---
_id: '14794'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the sparse
labeling of genetically defined neurons. We present a protocol for time-lapse
imaging of cortical projection neuron migration in mice using MADM. We describe
steps for the isolation, culturing, and 4D imaging of neuronal dynamics in MADM-labeled
brain tissue. While this protocol is compatible with other single-cell labeling
methods, the MADM approach provides a genetic platform for the functional assessment
of cell-autonomous candidate gene function and the relative contribution of non-cell-autonomous
effects.\r\n\r\nFor complete details on the use and execution of this protocol,
please refer to Hansen et al. (2022),1 Contreras et al. (2021),2 and Amberg and
Hippenmeyer (2021).3"
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We thank Florian Pauler for discussion and his expert technical support.
This research was supported by the Scientific Service Units (SSU) at IST Austria
through resources provided by the Imaging and Optics Facility (IOF) and Preclinical
Facility (PCF). A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian
Academy of Sciences.
article_number: '102795'
article_processing_charge: Yes
article_type: review
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Hippenmeyer S. Time-lapse imaging of cortical projection neuron
migration in mice using mosaic analysis with double markers. STAR Protocols.
2024;5(1). doi:10.1016/j.xpro.2023.102795
apa: Hansen, A. H., & Hippenmeyer, S. (2024). Time-lapse imaging of cortical
projection neuron migration in mice using mosaic analysis with double markers.
STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102795
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical
Projection Neuron Migration in Mice Using Mosaic Analysis with Double Markers.”
STAR Protocols. Elsevier, 2024. https://doi.org/10.1016/j.xpro.2023.102795.
ieee: A. H. Hansen and S. Hippenmeyer, “Time-lapse imaging of cortical projection
neuron migration in mice using mosaic analysis with double markers,” STAR Protocols,
vol. 5, no. 1. Elsevier, 2024.
ista: Hansen AH, Hippenmeyer S. 2024. Time-lapse imaging of cortical projection
neuron migration in mice using mosaic analysis with double markers. STAR Protocols.
5(1), 102795.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Time-Lapse Imaging of Cortical Projection
Neuron Migration in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols,
vol. 5, no. 1, 102795, Elsevier, 2024, doi:10.1016/j.xpro.2023.102795.
short: A.H. Hansen, S. Hippenmeyer, STAR Protocols 5 (2024).
date_created: 2024-01-14T23:00:56Z
date_published: 2024-01-01T00:00:00Z
date_updated: 2024-01-17T10:32:31Z
day: '01'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102795
external_id:
pmid:
- '38165800'
intvolume: ' 5'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102795
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
publication: STAR Protocols
publication_identifier:
eissn:
- 2666-1667
publication_status: epub_ahead
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- relation: software
url: http://github.com/hippenmeyerlab
scopus_import: '1'
status: public
title: Time-lapse imaging of cortical projection neuron migration in mice using mosaic
analysis with double markers
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2024'
...
---
_id: '12875'
abstract:
- lang: eng
text: The superior colliculus (SC) in the mammalian midbrain is essential for multisensory
integration and is composed of a rich diversity of excitatory and inhibitory neurons
and glia. However, the developmental principles directing the generation of SC
cell-type diversity are not understood. Here, we pursued systematic cell lineage
tracing in silico and in vivo, preserving full spatial information, using genetic
mosaic analysis with double markers (MADM)-based clonal analysis with single-cell
sequencing (MADM-CloneSeq). The analysis of clonally related cell lineages revealed
that radial glial progenitors (RGPs) in SC are exceptionally multipotent. Individual
resident RGPs have the capacity to produce all excitatory and inhibitory SC neuron
types, even at the stage of terminal division. While individual clonal units show
no pre-defined cellular composition, the establishment of appropriate relative
proportions of distinct neuronal types occurs in a PTEN-dependent manner. Collectively,
our findings provide an inaugural framework at the single-RGP/-cell level of the
mammalian SC ontogeny.
acknowledged_ssus:
- _id: Bio
- _id: M-Shop
- _id: LifeSc
- _id: PreCl
acknowledgement: "We thank Liqun Luo for his continued support, for providing essential
resources for generating Fzd10-CreER mice which were generated in his laboratory,
and for comments on the manuscript; W. Zhong for providing Nestin-Cre transgenic
mouse line for this study; A. Heger for mouse colony management; R. Beattie and
T. Asenov for designing and producing components of acute slice recovery chamber
for MADM-CloneSeq experiments; and K. Leopold, J. Rodarte and N. Amberg for initial
experiments, technical support and/or assistance. This study was supported by the
Scientific Service Units (SSU) of IST Austria through resources provided by the
Imaging & Optics Facility (IOF), Laboratory Support Facility (LSF), Miba Machine
Shop, and Pre-clinical Facility (PCF). G.C. received funding from European Commission
(IST plus postdoctoral fellowship). This work was supported by ISTA institutional\r\nfunds;
the Austrian Science Fund Special Research Programmes (FWF SFB F78 Neuro Stem Modulation)
to S.H. "
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Peter
full_name: Koppensteiner, Peter
id: 3B8B25A8-F248-11E8-B48F-1D18A9856A87
last_name: Koppensteiner
orcid: 0000-0002-3509-1948
- first_name: Thomas
full_name: Krausgruber, Thomas
last_name: Krausgruber
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Martin
full_name: Schrammel, Martin
id: f13e7cae-e8bd-11ed-841a-96dedf69f46d
last_name: Schrammel
- first_name: Natalie Y
full_name: Özgen, Natalie Y
id: e68ece33-f6e0-11ea-865d-ae1031dcc090
last_name: Özgen
- first_name: Alexis
full_name: Ivec, Alexis
id: 1d144691-e8be-11ed-9b33-bdd3077fad4c
last_name: Ivec
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Ryuichi
full_name: Shigemoto, Ryuichi
id: 499F3ABC-F248-11E8-B48F-1D18A9856A87
last_name: Shigemoto
orcid: 0000-0001-8761-9444
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Cheung GT, Pauler F, Koppensteiner P, et al. Multipotent progenitors instruct
ontogeny of the superior colliculus. Neuron. 2024;112(2):230-246.e11. doi:10.1016/j.neuron.2023.11.009
apa: Cheung, G. T., Pauler, F., Koppensteiner, P., Krausgruber, T., Streicher, C.,
Schrammel, M., … Hippenmeyer, S. (2024). Multipotent progenitors instruct ontogeny
of the superior colliculus. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.11.009
chicago: Cheung, Giselle T, Florian Pauler, Peter Koppensteiner, Thomas Krausgruber,
Carmen Streicher, Martin Schrammel, Natalie Y Özgen, et al. “Multipotent Progenitors
Instruct Ontogeny of the Superior Colliculus.” Neuron. Elsevier, 2024.
https://doi.org/10.1016/j.neuron.2023.11.009.
ieee: G. T. Cheung et al., “Multipotent progenitors instruct ontogeny of
the superior colliculus,” Neuron, vol. 112, no. 2. Elsevier, p. 230–246.e11,
2024.
ista: Cheung GT, Pauler F, Koppensteiner P, Krausgruber T, Streicher C, Schrammel
M, Özgen NY, Ivec A, Bock C, Shigemoto R, Hippenmeyer S. 2024. Multipotent progenitors
instruct ontogeny of the superior colliculus. Neuron. 112(2), 230–246.e11.
mla: Cheung, Giselle T., et al. “Multipotent Progenitors Instruct Ontogeny of the
Superior Colliculus.” Neuron, vol. 112, no. 2, Elsevier, 2024, p. 230–246.e11,
doi:10.1016/j.neuron.2023.11.009.
short: G.T. Cheung, F. Pauler, P. Koppensteiner, T. Krausgruber, C. Streicher, M.
Schrammel, N.Y. Özgen, A. Ivec, C. Bock, R. Shigemoto, S. Hippenmeyer, Neuron
112 (2024) 230–246.e11.
date_created: 2023-04-27T09:41:48Z
date_published: 2024-01-17T00:00:00Z
date_updated: 2024-03-05T09:43:02Z
day: '17'
ddc:
- '570'
department:
- _id: SiHi
- _id: RySh
doi: 10.1016/j.neuron.2023.11.009
external_id:
pmid:
- '38096816'
file:
- access_level: open_access
checksum: 32b3788f7085cf44a84108d8faaff3ce
content_type: application/pdf
creator: dernst
date_created: 2024-02-06T13:56:15Z
date_updated: 2024-02-06T13:56:15Z
file_id: '14944'
file_name: 2024_Neuron_Cheung.pdf
file_size: 5942467
relation: main_file
success: 1
file_date_updated: 2024-02-06T13:56:15Z
has_accepted_license: '1'
intvolume: ' 112'
issue: '2'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
page: 230-246.e11
pmid: 1
project:
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/the-pedigree-of-brain-cells/
scopus_import: '1'
status: public
title: Multipotent progenitors instruct ontogeny of the superior colliculus
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 112
year: '2024'
...
---
_id: '12542'
abstract:
- lang: eng
text: In this issue of Neuron, Espinosa-Medina et al.1 present the TEMPO (Temporal
Encoding and Manipulation in a Predefined Order) system, which enables the marking
and genetic manipulation of sequentially generated cell lineages in vertebrate
species in vivo.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Ana
full_name: Villalba Requena, Ana
id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247
last_name: Villalba Requena
orcid: 0000-0002-5615-5277
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Villalba Requena A, Hippenmeyer S. Going back in time with TEMPO. Neuron.
2023;111(3):291-293. doi:10.1016/j.neuron.2023.01.006
apa: Villalba Requena, A., & Hippenmeyer, S. (2023). Going back in time with
TEMPO. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2023.01.006
chicago: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with
TEMPO.” Neuron. Elsevier, 2023. https://doi.org/10.1016/j.neuron.2023.01.006.
ieee: A. Villalba Requena and S. Hippenmeyer, “Going back in time with TEMPO,” Neuron,
vol. 111, no. 3. Elsevier, pp. 291–293, 2023.
ista: Villalba Requena A, Hippenmeyer S. 2023. Going back in time with TEMPO. Neuron.
111(3), 291–293.
mla: Villalba Requena, Ana, and Simon Hippenmeyer. “Going Back in Time with TEMPO.”
Neuron, vol. 111, no. 3, Elsevier, 2023, pp. 291–93, doi:10.1016/j.neuron.2023.01.006.
short: A. Villalba Requena, S. Hippenmeyer, Neuron 111 (2023) 291–293.
date_created: 2023-02-12T23:00:58Z
date_published: 2023-02-01T00:00:00Z
date_updated: 2023-08-01T13:10:27Z
day: '01'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2023.01.006
external_id:
isi:
- '000994473300001'
intvolume: ' 111'
isi: 1
issue: '3'
language:
- iso: eng
month: '02'
oa_version: None
page: 291-293
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Going back in time with TEMPO
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 111
year: '2023'
...
---
_id: '12679'
abstract:
- lang: eng
text: How to generate a brain of correct size and with appropriate cell-type diversity
during development is a major question in Neuroscience. In the developing neocortex,
radial glial progenitor (RGP) cells are the main neural stem cells that produce
cortical excitatory projection neurons, glial cells, and establish the prospective
postnatal stem cell niche in the lateral ventricles. RGPs follow a tightly orchestrated
developmental program that when disrupted can result in severe cortical malformations
such as microcephaly and megalencephaly. The precise cellular and molecular mechanisms
instructing faithful RGP lineage progression are however not well understood.
This review will summarize recent conceptual advances that contribute to our understanding
of the general principles of RGP lineage progression.
acknowledgement: "I wish to thank all current and past members of the Hippenmeyer
laboratory at ISTA for exciting discussions on the subject of this review. I apologize
to colleagues whose work I could not cite and/or discuss in the frame of the available
space. Work in the Hippenmeyer laboratory on the\r\ndiscussed topic is supported
by ISTA institutional funds, FWF SFB F78 to S.H., and the European Research Council
(ERC) under the European Union’s Horizon 2020 Research and Innovation Programme
(grant agree-ment no. 725780 LinPro) to SH."
article_number: '102695'
article_processing_charge: Yes (via OA deal)
article_type: review
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Hippenmeyer S. Principles of neural stem cell lineage progression: Insights
from developing cerebral cortex. Current Opinion in Neurobiology. 2023;79(4).
doi:10.1016/j.conb.2023.102695'
apa: 'Hippenmeyer, S. (2023). Principles of neural stem cell lineage progression:
Insights from developing cerebral cortex. Current Opinion in Neurobiology.
Elsevier. https://doi.org/10.1016/j.conb.2023.102695'
chicago: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression:
Insights from Developing Cerebral Cortex.” Current Opinion in Neurobiology.
Elsevier, 2023. https://doi.org/10.1016/j.conb.2023.102695.'
ieee: 'S. Hippenmeyer, “Principles of neural stem cell lineage progression: Insights
from developing cerebral cortex,” Current Opinion in Neurobiology, vol.
79, no. 4. Elsevier, 2023.'
ista: 'Hippenmeyer S. 2023. Principles of neural stem cell lineage progression:
Insights from developing cerebral cortex. Current Opinion in Neurobiology. 79(4),
102695.'
mla: 'Hippenmeyer, Simon. “Principles of Neural Stem Cell Lineage Progression: Insights
from Developing Cerebral Cortex.” Current Opinion in Neurobiology, vol.
79, no. 4, 102695, Elsevier, 2023, doi:10.1016/j.conb.2023.102695.'
short: S. Hippenmeyer, Current Opinion in Neurobiology 79 (2023).
date_created: 2023-02-26T12:24:21Z
date_published: 2023-04-01T00:00:00Z
date_updated: 2023-08-16T12:30:25Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.conb.2023.102695
ec_funded: 1
external_id:
isi:
- '000953497700001'
pmid:
- '36842274'
file:
- access_level: open_access
checksum: 4d11c4ca87e6cbc4d2ac46d3225ea615
content_type: application/pdf
creator: dernst
date_created: 2023-08-16T12:29:06Z
date_updated: 2023-08-16T12:29:06Z
file_id: '14071'
file_name: 2023_CurrentOpinionNeurobio_Hippenmeyer.pdf
file_size: 1787894
relation: main_file
success: 1
file_date_updated: 2023-08-16T12:29:06Z
has_accepted_license: '1'
intvolume: ' 79'
isi: 1
issue: '4'
keyword:
- General Neuroscience
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Current Opinion in Neurobiology
publication_identifier:
issn:
- 0959-4388
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Principles of neural stem cell lineage progression: Insights from developing
cerebral cortex'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 79
year: '2023'
...
---
_id: '12562'
abstract:
- lang: eng
text: Presynaptic inputs determine the pattern of activation of postsynaptic neurons
in a neural circuit. Molecular and genetic pathways that regulate the selective
formation of subsets of presynaptic inputs are largely unknown, despite significant
understanding of the general process of synaptogenesis. In this study, we have
begun to identify such factors using the spinal monosynaptic stretch reflex circuit
as a model system. In this neuronal circuit, Ia proprioceptive afferents establish
monosynaptic connections with spinal motor neurons that project to the same muscle
(termed homonymous connections) or muscles with related or synergistic function.
However, monosynaptic connections are not formed with motor neurons innervating
muscles with antagonistic functions. The ETS transcription factor ER81 (also known
as ETV1) is expressed by all proprioceptive afferents, but only a small set of
motor neuron pools in the lumbar spinal cord of the mouse. Here we use conditional
mouse genetic techniques to eliminate Er81 expression selectively from motor neurons.
We find that ablation of Er81 in motor neurons reduces synaptic inputs from proprioceptive
afferents conveying information from homonymous and synergistic muscles, with
no change observed in the connectivity pattern from antagonistic proprioceptive
afferents. In summary, these findings suggest a role for ER81 in defined motor
neuron pools to control the assembly of specific presynaptic inputs and thereby
influence the profile of activation of these motor neurons.
acknowledgement: The authors gratefully thank Dr. Silvia Arber, University of Basel
and Friedrich Miescher Institute for Biomedical Research, for support and in whose
lab the data were collected. For advice on statistical analysis, we thank Michael
Bottomley from the Statistical Consulting Center, College of Science and Mathematics,
Wright State University.
article_processing_charge: No
article_type: original
author:
- first_name: David R.
full_name: Ladle, David R.
last_name: Ladle
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Ladle DR, Hippenmeyer S. Loss of ETV1/ER81 in motor neurons leads to reduced
monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology.
2023;129(3):501-512. doi:10.1152/jn.00172.2022
apa: Ladle, D. R., & Hippenmeyer, S. (2023). Loss of ETV1/ER81 in motor neurons
leads to reduced monosynaptic inputs from proprioceptive sensory neurons. Journal
of Neurophysiology. American Physiological Society. https://doi.org/10.1152/jn.00172.2022
chicago: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal
of Neurophysiology. American Physiological Society, 2023. https://doi.org/10.1152/jn.00172.2022.
ieee: D. R. Ladle and S. Hippenmeyer, “Loss of ETV1/ER81 in motor neurons leads
to reduced monosynaptic inputs from proprioceptive sensory neurons,” Journal
of Neurophysiology, vol. 129, no. 3. American Physiological Society, pp. 501–512,
2023.
ista: Ladle DR, Hippenmeyer S. 2023. Loss of ETV1/ER81 in motor neurons leads to
reduced monosynaptic inputs from proprioceptive sensory neurons. Journal of Neurophysiology.
129(3), 501–512.
mla: Ladle, David R., and Simon Hippenmeyer. “Loss of ETV1/ER81 in Motor Neurons
Leads to Reduced Monosynaptic Inputs from Proprioceptive Sensory Neurons.” Journal
of Neurophysiology, vol. 129, no. 3, American Physiological Society, 2023,
pp. 501–12, doi:10.1152/jn.00172.2022.
short: D.R. Ladle, S. Hippenmeyer, Journal of Neurophysiology 129 (2023) 501–512.
date_created: 2023-02-15T14:46:14Z
date_published: 2023-03-01T00:00:00Z
date_updated: 2023-09-05T12:13:34Z
day: '01'
department:
- _id: SiHi
doi: 10.1152/jn.00172.2022
external_id:
isi:
- '000957721600001'
pmid:
- '36695533'
intvolume: ' 129'
isi: 1
issue: '3'
keyword:
- Physiology
- General Neuroscience
language:
- iso: eng
month: '03'
oa_version: None
page: 501-512
pmid: 1
publication: Journal of Neurophysiology
publication_identifier:
eissn:
- 1522-1598
issn:
- 0022-3077
publication_status: published
publisher: American Physiological Society
quality_controlled: '1'
status: public
title: Loss of ETV1/ER81 in motor neurons leads to reduced monosynaptic inputs from
proprioceptive sensory neurons
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 129
year: '2023'
...
---
_id: '14647'
abstract:
- lang: eng
text: In the developing vertebrate central nervous system, neurons and glia typically
arise sequentially from common progenitors. Here, we report that the transcription
factor Forkhead Box G1 (Foxg1) regulates gliogenesis in the mouse neocortex via
distinct cell-autonomous roles in progenitors and in postmitotic neurons that
regulate different aspects of the gliogenic FGF signalling pathway. We demonstrate
that loss of Foxg1 in cortical progenitors at neurogenic stages causes premature
astrogliogenesis. We identify a novel FOXG1 target, the pro-gliogenic FGF pathway
component Fgfr3, which is suppressed by FOXG1 cell-autonomously to maintain neurogenesis.
Furthermore, FOXG1 can also suppress premature astrogliogenesis triggered by the
augmentation of FGF signalling. We identify a second novel function of FOXG1 in
regulating the expression of gliogenic ligand FGF18 in new born neocortical upper-layer
neurons. Loss of FOXG1 in postmitotic neurons increases Fgf18 expression and enhances
gliogenesis in the progenitors. These results fit well with the model that new
born neurons secrete cues that trigger progenitors to produce the next wave of
cell types, astrocytes. If FGF signalling is attenuated in Foxg1 null progenitors,
they progress to oligodendrocyte production. Therefore, loss of FOXG1 transitions
the progenitor to a gliogenic state, producing either astrocytes or oligodendrocytes
depending on FGF signalling levels. Our results uncover how FOXG1 integrates extrinsic
signalling via the FGF pathway to regulate the sequential generation of neurons,
astrocytes, and oligodendrocytes in the cerebral cortex.
acknowledgement: "We thank Dr. Shital Suryavanshi and the animal house staff of the
Tata Institute of\r\nFundamental Research (TIFR) for their excellent support; Gord
Fishell and Goichi Miyoshi for\r\nthe Foxg1 floxed mouse line; Hiroshi Kawasaki
for the plasmids pCAG-FGF8 and pCAGsFGFR3c. We thank Prof. S.K. Lee for the Foxg1lox/lox
genotyping primers and protocol. We thank Dr. Deepak Modi and Dr. Vainav Patel for
allowing us to use the NIRRCH FACS Facility and the staff of the NIRRCH and TIFR
FACS facilities for their assistance.\r\nWe thank Denis Jabaudon for his critical
comments on the manuscript and members of the\r\nJabaudon lab for helpful discussions.
This work was funded by the Department of Atomic\r\nEnergy (DAE), Govt. of India
(Project Identification no. RTI4003, DAE OM no.\r\n1303/2/2019/R&D-II/DAE/2079)."
article_processing_charge: No
author:
- first_name: Mahima
full_name: Bose, Mahima
last_name: Bose
- first_name: Varun
full_name: Suresh, Varun
last_name: Suresh
- first_name: Urvi
full_name: Mishra, Urvi
last_name: Mishra
- first_name: Ishita
full_name: Talwar, Ishita
last_name: Talwar
- first_name: Anuradha
full_name: Yadav, Anuradha
last_name: Yadav
- first_name: Shiona
full_name: Biswas, Shiona
last_name: Biswas
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Shubha
full_name: Tole, Shubha
last_name: Tole
citation:
ama: Bose M, Suresh V, Mishra U, et al. Dual role of FOXG1 in regulating gliogenesis
in the developing neocortex via the FGF signalling pathway. bioRxiv. doi:10.1101/2023.11.30.569337
apa: Bose, M., Suresh, V., Mishra, U., Talwar, I., Yadav, A., Biswas, S., … Tole,
S. (n.d.). Dual role of FOXG1 in regulating gliogenesis in the developing neocortex
via the FGF signalling pathway. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2023.11.30.569337
chicago: Bose, Mahima, Varun Suresh, Urvi Mishra, Ishita Talwar, Anuradha Yadav,
Shiona Biswas, Simon Hippenmeyer, and Shubha Tole. “Dual Role of FOXG1 in Regulating
Gliogenesis in the Developing Neocortex via the FGF Signalling Pathway.” BioRxiv.
Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2023.11.30.569337.
ieee: M. Bose et al., “Dual role of FOXG1 in regulating gliogenesis in the
developing neocortex via the FGF signalling pathway,” bioRxiv. Cold Spring
Harbor Laboratory.
ista: Bose M, Suresh V, Mishra U, Talwar I, Yadav A, Biswas S, Hippenmeyer S, Tole
S. Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via
the FGF signalling pathway. bioRxiv, 10.1101/2023.11.30.569337.
mla: Bose, Mahima, et al. “Dual Role of FOXG1 in Regulating Gliogenesis in the Developing
Neocortex via the FGF Signalling Pathway.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/2023.11.30.569337.
short: M. Bose, V. Suresh, U. Mishra, I. Talwar, A. Yadav, S. Biswas, S. Hippenmeyer,
S. Tole, BioRxiv (n.d.).
date_created: 2023-12-06T13:07:01Z
date_published: 2023-12-01T00:00:00Z
date_updated: 2023-12-11T07:37:17Z
day: '01'
department:
- _id: SiHi
doi: 10.1101/2023.11.30.569337
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2023.11.30.569337
month: '12'
oa: 1
oa_version: Preprint
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Dual role of FOXG1 in regulating gliogenesis in the developing neocortex via
the FGF signalling pathway
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '14683'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice and high-resolution phenotyping at the individual
cell level. Here, we present a protocol for isolating MADM-labeled cells with
high yield for downstream molecular analyses using fluorescence-activated cell
sorting (FACS). We describe steps for generating MADM-labeled mice, perfusion,
single-cell suspension, and debris removal. We then detail procedures for cell
sorting by FACS and downstream analysis. This protocol is suitable for embryonic
to adult mice.\r\nFor complete details on the use and execution of this protocol,
please refer to Contreras et al. (2021).1"
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Imaging & Optics Facility (IOF)
and Preclinical Facilities (PCF). N.A. received support from FWF Firnberg-Programme
(T 1031). G.C. received support from the European Union’s Horizon 2020 research
and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411
as an ISTplus postdoctoral fellow. This work was also supported by IST Austria institutional
funds, FWF SFB F78 to S.H., and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation programme (grant agreement no. 725780
LinPro) to S.H.
article_number: '102771'
article_processing_charge: No
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Cheung GT, Hippenmeyer S. Protocol for sorting cells from mouse brains
labeled with mosaic analysis with double markers by flow cytometry. STAR Protocols.
2023;5(1). doi:10.1016/j.xpro.2023.102771
apa: Amberg, N., Cheung, G. T., & Hippenmeyer, S. (2023). Protocol for sorting
cells from mouse brains labeled with mosaic analysis with double markers by flow
cytometry. STAR Protocols. Elsevier. https://doi.org/10.1016/j.xpro.2023.102771
chicago: Amberg, Nicole, Giselle T Cheung, and Simon Hippenmeyer. “Protocol for
Sorting Cells from Mouse Brains Labeled with Mosaic Analysis with Double Markers
by Flow Cytometry.” STAR Protocols. Elsevier, 2023. https://doi.org/10.1016/j.xpro.2023.102771.
ieee: N. Amberg, G. T. Cheung, and S. Hippenmeyer, “Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry,”
STAR Protocols, vol. 5, no. 1. Elsevier, 2023.
ista: Amberg N, Cheung GT, Hippenmeyer S. 2023. Protocol for sorting cells from
mouse brains labeled with mosaic analysis with double markers by flow cytometry.
STAR Protocols. 5(1), 102771.
mla: Amberg, Nicole, et al. “Protocol for Sorting Cells from Mouse Brains Labeled
with Mosaic Analysis with Double Markers by Flow Cytometry.” STAR Protocols,
vol. 5, no. 1, 102771, Elsevier, 2023, doi:10.1016/j.xpro.2023.102771.
short: N. Amberg, G.T. Cheung, S. Hippenmeyer, STAR Protocols 5 (2023).
date_created: 2023-12-13T11:48:05Z
date_published: 2023-12-08T00:00:00Z
date_updated: 2023-12-18T08:06:14Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2023.102771
ec_funded: 1
external_id:
pmid:
- '38070137'
intvolume: ' 5'
issue: '1'
keyword:
- General Immunology and Microbiology
- General Biochemistry
- Genetics and Molecular Biology
- General Neuroscience
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.xpro.2023.102771
month: '12'
oa: 1
oa_version: Submitted Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: epub_ahead
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Protocol for sorting cells from mouse brains labeled with mosaic analysis with
double markers by flow cytometry
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2023'
...
---
_id: '14757'
abstract:
- lang: eng
text: The cerebral cortex is comprised of a vast cell-type diversity sequentially
generated by cortical progenitor cells. Faithful progenitor lineage progression
requires the tight orchestration of distinct molecular and cellular mechanisms
regulating proper progenitor proliferation behavior and differentiation. Correct
execution of developmental programs involves a complex interplay of cell intrinsic
and tissue-wide mechanisms. Many studies over the past decades have been able
to determine a plethora of genes critically involved in cortical development.
However, only a few made use of genetic paradigms with sparse and global gene
deletion to probe cell-autonomous vs. tissue-wide contribution. In this chapter,
we will elaborate on the importance of dissecting the cell-autonomous and tissue-wide
mechanisms to gain a precise understanding of gene function during radial glial
progenitor lineage progression.
article_processing_charge: No
author:
- first_name: Ana
full_name: Villalba Requena, Ana
id: 68cb85a0-39f7-11eb-9559-9aaab4f6a247
last_name: Villalba Requena
orcid: 0000-0002-5615-5277
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Villalba Requena A, Amberg N, Hippenmeyer S. Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression. In: Huttner W, ed. Neocortical Neurogenesis in Development and
Evolution. Wiley; 2023:169-191. doi:10.1002/9781119860914.ch10'
apa: Villalba Requena, A., Amberg, N., & Hippenmeyer, S. (2023). Interplay of
Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial
Progenitor Lineage Progression. In W. Huttner (Ed.), Neocortical Neurogenesis
in Development and Evolution (pp. 169–191). Wiley. https://doi.org/10.1002/9781119860914.ch10
chicago: Villalba Requena, Ana, Nicole Amberg, and Simon Hippenmeyer. “Interplay
of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating Radial
Glial Progenitor Lineage Progression.” In Neocortical Neurogenesis in Development
and Evolution, edited by Wieland Huttner, 169–91. Wiley, 2023. https://doi.org/10.1002/9781119860914.ch10.
ieee: A. Villalba Requena, N. Amberg, and S. Hippenmeyer, “Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression,” in Neocortical Neurogenesis in Development and Evolution,
W. Huttner, Ed. Wiley, 2023, pp. 169–191.
ista: 'Villalba Requena A, Amberg N, Hippenmeyer S. 2023.Interplay of Cell‐autonomous
Gene Function and Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage
Progression. In: Neocortical Neurogenesis in Development and Evolution. , 169–191.'
mla: Villalba Requena, Ana, et al. “Interplay of Cell‐autonomous Gene Function and
Tissue‐wide Mechanisms Regulating Radial Glial Progenitor Lineage Progression.”
Neocortical Neurogenesis in Development and Evolution, edited by Wieland
Huttner, Wiley, 2023, pp. 169–91, doi:10.1002/9781119860914.ch10.
short: A. Villalba Requena, N. Amberg, S. Hippenmeyer, in:, W. Huttner (Ed.), Neocortical
Neurogenesis in Development and Evolution, Wiley, 2023, pp. 169–191.
date_created: 2024-01-08T13:16:36Z
date_published: 2023-08-08T00:00:00Z
date_updated: 2024-01-09T09:46:57Z
day: '08'
department:
- _id: SiHi
doi: 10.1002/9781119860914.ch10
editor:
- first_name: Wieland
full_name: Huttner, Wieland
last_name: Huttner
language:
- iso: eng
month: '08'
oa_version: None
page: 169-191
publication: Neocortical Neurogenesis in Development and Evolution
publication_identifier:
eisbn:
- '9781119860914'
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Interplay of Cell‐autonomous Gene Function and Tissue‐wide Mechanisms Regulating
Radial Glial Progenitor Lineage Progression
type: book_chapter
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2023'
...
---
_id: '12802'
abstract:
- lang: eng
text: Little is known about the critical metabolic changes that neural cells have
to undergo during development and how temporary shifts in this program can influence
brain circuitries and behavior. Inspired by the discovery that mutations in SLC7A5,
a transporter of metabolically essential large neutral amino acids (LNAAs), lead
to autism, we employed metabolomic profiling to study the metabolic states of
the cerebral cortex across different developmental stages. We found that the forebrain
undergoes significant metabolic remodeling throughout development, with certain
groups of metabolites showing stage-specific changes, but what are the consequences
of perturbing this metabolic program? By manipulating Slc7a5 expression in neural
cells, we found that the metabolism of LNAAs and lipids are interconnected in
the cortex. Deletion of Slc7a5 in neurons affects the postnatal metabolic state,
leading to a shift in lipid metabolism. Additionally, it causes stage- and cell-type-specific
alterations in neuronal activity patterns, resulting in a long-term circuit dysfunction.
acknowledged_ssus:
- _id: PreCl
- _id: EM-Fac
- _id: Bio
- _id: LifeSc
acknowledgement: We thank A. Freeman and V. Voronin for technical assistance, S. Deixler,
A. Stichelberger, M. Schunn, and the Preclinical Facility for managing our animal
colony. We thank L. Andersen and J. Sonntag, who were involved in generating the
MADM lines. We thank the ISTA LSF Mass Spectrometry Core Facility for assistance
with the proteomic analysis, as well as the ISTA electron microscopy and Imaging
and Optics facility for technical support. Metabolomics LC-MS/MS analysis was performed
by the Metabolomics Facility at Vienna BioCenter Core Facilities (VBCF). We acknowledge
the support of the EMBL Metabolomics Core Facility (MCF) for lipidomics and intracellular
metabolomics mass spectrometry data acquisition and analysis. RNA sequencing was
performed by the Next Generation Sequencing Facility at VBCF. Schematics were generated
using Biorender.com. This work was supported by the Austrian Science Fund (FWF,
DK W1232-B24) and by the European Union’s Horizon 2020 research and innovation program
(ERC) grant 725780 (LinPro) to S.H. and 715508 (REVERSEAUTISM) to G.N.
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Lisa
full_name: Knaus, Lisa
id: 3B2ABCF4-F248-11E8-B48F-1D18A9856A87
last_name: Knaus
- first_name: Bernadette
full_name: Basilico, Bernadette
id: 36035796-5ACA-11E9-A75E-7AF2E5697425
last_name: Basilico
orcid: 0000-0003-1843-3173
- first_name: Daniel
full_name: Malzl, Daniel
last_name: Malzl
- first_name: Maria
full_name: Gerykova Bujalkova, Maria
last_name: Gerykova Bujalkova
- first_name: Mateja
full_name: Smogavec, Mateja
last_name: Smogavec
- first_name: Lena A.
full_name: Schwarz, Lena A.
last_name: Schwarz
- first_name: Sarah
full_name: Gorkiewicz, Sarah
id: f141a35d-15a9-11ec-9fb2-fef6becc7b6f
last_name: Gorkiewicz
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Christian
full_name: Knittl-Frank, Christian
last_name: Knittl-Frank
- first_name: Marianna
full_name: Tassinari, Marianna
id: 7af593f1-d44a-11ed-bf94-a3646a6bb35e
last_name: Tassinari
- first_name: Nuno
full_name: Maulide, Nuno
last_name: Maulide
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Jörg
full_name: Menche, Jörg
last_name: Menche
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Knaus L, Basilico B, Malzl D, et al. Large neutral amino acid levels tune perinatal
neuronal excitability and survival. Cell. 2023;186(9):1950-1967.e25. doi:10.1016/j.cell.2023.02.037
apa: Knaus, L., Basilico, B., Malzl, D., Gerykova Bujalkova, M., Smogavec, M., Schwarz,
L. A., … Novarino, G. (2023). Large neutral amino acid levels tune perinatal neuronal
excitability and survival. Cell. Elsevier. https://doi.org/10.1016/j.cell.2023.02.037
chicago: Knaus, Lisa, Bernadette Basilico, Daniel Malzl, Maria Gerykova Bujalkova,
Mateja Smogavec, Lena A. Schwarz, Sarah Gorkiewicz, et al. “Large Neutral Amino
Acid Levels Tune Perinatal Neuronal Excitability and Survival.” Cell. Elsevier,
2023. https://doi.org/10.1016/j.cell.2023.02.037.
ieee: L. Knaus et al., “Large neutral amino acid levels tune perinatal neuronal
excitability and survival,” Cell, vol. 186, no. 9. Elsevier, p. 1950–1967.e25,
2023.
ista: Knaus L, Basilico B, Malzl D, Gerykova Bujalkova M, Smogavec M, Schwarz LA,
Gorkiewicz S, Amberg N, Pauler F, Knittl-Frank C, Tassinari M, Maulide N, Rülicke
T, Menche J, Hippenmeyer S, Novarino G. 2023. Large neutral amino acid levels
tune perinatal neuronal excitability and survival. Cell. 186(9), 1950–1967.e25.
mla: Knaus, Lisa, et al. “Large Neutral Amino Acid Levels Tune Perinatal Neuronal
Excitability and Survival.” Cell, vol. 186, no. 9, Elsevier, 2023, p. 1950–1967.e25,
doi:10.1016/j.cell.2023.02.037.
short: L. Knaus, B. Basilico, D. Malzl, M. Gerykova Bujalkova, M. Smogavec, L.A.
Schwarz, S. Gorkiewicz, N. Amberg, F. Pauler, C. Knittl-Frank, M. Tassinari, N.
Maulide, T. Rülicke, J. Menche, S. Hippenmeyer, G. Novarino, Cell 186 (2023) 1950–1967.e25.
date_created: 2023-04-05T08:15:40Z
date_published: 2023-04-27T00:00:00Z
date_updated: 2024-02-07T08:03:32Z
day: '27'
ddc:
- '570'
department:
- _id: SiHi
- _id: GaNo
doi: 10.1016/j.cell.2023.02.037
ec_funded: 1
external_id:
isi:
- '000991468700001'
file:
- access_level: open_access
checksum: 47e94fbe19e86505b429cb7a5b503ce6
content_type: application/pdf
creator: dernst
date_created: 2023-05-02T09:26:21Z
date_updated: 2023-05-02T09:26:21Z
file_id: '12889'
file_name: 2023_Cell_Knaus.pdf
file_size: 15712841
relation: main_file
success: 1
file_date_updated: 2023-05-02T09:26:21Z
has_accepted_license: '1'
intvolume: ' 186'
isi: 1
issue: '9'
keyword:
- General Biochemistry
- Genetics and Molecular Biology
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 1950-1967.e25
project:
- _id: 2548AE96-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: W1232-B24
name: Molecular Drug Targets
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25444568-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '715508'
name: Probing the Reversibility of Autism Spectrum Disorders by Employing in vivo
and in vitro Models
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on ISTA Website
relation: press_release
url: https://ista.ac.at/en/news/feed-them-or-lose-them/
record:
- id: '13107'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Large neutral amino acid levels tune perinatal neuronal excitability and survival
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 186
year: '2023'
...
---
_id: '11336'
abstract:
- lang: eng
text: The generation of a correctly-sized cerebral cortex with all-embracing neuronal
and glial cell-type diversity critically depends on faithful radial glial progenitor
(RGP) cell proliferation/differentiation programs. Temporal RGP lineage progression
is regulated by Polycomb Repressive Complex 2 (PRC2) and loss of PRC2 activity
results in severe neurogenesis defects and microcephaly. How PRC2-dependent gene
expression instructs RGP lineage progression is unknown. Here we utilize Mosaic
Analysis with Double Markers (MADM)-based single cell technology and demonstrate
that PRC2 is not cell-autonomously required in neurogenic RGPs but rather acts
at the global tissue-wide level. Conversely, cortical astrocyte production and
maturation is cell-autonomously controlled by PRC2-dependent transcriptional regulation.
We thus reveal highly distinct and sequential PRC2 functions in RGP lineage progression
that are dependent on complex interplays between intrinsic and tissue-wide properties.
In a broader context our results imply a critical role for the genetic and cellular
niche environment in neural stem cell behavior.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
- _id: LifeSc
acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and
C. Czepe (VBCF GmbH, NGS Unit) and S. Gharagozlou for technical support. This research was supported by the Scientific Service Units (SSU) of IST Austria through resources provided by the Imaging & Optics
Facility (IOF), Lab Support Facility (LSF), and Preclinical Facility (PCF). N.A.
received funding from the FWF Firnberg-Programm (T 1031). The work was supported by IST institutional funds and by the European Research Council (ERC) under the European Union’s Horizon
2020 research and innovation program (grant agreement 725780 LinPro) to S.H.
article_number: abq1263
article_processing_charge: No
article_type: original
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Pauler F, Streicher C, Hippenmeyer S. Tissue-wide genetic and cellular
landscape shapes the execution of sequential PRC2 functions in neural stem cell
lineage progression. Science Advances. 2022;8(44). doi:10.1126/sciadv.abq1263
apa: Amberg, N., Pauler, F., Streicher, C., & Hippenmeyer, S. (2022). Tissue-wide
genetic and cellular landscape shapes the execution of sequential PRC2 functions
in neural stem cell lineage progression. Science Advances. American Association
for the Advancement of Science. https://doi.org/10.1126/sciadv.abq1263
chicago: Amberg, Nicole, Florian Pauler, Carmen Streicher, and Simon Hippenmeyer.
“Tissue-Wide Genetic and Cellular Landscape Shapes the Execution of Sequential
PRC2 Functions in Neural Stem Cell Lineage Progression.” Science Advances.
American Association for the Advancement of Science, 2022. https://doi.org/10.1126/sciadv.abq1263.
ieee: N. Amberg, F. Pauler, C. Streicher, and S. Hippenmeyer, “Tissue-wide genetic
and cellular landscape shapes the execution of sequential PRC2 functions in neural
stem cell lineage progression,” Science Advances, vol. 8, no. 44. American
Association for the Advancement of Science, 2022.
ista: Amberg N, Pauler F, Streicher C, Hippenmeyer S. 2022. Tissue-wide genetic
and cellular landscape shapes the execution of sequential PRC2 functions in neural
stem cell lineage progression. Science Advances. 8(44), abq1263.
mla: Amberg, Nicole, et al. “Tissue-Wide Genetic and Cellular Landscape Shapes the
Execution of Sequential PRC2 Functions in Neural Stem Cell Lineage Progression.”
Science Advances, vol. 8, no. 44, abq1263, American Association for the
Advancement of Science, 2022, doi:10.1126/sciadv.abq1263.
short: N. Amberg, F. Pauler, C. Streicher, S. Hippenmeyer, Science Advances 8 (2022).
date_created: 2022-04-26T15:04:50Z
date_published: 2022-11-01T00:00:00Z
date_updated: 2023-05-31T12:24:10Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1126/sciadv.abq1263
ec_funded: 1
file:
- access_level: open_access
checksum: 0117023e188542082ca6693cf39e7f03
content_type: application/pdf
creator: patrickd
date_created: 2023-03-21T14:18:10Z
date_updated: 2023-03-21T14:18:10Z
file_id: '12742'
file_name: sciadv.abq1263.pdf
file_size: 2973998
relation: main_file
success: 1
file_date_updated: 2023-03-21T14:18:10Z
has_accepted_license: '1'
intvolume: ' 8'
issue: '44'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
publication: Science Advances
publication_identifier:
issn:
- 2375-2548
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
related_material:
link:
- description: News on ISTA website
relation: press_release
url: https://ista.ac.at/en/news/whole-tissue-shapes-brain-development/
scopus_import: '1'
status: public
title: Tissue-wide genetic and cellular landscape shapes the execution of sequential
PRC2 functions in neural stem cell lineage progression
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2022'
...
---
_id: '9794'
abstract:
- lang: eng
text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular
cells that form dedicated niches for immune cell interaction and capsular fibroblasts
that build a shell around the organ. Immunological challenge causes LNs to increase
more than tenfold in size within a few days. Here, we characterized the biomechanics
of LN swelling on the cellular and organ scale. We identified lymphocyte trapping
by influx and proliferation as drivers of an outward pressure force, causing fibroblastic
reticular cells of the T-zone (TRCs) and their associated conduits to stretch.
After an initial phase of relaxation, TRCs sensed the resulting strain through
cell matrix adhesions, which coordinated local growth and remodeling of the stromal
network. While the expanded TRC network readopted its typical configuration, a
massive fibrotic reaction of the organ capsule set in and countered further organ
expansion. Thus, different fibroblast populations mechanically control LN swelling
in a multitier fashion.'
acknowledged_ssus:
- _id: Bio
- _id: EM-Fac
- _id: PreCl
- _id: LifeSc
acknowledgement: This research was supported by the Scientific Service Units of IST
Austria through resources provided by the Imaging and Optics, Electron Microscopy,
Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd
antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing
a custom 3D channel alignment script. This work was supported by a European Research
Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR
20-24603Y and Charles University PRIMUS/20/MED/013.
article_processing_charge: No
article_type: original
author:
- first_name: Frank P
full_name: Assen, Frank P
id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87
last_name: Assen
orcid: 0000-0003-3470-6119
- first_name: Jun
full_name: Abe, Jun
last_name: Abe
- first_name: Miroslav
full_name: Hons, Miroslav
id: 4167FE56-F248-11E8-B48F-1D18A9856A87
last_name: Hons
orcid: 0000-0002-6625-3348
- first_name: Robert
full_name: Hauschild, Robert
id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87
last_name: Hauschild
orcid: 0000-0001-9843-3522
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Walter
full_name: Kaufmann, Walter
id: 3F99E422-F248-11E8-B48F-1D18A9856A87
last_name: Kaufmann
orcid: 0000-0001-9735-5315
- first_name: Tommaso
full_name: Costanzo, Tommaso
id: D93824F4-D9BA-11E9-BB12-F207E6697425
last_name: Costanzo
orcid: 0000-0001-9732-3815
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Markus
full_name: Brown, Markus
id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87
last_name: Brown
- first_name: Burkhard
full_name: Ludewig, Burkhard
last_name: Ludewig
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
- first_name: Wolfgang
full_name: Weninger, Wolfgang
last_name: Weninger
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Sanjiv A.
full_name: Luther, Sanjiv A.
last_name: Luther
- first_name: Jens V.
full_name: Stein, Jens V.
last_name: Stein
- first_name: Michael K
full_name: Sixt, Michael K
id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
last_name: Sixt
orcid: 0000-0002-4561-241X
citation:
ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4
apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W.,
… Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling
lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4
chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour,
Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal
Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature,
2022. https://doi.org/10.1038/s41590-022-01257-4.
ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations
in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature,
pp. 1246–1255, 2022.
ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T,
Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo
EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations
in swelling lymph nodes. Nature Immunology. 23, 1246–1255.
mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in
Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022,
pp. 1246–55, doi:10.1038/s41590-022-01257-4.
short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T.
Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg,
W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology
23 (2022) 1246–1255.
date_created: 2021-08-06T09:09:11Z
date_published: 2022-07-11T00:00:00Z
date_updated: 2023-08-02T06:53:07Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
- _id: CaHe
- _id: EdHa
- _id: EM-Fac
- _id: Bio
- _id: MiSi
doi: 10.1038/s41590-022-01257-4
ec_funded: 1
external_id:
isi:
- '000822975900002'
file:
- access_level: open_access
checksum: 628e7b49809f22c75b428842efe70c68
content_type: application/pdf
creator: dernst
date_created: 2022-07-25T07:11:32Z
date_updated: 2022-07-25T07:11:32Z
file_id: '11642'
file_name: 2022_NatureImmunology_Assen.pdf
file_size: 11475325
relation: main_file
success: 1
file_date_updated: 2022-07-25T07:11:32Z
has_accepted_license: '1'
intvolume: ' 23'
isi: 1
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 1246-1255
project:
- _id: 25FE9508-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '724373'
name: Cellular navigation along spatial gradients
publication: Nature Immunology
publication_identifier:
eissn:
- 1529-2916
issn:
- 1529-2908
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multitier mechanics control stromal adaptations in swelling lymph nodes
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 23
year: '2022'
...
---
_id: '11460'
abstract:
- lang: eng
text: "Background: Proper cerebral cortical development depends on the tightly orchestrated
migration of newly born neurons from the inner ventricular and subventricular
zones to the outer cortical plate. Any disturbance in this process during prenatal
stages may lead to neuronal migration disorders (NMDs), which can vary in extent
from focal to global. Furthermore, NMDs show a substantial comorbidity with other
neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous
work demonstrated focal neuronal migration defects in mice carrying loss-of-function
alleles of the recognized autism risk gene WDFY3. However, the cellular origins
of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide
critical insight into WDFY3-dependent disease pathology.\r\nMethods: Here, in
an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic
analysis with double markers (MADM). MADM technology enabled us to genetically
distinctly track and phenotypically analyze mutant and wild-type cells concomitantly
in vivo using immunofluorescent techniques.\r\nResults: We revealed a cell autonomous
requirement of WDFY3 for accurate laminar positioning of cortical projection neurons
and elimination of mispositioned cells during early postnatal life. In addition,
we identified significant deviations in dendritic arborization, as well as synaptic
density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant
neurons in Wdfy3-MADM reporter mice at postnatal stages.\r\nLimitations: While
Wdfy3 mutant mice have provided valuable insight into prenatal aspects of ASD
pathology that remain inaccessible to investigation in humans, like most animal
models, they do not a perfectly replicate all aspects of human ASD biology. The
lack of human data makes it indeterminate whether morphological deviations described
here apply to ASD patients or some of the other neurodevelopmental conditions
associated with WDFY3 mutation.\r\nConclusions: Our genetic approach revealed
several cell autonomous requirements of WDFY3 in neuronal development that could
underlie the pathogenic mechanisms of WDFY3-related neurodevelopmental conditions.
The results are also consistent with findings in other ASD animal models and patients
and suggest an important role for WDFY3 in regulating neuronal function and interconnectivity
in postnatal life."
acknowledgement: "This study was funded by NIMH R21MH115347 to KSZ. KSZ is further
supported by Shriners Hospitals for Children.\r\nWe would like to thank Angelo Harlan
de Crescenzo for early contributions to this project."
article_number: '27'
article_processing_charge: No
article_type: original
author:
- first_name: Zachary A.
full_name: Schaaf, Zachary A.
last_name: Schaaf
- first_name: Lyvin
full_name: Tat, Lyvin
last_name: Tat
- first_name: Noemi
full_name: Cannizzaro, Noemi
last_name: Cannizzaro
- first_name: Ralph
full_name: Green, Ralph
last_name: Green
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Konstantinos S.
full_name: Zarbalis, Konstantinos S.
last_name: Zarbalis
citation:
ama: Schaaf ZA, Tat L, Cannizzaro N, et al. WDFY3 mutation alters laminar position
and morphology of cortical neurons. Molecular Autism. 2022;13. doi:10.1186/s13229-022-00508-3
apa: Schaaf, Z. A., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer,
S., & Zarbalis, K. S. (2022). WDFY3 mutation alters laminar position and morphology
of cortical neurons. Molecular Autism. Springer Nature. https://doi.org/10.1186/s13229-022-00508-3
chicago: Schaaf, Zachary A., Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke,
Simon Hippenmeyer, and Konstantinos S. Zarbalis. “WDFY3 Mutation Alters Laminar
Position and Morphology of Cortical Neurons.” Molecular Autism. Springer
Nature, 2022. https://doi.org/10.1186/s13229-022-00508-3.
ieee: Z. A. Schaaf et al., “WDFY3 mutation alters laminar position and morphology
of cortical neurons,” Molecular Autism, vol. 13. Springer Nature, 2022.
ista: Schaaf ZA, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis
KS. 2022. WDFY3 mutation alters laminar position and morphology of cortical neurons.
Molecular Autism. 13, 27.
mla: Schaaf, Zachary A., et al. “WDFY3 Mutation Alters Laminar Position and Morphology
of Cortical Neurons.” Molecular Autism, vol. 13, 27, Springer Nature, 2022,
doi:10.1186/s13229-022-00508-3.
short: Z.A. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer,
K.S. Zarbalis, Molecular Autism 13 (2022).
date_created: 2022-06-23T14:28:55Z
date_published: 2022-06-22T00:00:00Z
date_updated: 2023-08-03T07:21:32Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1186/s13229-022-00508-3
external_id:
isi:
- '000814641400001'
file:
- access_level: open_access
checksum: 525d2618e855139089bbfc3e3d49d1b2
content_type: application/pdf
creator: dernst
date_created: 2022-06-24T08:22:59Z
date_updated: 2022-06-24T08:22:59Z
file_id: '11461'
file_name: 2022_MolecularAutism_Schaaf.pdf
file_size: 7552298
relation: main_file
success: 1
file_date_updated: 2022-06-24T08:22:59Z
has_accepted_license: '1'
intvolume: ' 13'
isi: 1
keyword:
- Psychiatry and Mental health
- Developmental Biology
- Developmental Neuroscience
- Molecular Biology
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: Molecular Autism
publication_identifier:
issn:
- 2040-2392
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1186/s13229-023-00539-4
status: public
title: WDFY3 mutation alters laminar position and morphology of cortical neurons
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '11449'
abstract:
- lang: eng
text: Mutations are acquired frequently, such that each cell's genome inscribes
its history of cell divisions. Common genomic alterations involve loss of heterozygosity
(LOH). LOH accumulates throughout the genome, offering large encoding capacity
for inferring cell lineage. Using only single-cell RNA sequencing (scRNA-seq)
of mouse brain cells, we found that LOH events spanning multiple genes are revealed
as tracts of monoallelically expressed, constitutionally heterozygous single-nucleotide
variants (SNVs). We simultaneously inferred cell lineage and marked developmental
time points based on X chromosome inactivation and the total number of LOH events
while identifying cell types from gene expression patterns. Our results are consistent
with progenitor cells giving rise to multiple cortical cell types through stereotyped
expansion and distinct waves of neurogenesis. This type of retrospective analysis
could be incorporated into scRNA-seq pipelines and, compared with experimental
approaches for determining lineage in model organisms, is applicable where genetic
engineering is prohibited, such as humans.
acknowledgement: D.J.A. thanks Wayne K. Potts, Alan R. Rogers, Kristen Hawkes, Ryk
Ward, and Jon Seger for inspiring a young undergraduate to apply evolutionary theory
to intraorganism development. Supported by the Paul G. Allen Frontiers Group (University
of Washington); NIH R00HG010152 (Dartmouth); and NÖ Forschung und Bildung n[f+b]
life science call grant (C13-002) and the European Research Council (ERC) under
the European Union’s Horizon 2020 research and innovation program 725780 LinPro
to S.H.
article_processing_charge: No
article_type: original
author:
- first_name: Donovan J.
full_name: Anderson, Donovan J.
last_name: Anderson
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Aaron
full_name: Mckenna, Aaron
last_name: Mckenna
- first_name: Jay
full_name: Shendure, Jay
last_name: Shendure
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Marshall S.
full_name: Horwitz, Marshall S.
last_name: Horwitz
citation:
ama: Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous
brain cell type and lineage determined by scRNA-seq reveals stereotyped cortical
development. Cell Systems. 2022;13(6):438-453.e5. doi:10.1016/j.cels.2022.03.006
apa: Anderson, D. J., Pauler, F., Mckenna, A., Shendure, J., Hippenmeyer, S., &
Horwitz, M. S. (2022). Simultaneous brain cell type and lineage determined by
scRNA-seq reveals stereotyped cortical development. Cell Systems. Elsevier.
https://doi.org/10.1016/j.cels.2022.03.006
chicago: Anderson, Donovan J., Florian Pauler, Aaron Mckenna, Jay Shendure, Simon
Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Brain Cell Type and Lineage
Determined by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems.
Elsevier, 2022. https://doi.org/10.1016/j.cels.2022.03.006.
ieee: D. J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, and M.
S. Horwitz, “Simultaneous brain cell type and lineage determined by scRNA-seq
reveals stereotyped cortical development,” Cell Systems, vol. 13, no. 6.
Elsevier, p. 438–453.e5, 2022.
ista: Anderson DJ, Pauler F, Mckenna A, Shendure J, Hippenmeyer S, Horwitz MS. 2022.
Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped
cortical development. Cell Systems. 13(6), 438–453.e5.
mla: Anderson, Donovan J., et al. “Simultaneous Brain Cell Type and Lineage Determined
by ScRNA-Seq Reveals Stereotyped Cortical Development.” Cell Systems, vol.
13, no. 6, Elsevier, 2022, p. 438–453.e5, doi:10.1016/j.cels.2022.03.006.
short: D.J. Anderson, F. Pauler, A. Mckenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz,
Cell Systems 13 (2022) 438–453.e5.
date_created: 2022-06-19T22:01:57Z
date_published: 2022-06-15T00:00:00Z
date_updated: 2023-08-03T07:19:43Z
day: '15'
department:
- _id: SiHi
doi: 10.1016/j.cels.2022.03.006
ec_funded: 1
external_id:
isi:
- '000814124400002'
pmid:
- '35452605'
intvolume: ' 13'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cels.2022.03.006
month: '06'
oa: 1
oa_version: Published Version
page: 438-453.e5
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Cell Systems
publication_identifier:
eissn:
- 2405-4720
issn:
- 2405-4712
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Simultaneous brain cell type and lineage determined by scRNA-seq reveals stereotyped
cortical development
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 13
year: '2022'
...
---
_id: '10792'
abstract:
- lang: eng
text: "Background\r\nProper cerebral cortical development depends on the tightly
orchestrated migration of newly born neurons from the inner ventricular and subventricular
zones to the outer cortical plate. Any disturbance in this process during prenatal
stages may lead to neuronal migration disorders (NMDs), which can vary in extent
from focal to global. Furthermore, NMDs show a substantial comorbidity with other
neurodevelopmental disorders, notably autism spectrum disorders (ASDs). Our previous
work demonstrated focal neuronal migration defects in mice carrying loss-of-function
alleles of the recognized autism risk gene WDFY3. However, the cellular origins
of these defects in Wdfy3 mutant mice remain elusive and uncovering it will provide
critical insight into WDFY3-dependent disease pathology .\r\nMethods\r\nHere,
in an effort to untangle the origins of NMDs in Wdfy3lacZ mice, we employed mosaic
analysis with double markers (MADM). MADM technology enabled us to genetically
distinctly track and phenotypically analyze mutant and wild type cells concomitantly
in vivo using immunofluorescent techniques.\r\nResults\r\nWe revealed a cell autonomous
requirement of WDFY3 for accurate laminar positioning of cortical projection neurons
and elimination of mispositioned cells during early postnatal life. In addition,
we identified significant deviations in dendritic arborization, as well as synaptic
density and morphology between wild type, heterozygous, and homozygous Wdfy3 mutant
neurons in Wdfy3-MADM reporter mice at postnatal stages. Limitations While Wdfy3
mutant mice have provided valuable insight into prenatal aspects of ASD pathology
that remain inaccessible to investigation in humans, like most animal models,
they do not a perfectly replicate all aspects of human ASD biology. The lack of
human data makes it indeterminate whether morphological deviations described here
apply to ASD patients.\r\nConclusions\r\n\uFEFFOur genetic approach revealed several
cell autonomous requirements of Wdfy3 in neuronal development that could underly
the pathogenic mechanisms of WDFY3-related ASD conditions. The results are also
consistent with findings in other ASD animal models and patients and suggest an
important role for Wdfy3 in regulating neuronal function and interconnectivity
in postnatal life."
article_processing_charge: No
author:
- first_name: Zachary
full_name: Schaaf, Zachary
last_name: Schaaf
- first_name: Lyvin
full_name: Tat, Lyvin
last_name: Tat
- first_name: Noemi
full_name: Cannizzaro, Noemi
last_name: Cannizzaro
- first_name: Ralph
full_name: Green, Ralph
last_name: Green
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: K
full_name: Zarbalis, K
last_name: Zarbalis
citation:
ama: Schaaf Z, Tat L, Cannizzaro N, et al. WDFY3 cell autonomously controls neuronal
migration. doi:10.21203/rs.3.rs-1316167/v1
apa: Schaaf, Z., Tat, L., Cannizzaro, N., Green, R., Rülicke, T., Hippenmeyer, S.,
& Zarbalis, K. (n.d.). WDFY3 cell autonomously controls neuronal migration.
Research Square. https://doi.org/10.21203/rs.3.rs-1316167/v1
chicago: Schaaf, Zachary, Lyvin Tat, Noemi Cannizzaro, Ralph Green, Thomas Rülicke,
Simon Hippenmeyer, and K Zarbalis. “WDFY3 Cell Autonomously Controls Neuronal
Migration.” Research Square, n.d. https://doi.org/10.21203/rs.3.rs-1316167/v1.
ieee: Z. Schaaf et al., “WDFY3 cell autonomously controls neuronal migration.”
Research Square.
ista: Schaaf Z, Tat L, Cannizzaro N, Green R, Rülicke T, Hippenmeyer S, Zarbalis
K. WDFY3 cell autonomously controls neuronal migration. 10.21203/rs.3.rs-1316167/v1.
mla: Schaaf, Zachary, et al. WDFY3 Cell Autonomously Controls Neuronal Migration.
Research Square, doi:10.21203/rs.3.rs-1316167/v1.
short: Z. Schaaf, L. Tat, N. Cannizzaro, R. Green, T. Rülicke, S. Hippenmeyer, K.
Zarbalis, (n.d.).
date_created: 2022-02-25T07:53:26Z
date_published: 2022-02-16T00:00:00Z
date_updated: 2023-10-17T13:06:52Z
day: '16'
department:
- _id: SiHi
doi: 10.21203/rs.3.rs-1316167/v1
external_id:
pmid:
- PPR454733
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.21203/rs.3.rs-1316167/v1
month: '02'
oa: 1
oa_version: Preprint
page: '30'
pmid: 1
publication_identifier:
eissn:
- 2693-5015
publication_status: submitted
publisher: Research Square
status: public
title: WDFY3 cell autonomously controls neuronal migration
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2022'
...
---
_id: '10791'
abstract:
- lang: eng
text: The mammalian neocortex is composed of diverse neuronal and glial cell classes
that broadly arrange in six distinct laminae. Cortical layers emerge during development
and defects in the developmental programs that orchestrate cortical lamination
are associated with neurodevelopmental diseases. The developmental principle of
cortical layer formation depends on concerted radial projection neuron migration,
from their birthplace to their final target position. Radial migration occurs
in defined sequential steps, regulated by a large array of signaling pathways.
However, based on genetic loss-of-function experiments, most studies have thus
far focused on the role of cell-autonomous gene function. Yet, cortical neuron
migration in situ is a complex process and migrating neurons traverse along diverse
cellular compartments and environments. The role of tissue-wide properties and
genetic state in radial neuron migration is however not clear. Here we utilized
mosaic analysis with double markers (MADM) technology to either sparsely or globally
delete gene function, followed by quantitative single-cell phenotyping. The MADM-based
gene ablation paradigms in combination with computational modeling demonstrated
that global tissue-wide effects predominate cell-autonomous gene function albeit
in a gene-specific manner. Our results thus suggest that the genetic landscape
in a tissue critically affects the overall migration phenotype of individual cortical
projection neurons. In a broader context, our findings imply that global tissue-wide
effects represent an essential component of the underlying etiology associated
with focal malformations of cortical development in particular, and neurological
diseases in general.
acknowledged_ssus:
- _id: LifeSc
- _id: PreCl
- _id: Bio
acknowledgement: "A.H.H. was a recipient of a DOC Fellowship (24812) of the Austrian
Academy of Sciences. This work also received support from IST Austria institutional
funds; the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme (FP7/2007–2013) under REA grant agreement No 618444 to S.H.\r\nAPC
funding was obtained by IST Austria institutional funds.\r\nWe thank A. Sommer and
C. Czepe (VBCF GmbH, NGS Unit), L. Andersen, J. Sonntag and J. Renno for technical
support and/or initial experiments; M. Sixt, J. Nimpf and all members of the Hippenmeyer
lab for discussion. This research was supported by the Scientific Service Units
of IST Austria through resources provided by the Imaging and Optics Facility, Lab
Support Facility and Preclinical Facility."
article_number: kvac009
article_processing_charge: No
article_type: original
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Michael
full_name: Riedl, Michael
id: 3BE60946-F248-11E8-B48F-1D18A9856A87
last_name: Riedl
orcid: 0000-0003-4844-6311
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Anna-Magdalena
full_name: Heger, Anna-Magdalena
id: 4B76FFD2-F248-11E8-B48F-1D18A9856A87
last_name: Heger
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Christoph M
full_name: Sommer, Christoph M
id: 4DF26D8C-F248-11E8-B48F-1D18A9856A87
last_name: Sommer
orcid: 0000-0003-1216-9105
- first_name: Armel
full_name: Nicolas, Armel
id: 2A103192-F248-11E8-B48F-1D18A9856A87
last_name: Nicolas
- first_name: Björn
full_name: Hof, Björn
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
- first_name: Li Huei
full_name: Tsai, Li Huei
last_name: Tsai
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Pauler F, Riedl M, et al. Tissue-wide effects override cell-intrinsic
gene function in radial neuron migration. Oxford Open Neuroscience. 2022;1(1).
doi:10.1093/oons/kvac009
apa: Hansen, A. H., Pauler, F., Riedl, M., Streicher, C., Heger, A.-M., Laukoter,
S., … Hippenmeyer, S. (2022). Tissue-wide effects override cell-intrinsic gene
function in radial neuron migration. Oxford Open Neuroscience. Oxford Academic.
https://doi.org/10.1093/oons/kvac009
chicago: Hansen, Andi H, Florian Pauler, Michael Riedl, Carmen Streicher, Anna-Magdalena
Heger, Susanne Laukoter, Christoph M Sommer, et al. “Tissue-Wide Effects Override
Cell-Intrinsic Gene Function in Radial Neuron Migration.” Oxford Open Neuroscience.
Oxford Academic, 2022. https://doi.org/10.1093/oons/kvac009.
ieee: A. H. Hansen et al., “Tissue-wide effects override cell-intrinsic gene
function in radial neuron migration,” Oxford Open Neuroscience, vol. 1,
no. 1. Oxford Academic, 2022.
ista: Hansen AH, Pauler F, Riedl M, Streicher C, Heger A-M, Laukoter S, Sommer CM,
Nicolas A, Hof B, Tsai LH, Rülicke T, Hippenmeyer S. 2022. Tissue-wide effects
override cell-intrinsic gene function in radial neuron migration. Oxford Open
Neuroscience. 1(1), kvac009.
mla: Hansen, Andi H., et al. “Tissue-Wide Effects Override Cell-Intrinsic Gene Function
in Radial Neuron Migration.” Oxford Open Neuroscience, vol. 1, no. 1, kvac009,
Oxford Academic, 2022, doi:10.1093/oons/kvac009.
short: A.H. Hansen, F. Pauler, M. Riedl, C. Streicher, A.-M. Heger, S. Laukoter,
C.M. Sommer, A. Nicolas, B. Hof, L.H. Tsai, T. Rülicke, S. Hippenmeyer, Oxford
Open Neuroscience 1 (2022).
date_created: 2022-02-25T07:52:11Z
date_published: 2022-07-07T00:00:00Z
date_updated: 2023-11-30T10:55:12Z
day: '07'
ddc:
- '570'
department:
- _id: SiHi
- _id: BjHo
- _id: LifeSc
- _id: EM-Fac
doi: 10.1093/oons/kvac009
ec_funded: 1
file:
- access_level: open_access
checksum: 822e76e056c07099d1fb27d1ece5941b
content_type: application/pdf
creator: dernst
date_created: 2023-08-16T08:00:30Z
date_updated: 2023-08-16T08:00:30Z
file_id: '14061'
file_name: 2023_OxfordOpenNeuroscience_Hansen.pdf
file_size: 4846551
relation: main_file
success: 1
file_date_updated: 2023-08-16T08:00:30Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
publication: Oxford Open Neuroscience
publication_identifier:
eissn:
- 2753-149X
publication_status: published
publisher: Oxford Academic
quality_controlled: '1'
related_material:
record:
- id: '12726'
relation: dissertation_contains
status: public
- id: '14530'
relation: dissertation_contains
status: public
status: public
title: Tissue-wide effects override cell-intrinsic gene function in radial neuron
migration
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2022'
...
---
_id: '9082'
abstract:
- lang: eng
text: Acquired mutations are sufficiently frequent such that the genome of a single
cell offers a record of its history of cell divisions. Among more common somatic
genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially
detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic
expression for constitutionally heterozygous single nucleotide variants (SNVs)
located among contiguous genes. We identified runs of monoallelic expression,
consistent with LOH, uniquely distributed throughout the genome in single cell
brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains.
We then phylogenetically reconstructed single cell lineages and simultaneously
identified cell types by corresponding gene expression patterns. Our results are
consistent with progenitor cells giving rise to multiple cortical cell types through
stereotyped expansion and distinct waves of neurogenesis. Compared to engineered
recording systems, LOH events accumulate throughout the genome and across the
lifetime of an organism, affording tremendous capacity for encoding lineage information
and increasing resolution for later cell divisions. This approach can conceivably
be computationally incorporated into scRNA-seq analysis and may be useful for
organisms where genetic engineering is prohibitive, such as humans.
acknowledgement: "We thank Bill Bolosky, Microsoft Research, for earlier work showing
proof of concept in TCGA\r\nbulk RNA-seq data. Supported by the Paul G. Allen Frontiers
Group (University of Washington);\r\nNIH R00HG010152 (Dartmouth); and NÖ Forschung
und Bildung n[f+b] life science call grant\r\n(C13-002) to SH, and the European
Research Council (ERC) under the European Union’s\r\nHorizon 2020 research and innovation
program 725780 LinPro to SH."
article_processing_charge: No
author:
- first_name: Donovan J.
full_name: Anderson, Donovan J.
last_name: Anderson
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Aaron
full_name: McKenna, Aaron
last_name: McKenna
- first_name: Jay
full_name: Shendure, Jay
last_name: Shendure
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Marshall S.
full_name: Horwitz, Marshall S.
last_name: Horwitz
citation:
ama: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous
identification of brain cell type and lineage via single cell RNA sequencing.
bioRxiv. doi:10.1101/2020.12.31.425016
apa: Anderson, D. J., Pauler, F., McKenna, A., Shendure, J., Hippenmeyer, S., &
Horwitz, M. S. (n.d.). Simultaneous identification of brain cell type and lineage
via single cell RNA sequencing. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/2020.12.31.425016
chicago: Anderson, Donovan J., Florian Pauler, Aaron McKenna, Jay Shendure, Simon
Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Identification of Brain Cell
Type and Lineage via Single Cell RNA Sequencing.” BioRxiv. Cold Spring
Harbor Laboratory, n.d. https://doi.org/10.1101/2020.12.31.425016.
ieee: D. J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, and M.
S. Horwitz, “Simultaneous identification of brain cell type and lineage via single
cell RNA sequencing,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous
identification of brain cell type and lineage via single cell RNA sequencing.
bioRxiv, 10.1101/2020.12.31.425016.
mla: Anderson, Donovan J., et al. “Simultaneous Identification of Brain Cell Type
and Lineage via Single Cell RNA Sequencing.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/2020.12.31.425016.
short: D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz,
BioRxiv (n.d.).
date_created: 2021-02-04T07:23:23Z
date_published: 2021-01-01T00:00:00Z
date_updated: 2021-02-04T07:29:53Z
day: '01'
department:
- _id: SiHi
doi: 10.1101/2020.12.31.425016
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.12.31.425016
month: '01'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Simultaneous identification of brain cell type and lineage via single cell
RNA sequencing
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2021'
...
---
_id: '8546'
abstract:
- lang: eng
text: Brain neurons arise from relatively few progenitors generating an enormous
diversity of neuronal types. Nonetheless, a cardinal feature of mammalian brain
neurogenesis is thought to be that excitatory and inhibitory neurons derive from
separate, spatially segregated progenitors. Whether bi-potential progenitors with
an intrinsic capacity to generate both lineages exist and how such a fate decision
may be regulated are unknown. Using cerebellar development as a model, we discover
that individual progenitors can give rise to both inhibitory and excitatory lineages.
Gradations of Notch activity determine the fates of the progenitors and their
daughters. Daughters with the highest levels of Notch activity retain the progenitor
fate, while intermediate levels of Notch activity generate inhibitory neurons,
and daughters with very low levels of Notch signaling adopt the excitatory fate.
Therefore, Notch-mediated binary cell fate choice is a mechanism for regulating
the ratio of excitatory to inhibitory neurons from common progenitors.
acknowledgement: This work was supported by the program “Investissements d’avenir”
ANR-10-IAIHU-06 , ICM , a Sorbonne Université Emergence grant, an Allen Distinguished
Investigator Award , and the Roger De Spoelberch Foundation Prize (to B.A.H.); Armenise-Harvard
Foundation , AIRC , and CARITRO (to L.T.); and the European Research Council under
the European Union’s Horizon 2020 research and innovation programme grant agreement
no. 725780 LinPro (to S.H.). T.Z. and T.L. were supported by doctoral fellowships
from the China Scholarship Council and A.H.H. by a doctoral DOC fellowship of the
Austrian Academy of Sciences ( 24812 ). All animal work was conducted at the PHENO-ICMice
facility. The Core is supported by 2 “Investissements d’avenir” (ANR-10- IAIHU-06
and ANR-11-INBS-0011-NeurATRIS) and the “Fondation pour la Recherche Médicale.”
Light microscopy work was carried out at ICM’s imaging core facility, ICM.Quant,
and analysis of scRNA-seq data was carried out at ICM’s bioinformatics core facility,
iCONICS. We thank Paulina Ejsmont, Natalia Danda, and Nathalie De Geest for technical
support. We are grateful to Dr. Shahragim TAJBAKHSH for providing R26Rstop-NICD-nGFP
transgenic mice, Dr. Bart De Strooper for Psn1-deficient mice, Dr. Jean-Christophe
Marine for Gt(ROSA)26SortdTom reporter mice, and Dr. Martinez Barbera for Sox2CreERT2
mice. We also give thanks to Dr. Mikio Hoshino for providing Atoh1 and Ptf1a antibodies.
B.A.H. is an Einstein Visiting Fellow of the Berlin Institute of Health .
article_number: '109208'
article_processing_charge: No
article_type: original
author:
- first_name: Tingting
full_name: Zhang, Tingting
last_name: Zhang
- first_name: Tengyuan
full_name: Liu, Tengyuan
last_name: Liu
- first_name: Natalia
full_name: Mora, Natalia
last_name: Mora
- first_name: Justine
full_name: Guegan, Justine
last_name: Guegan
- first_name: Mathilde
full_name: Bertrand, Mathilde
last_name: Bertrand
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Marica
full_name: Anderle, Marica
last_name: Anderle
- first_name: Natasha
full_name: Danda, Natasha
last_name: Danda
- first_name: Luca
full_name: Tiberi, Luca
last_name: Tiberi
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Bassem A.
full_name: Hassan, Bassem A.
last_name: Hassan
citation:
ama: Zhang T, Liu T, Mora N, et al. Generation of excitatory and inhibitory neurons
from common progenitors via Notch signaling in the cerebellum. Cell Reports.
2021;35(10). doi:10.1016/j.celrep.2021.109208
apa: Zhang, T., Liu, T., Mora, N., Guegan, J., Bertrand, M., Contreras, X., … Hassan,
B. A. (2021). Generation of excitatory and inhibitory neurons from common progenitors
via Notch signaling in the cerebellum. Cell Reports. Elsevier. https://doi.org/10.1016/j.celrep.2021.109208
chicago: Zhang, Tingting, Tengyuan Liu, Natalia Mora, Justine Guegan, Mathilde Bertrand,
Ximena Contreras, Andi H Hansen, et al. “Generation of Excitatory and Inhibitory
Neurons from Common Progenitors via Notch Signaling in the Cerebellum.” Cell
Reports. Elsevier, 2021. https://doi.org/10.1016/j.celrep.2021.109208.
ieee: T. Zhang et al., “Generation of excitatory and inhibitory neurons from
common progenitors via Notch signaling in the cerebellum,” Cell Reports,
vol. 35, no. 10. Elsevier, 2021.
ista: Zhang T, Liu T, Mora N, Guegan J, Bertrand M, Contreras X, Hansen AH, Streicher
C, Anderle M, Danda N, Tiberi L, Hippenmeyer S, Hassan BA. 2021. Generation of
excitatory and inhibitory neurons from common progenitors via Notch signaling
in the cerebellum. Cell Reports. 35(10), 109208.
mla: Zhang, Tingting, et al. “Generation of Excitatory and Inhibitory Neurons from
Common Progenitors via Notch Signaling in the Cerebellum.” Cell Reports,
vol. 35, no. 10, 109208, Elsevier, 2021, doi:10.1016/j.celrep.2021.109208.
short: T. Zhang, T. Liu, N. Mora, J. Guegan, M. Bertrand, X. Contreras, A.H. Hansen,
C. Streicher, M. Anderle, N. Danda, L. Tiberi, S. Hippenmeyer, B.A. Hassan, Cell
Reports 35 (2021).
date_created: 2020-09-21T12:00:48Z
date_published: 2021-06-08T00:00:00Z
date_updated: 2023-08-04T11:00:48Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2021.109208
ec_funded: 1
external_id:
isi:
- '000659894300001'
pmid:
- '34107249 '
file:
- access_level: open_access
checksum: 7def3d42ebc8f5675efb6f38819e3e2e
content_type: application/pdf
creator: cziletti
date_created: 2021-06-15T14:01:35Z
date_updated: 2021-06-15T14:01:35Z
file_id: '9554'
file_name: 2021_CellReports_Zhang.pdf
file_size: 8900385
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file_date_updated: 2021-06-15T14:01:35Z
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intvolume: ' 35'
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issue: '10'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
publication: Cell Reports
publication_identifier:
eissn:
- ' 22111247'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- relation: earlier_version
url: https://doi.org/10.1101/2020.03.18.997205
scopus_import: '1'
status: public
title: Generation of excitatory and inhibitory neurons from common progenitors via
Notch signaling in the cerebellum
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 35
year: '2021'
...
---
_id: '9188'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic mechanism that results in parental allele-specific
expression of ~1% of all genes in mouse and human. Imprinted genes are key developmental
regulators and play pivotal roles in many biological processes such as nutrient
transfer from the mother to offspring and neuronal development. Imprinted genes
are also involved in human disease, including neurodevelopmental disorders, and
often occur in clusters that are regulated by a common imprint control region
(ICR). In extra-embryonic tissues ICRs can act over large distances, with the
largest surrounding Igf2r spanning over 10 million base-pairs. Besides classical
imprinted expression that shows near exclusive maternal or paternal expression,
widespread biased imprinted expression has been identified mainly in brain. In
this review we discuss recent developments mapping cell type specific imprinted
expression in extra-embryonic tissues and neocortex in the mouse. We highlight
the advantages of using an inducible uniparental chromosome disomy (UPD) system
to generate cells carrying either two maternal or two paternal copies of a specific
chromosome to analyze the functional consequences of genomic imprinting. Mosaic
Analysis with Double Markers (MADM) allows fluorescent labeling and concomitant
induction of UPD sparsely in specific cell types, and thus to over-express or
suppress all imprinted genes on that chromosome. To illustrate the utility of
this technique, we explain how MADM-induced UPD revealed new insights about the
function of the well-studied Cdkn1c imprinted gene, and how MADM-induced UPDs
led to identification of highly cell type specific phenotypes related to perturbed
imprinted expression in the mouse neocortex. Finally, we give an outlook on how
MADM could be used to probe cell type specific imprinted expression in other tissues
in mouse, particularly in extra-embryonic tissues.
acknowledgement: We thank Melissa Stouffer for critically reading the manuscript.
This work was supported by IST Austria institutional funds; NÖ Forschung und Bildung
n[f + b] life science call grant (C13-002) to S.H. and the European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation program (grant
agreement 725780 LinPro) to S.H.
article_number: '104986'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. Inducible uniparental chromosome
disomy to probe genomic imprinting at single-cell level in brain and beyond. Neurochemistry
International. 2021;145(5). doi:10.1016/j.neuint.2021.104986
apa: Pauler, F., Hudson, Q., Laukoter, S., & Hippenmeyer, S. (2021). Inducible
uniparental chromosome disomy to probe genomic imprinting at single-cell level
in brain and beyond. Neurochemistry International. Elsevier. https://doi.org/10.1016/j.neuint.2021.104986
chicago: Pauler, Florian, Quanah Hudson, Susanne Laukoter, and Simon Hippenmeyer.
“Inducible Uniparental Chromosome Disomy to Probe Genomic Imprinting at Single-Cell
Level in Brain and Beyond.” Neurochemistry International. Elsevier, 2021.
https://doi.org/10.1016/j.neuint.2021.104986.
ieee: F. Pauler, Q. Hudson, S. Laukoter, and S. Hippenmeyer, “Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond,” Neurochemistry International, vol. 145, no. 5. Elsevier, 2021.
ista: Pauler F, Hudson Q, Laukoter S, Hippenmeyer S. 2021. Inducible uniparental
chromosome disomy to probe genomic imprinting at single-cell level in brain and
beyond. Neurochemistry International. 145(5), 104986.
mla: Pauler, Florian, et al. “Inducible Uniparental Chromosome Disomy to Probe Genomic
Imprinting at Single-Cell Level in Brain and Beyond.” Neurochemistry International,
vol. 145, no. 5, 104986, Elsevier, 2021, doi:10.1016/j.neuint.2021.104986.
short: F. Pauler, Q. Hudson, S. Laukoter, S. Hippenmeyer, Neurochemistry International
145 (2021).
date_created: 2021-02-23T12:31:43Z
date_published: 2021-05-01T00:00:00Z
date_updated: 2023-08-07T13:48:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuint.2021.104986
ec_funded: 1
external_id:
isi:
- '000635575000005'
pmid:
- '33600873'
file:
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checksum: c6d7a40089cd29e289f9b22e75768304
content_type: application/pdf
creator: kschuh
date_created: 2021-08-11T12:30:38Z
date_updated: 2021-08-11T12:30:38Z
file_id: '9883'
file_name: 2021_NCI_Pauler.pdf
file_size: 7083499
relation: main_file
success: 1
file_date_updated: 2021-08-11T12:30:38Z
has_accepted_license: '1'
intvolume: ' 145'
isi: 1
issue: '5'
keyword:
- Cell Biology
- Cellular and Molecular Neuroscience
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Neurochemistry International
publication_identifier:
issn:
- 0197-0186
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Inducible uniparental chromosome disomy to probe genomic imprinting at single-cell
level in brain and beyond
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 145
year: '2021'
...
---
_id: '9601'
abstract:
- lang: eng
text: 'In mammalian genomes, differentially methylated regions (DMRs) and histone
marks including trimethylation of histone 3 lysine 27 (H3K27me3) at imprinted
genes are asymmetrically inherited to control parentally-biased gene expression.
However, neither parent-of-origin-specific transcription nor imprints have been
comprehensively mapped at the blastocyst stage of preimplantation development.
Here, we address this by integrating transcriptomic and epigenomic approaches
in mouse preimplantation embryos. We find that seventy-one genes exhibit previously
unreported parent-of-origin-specific expression in blastocysts (nBiX: novel blastocyst-imprinted
expressed). Uniparental expression of nBiX genes disappears soon after implantation.
Micro-whole-genome bisulfite sequencing (µWGBS) of individual uniparental blastocysts
detects 859 DMRs. We further find that 16% of nBiX genes are associated with a
DMR, whereas most are associated with parentally-biased H3K27me3, suggesting a
role for Polycomb-mediated imprinting in blastocysts. nBiX genes are clustered:
five clusters contained at least one published imprinted gene, and five clusters
exclusively contained nBiX genes. These data suggest that early development undergoes
a complex program of stage-specific imprinting involving different tiers of regulation.'
acknowledgement: The authors thank Robert Feil and Anton Wutz for helpful discussions
and comments, Samuel Collombet and Peter Fraser for sharing embryo TAD coordinates,
and Andy Riddel at the Cambridge Stem Cell Institute and Thomas Sauer at the Max
Perutz Laboratories FACS facility for flow-sorting. We thank the team of the Biomedical
Sequencing Facility at the CeMM and the Vienna Biocenter Core Facilities (VBCF)
for support with next-generation sequencing. We are grateful to animal care teams
at the University of Bath and MRC Harwell. A.C.F.P. acknowledges support from the
UK Medical Research Council (MR/N000080/1 and MR/N020294/1) and Biotechnology and
Biological Sciences Research Council (BB/P009506/1). L.S. is part of the FWF doctoral
programme SMICH and supported by an Austrian Academy of Sciences DOC Fellowship.
M.L. is funded by a Vienna Research Group for Young Investigators grant (VRG14-006)
by the Vienna Science and Technology Fund (WWTF) and by the Austrian Science Fund
FWF (I3786 and P31334).
article_number: '3804'
article_processing_charge: No
article_type: original
author:
- first_name: Laura
full_name: Santini, Laura
last_name: Santini
- first_name: Florian
full_name: Halbritter, Florian
last_name: Halbritter
- first_name: Fabian
full_name: Titz-Teixeira, Fabian
last_name: Titz-Teixeira
- first_name: Toru
full_name: Suzuki, Toru
last_name: Suzuki
- first_name: Maki
full_name: Asami, Maki
last_name: Asami
- first_name: Xiaoyan
full_name: Ma, Xiaoyan
last_name: Ma
- first_name: Julia
full_name: Ramesmayer, Julia
last_name: Ramesmayer
- first_name: Andreas
full_name: Lackner, Andreas
last_name: Lackner
- first_name: Nick
full_name: Warr, Nick
last_name: Warr
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ernest
full_name: Laue, Ernest
last_name: Laue
- first_name: Matthias
full_name: Farlik, Matthias
last_name: Farlik
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Andreas
full_name: Beyer, Andreas
last_name: Beyer
- first_name: Anthony C.F.
full_name: Perry, Anthony C.F.
last_name: Perry
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
citation:
ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Genomic imprinting in mouse
blastocysts is predominantly associated with H3K27me3. Nature Communications.
2021;12(1). doi:10.1038/s41467-021-23510-4
apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ma,
X., … Leeb, M. (2021). Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-021-23510-4
chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki,
Maki Asami, Xiaoyan Ma, Julia Ramesmayer, et al. “Genomic Imprinting in Mouse
Blastocysts Is Predominantly Associated with H3K27me3.” Nature Communications.
Springer Nature, 2021. https://doi.org/10.1038/s41467-021-23510-4.
ieee: L. Santini et al., “Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3,” Nature Communications, vol. 12, no. 1. Springer
Nature, 2021.
ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ma X, Ramesmayer
J, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer
A, Perry ACF, Leeb M. 2021. Genomic imprinting in mouse blastocysts is predominantly
associated with H3K27me3. Nature Communications. 12(1), 3804.
mla: Santini, Laura, et al. “Genomic Imprinting in Mouse Blastocysts Is Predominantly
Associated with H3K27me3.” Nature Communications, vol. 12, no. 1, 3804,
Springer Nature, 2021, doi:10.1038/s41467-021-23510-4.
short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, X. Ma,
J. Ramesmayer, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik,
C. Bock, A. Beyer, A.C.F. Perry, M. Leeb, Nature Communications 12 (2021).
date_created: 2021-06-27T22:01:46Z
date_published: 2021-07-12T00:00:00Z
date_updated: 2023-08-10T13:53:23Z
day: '12'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1038/s41467-021-23510-4
external_id:
isi:
- '000667248600005'
file:
- access_level: open_access
checksum: 75dd89d09945185b2d14b2434a0bcb50
content_type: application/pdf
creator: asandaue
date_created: 2021-06-28T08:04:22Z
date_updated: 2021-06-28T08:04:22Z
file_id: '9608'
file_name: 2021_NatureCommunications_Santini.pdf
file_size: 2156554
relation: main_file
success: 1
file_date_updated: 2021-06-28T08:04:22Z
has_accepted_license: '1'
intvolume: ' 12'
isi: 1
issue: '1'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_identifier:
eissn:
- '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genomic imprinting in mouse blastocysts is predominantly associated with H3K27me3
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 12
year: '2021'
...
---
_id: '9603'
abstract:
- lang: eng
text: Mosaic analysis with double markers (MADM) offers one approach to visualize
and concomitantly manipulate genetically defined cells in mice with single-cell
resolution. MADM applications include the analysis of lineage, single-cell morphology
and physiology, genomic imprinting phenotypes, and dissection of cell-autonomous
gene functions in vivo in health and disease. Yet, MADM can only be applied to
<25% of all mouse genes on select chromosomes to date. To overcome this limitation,
we generate transgenic mice with knocked-in MADM cassettes near the centromeres
of all 19 autosomes and validate their use across organs. With this resource,
>96% of the entire mouse genome can now be subjected to single-cell genetic mosaic
analysis. Beyond a proof of principle, we apply our MADM library to systematically
trace sister chromatid segregation in distinct mitotic cell lineages. We find
striking chromosome-specific biases in segregation patterns, reflecting a putative
mechanism for the asymmetric segregation of genetic determinants in somatic stem
cell division.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: We thank the Bioimaging, Life Science, and Pre-Clinical Facilities
at IST Austria; M.P. Postiglione, C. Simbriger, K. Valoskova, C. Schwayer, T. Hussain,
M. Pieber, and V. Wimmer for initial experiments, technical support, and/or assistance;
R. Shigemoto for sharing iv (Dnah11 mutant) mice; and M. Sixt and all members of
the Hippenmeyer lab for discussion. This work was supported by National Institutes
of Health grants ( R01-NS050580 to L.L. and F32MH096361 to L.A.S.). L.L. is an investigator
of HHMI. N.A. received support from FWF Firnberg-Programm ( T 1031 ). A.H.H. is
a recipient of a DOC Fellowship (24812) of the Austrian Academy of Sciences . This
work also received support from IST Austria institutional funds , FWF SFB F78 to
S.H., the People Programme (Marie Curie Actions) of the European Union’s Seventh
Framework Programme ( FP7/2007-2013 ) under REA grant agreement no 618444 to S.H.,
and the European Research Council (ERC) under the European Union’s Horizon 2020
Research and Innovation Programme (grant agreement no. 725780 LinPro ) to S.H.
article_number: '109274'
article_processing_charge: No
article_type: original
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Amarbayasgalan
full_name: Davaatseren, Amarbayasgalan
id: 70ADC922-B424-11E9-99E3-BA18E6697425
last_name: Davaatseren
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Johanna
full_name: Sonntag, Johanna
id: 32FE7D7C-F248-11E8-B48F-1D18A9856A87
last_name: Sonntag
- first_name: Lill
full_name: Andersen, Lill
last_name: Andersen
- first_name: Tina
full_name: Bernthaler, Tina
last_name: Bernthaler
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Anna-Magdalena
full_name: Heger, Anna-Magdalena
id: 4B76FFD2-F248-11E8-B48F-1D18A9856A87
last_name: Heger
- first_name: Randy L.
full_name: Johnson, Randy L.
last_name: Johnson
- first_name: Lindsay A.
full_name: Schwarz, Lindsay A.
last_name: Schwarz
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Amberg N, Davaatseren A, et al. A genome-wide library of MADM
mice for single-cell genetic mosaic analysis. Cell Reports. 2021;35(12).
doi:10.1016/j.celrep.2021.109274
apa: Contreras, X., Amberg, N., Davaatseren, A., Hansen, A. H., Sonntag, J., Andersen,
L., … Hippenmeyer, S. (2021). A genome-wide library of MADM mice for single-cell
genetic mosaic analysis. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2021.109274
chicago: Contreras, Ximena, Nicole Amberg, Amarbayasgalan Davaatseren, Andi H Hansen,
Johanna Sonntag, Lill Andersen, Tina Bernthaler, et al. “A Genome-Wide Library
of MADM Mice for Single-Cell Genetic Mosaic Analysis.” Cell Reports. Cell
Press, 2021. https://doi.org/10.1016/j.celrep.2021.109274.
ieee: X. Contreras et al., “A genome-wide library of MADM mice for single-cell
genetic mosaic analysis,” Cell Reports, vol. 35, no. 12. Cell Press, 2021.
ista: Contreras X, Amberg N, Davaatseren A, Hansen AH, Sonntag J, Andersen L, Bernthaler
T, Streicher C, Heger A-M, Johnson RL, Schwarz LA, Luo L, Rülicke T, Hippenmeyer
S. 2021. A genome-wide library of MADM mice for single-cell genetic mosaic analysis.
Cell Reports. 35(12), 109274.
mla: Contreras, Ximena, et al. “A Genome-Wide Library of MADM Mice for Single-Cell
Genetic Mosaic Analysis.” Cell Reports, vol. 35, no. 12, 109274, Cell Press,
2021, doi:10.1016/j.celrep.2021.109274.
short: X. Contreras, N. Amberg, A. Davaatseren, A.H. Hansen, J. Sonntag, L. Andersen,
T. Bernthaler, C. Streicher, A.-M. Heger, R.L. Johnson, L.A. Schwarz, L. Luo,
T. Rülicke, S. Hippenmeyer, Cell Reports 35 (2021).
date_created: 2021-06-27T22:01:48Z
date_published: 2021-06-22T00:00:00Z
date_updated: 2023-08-10T13:55:00Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
- _id: LoSw
- _id: PreCl
doi: 10.1016/j.celrep.2021.109274
ec_funded: 1
external_id:
isi:
- '000664463600016'
file:
- access_level: open_access
checksum: d49520fdcbbb5c2f883bddb67cee5d77
content_type: application/pdf
creator: asandaue
date_created: 2021-06-28T14:06:24Z
date_updated: 2021-06-28T14:06:24Z
file_id: '9613'
file_name: 2021_CellReports_Contreras.pdf
file_size: 7653149
relation: main_file
success: 1
file_date_updated: 2021-06-28T14:06:24Z
has_accepted_license: '1'
intvolume: ' 35'
isi: 1
issue: '12'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Cell Reports
publication_identifier:
eissn:
- '22111247'
publication_status: published
publisher: Cell Press
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/boost-for-mouse-genetic-analysis/
scopus_import: '1'
status: public
title: A genome-wide library of MADM mice for single-cell genetic mosaic analysis
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 35
year: '2021'
...
---
_id: '9073'
abstract:
- lang: eng
text: The sensory and cognitive abilities of the mammalian neocortex are underpinned
by intricate columnar and laminar circuits formed from an array of diverse neuronal
populations. One approach to determining how interactions between these circuit
components give rise to complex behavior is to investigate the rules by which
cortical circuits are formed and acquire functionality during development. This
review summarizes recent research on the development of the neocortex, from genetic
determination in neural stem cells through to the dynamic role that specific neuronal
populations play in the earliest circuits of neocortex, and how they contribute
to emergent function and cognition. While many of these endeavors take advantage
of model systems, consideration will also be given to advances in our understanding
of activity in nascent human circuits. Such cross-species perspective is imperative
when investigating the mechanisms underlying the dysfunction of early neocortical
circuits in neurodevelopmental disorders, so that one can identify targets amenable
to therapeutic intervention.
acknowledgement: Work in the I.L.H.-O. laboratory was supported by European Research
Council Grant ERC-2015-CoG 681577 and German Research Foundation Ha 4466/10-1, Ha4466/11-1,
Ha4466/12-1, SPP 1665, and SFB 936B5. Work in the S.J.B.B. laboratory was supported
by Biotechnology and Biological Sciences Research Council BB/P003796/1, Medical
Research Council MR/K004387/1 and MR/T033320/1, Wellcome Trust 215199/Z/19/Z and
102386/Z/13/Z, and John Fell Fund. Work in the S.H. laboratory was supported by
European Research Council Grants ERC-2016-CoG 725780 LinPro and FWF SFB F78. This
work was supported by National Institutes of Health Grant NIMH 1R01MH110553 to N.V.D.M.G.
Work in the J.A.C. laboratory was supported by the Ludwig Family Foundation, Simons
Foundation SFARI Research Award, and National Institutes of Health/National Institute
of Mental Health R01 MH102365 and R01MH113852. The B.V. laboratory was supported
by Whitehall Foundation 2017-12-73, National Science Foundation 1736028, National
Institutes of Health, National Institute of General Medical Sciences R01GM134363-01,
and Halıcıoğlu Data Science Institute Fellowship. This work was supported by the
University of California San Diego School of Medicine.
article_processing_charge: No
article_type: original
author:
- first_name: Ileana L.
full_name: Hanganu-Opatz, Ileana L.
last_name: Hanganu-Opatz
- first_name: Simon J. B.
full_name: Butt, Simon J. B.
last_name: Butt
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Natalia V.
full_name: De Marco García, Natalia V.
last_name: De Marco García
- first_name: Jessica A.
full_name: Cardin, Jessica A.
last_name: Cardin
- first_name: Bradley
full_name: Voytek, Bradley
last_name: Voytek
- first_name: Alysson R.
full_name: Muotri, Alysson R.
last_name: Muotri
citation:
ama: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, et al. The logic of developing neocortical
circuits in health and disease. The Journal of Neuroscience. 2021;41(5):813-822.
doi:10.1523/jneurosci.1655-20.2020
apa: Hanganu-Opatz, I. L., Butt, S. J. B., Hippenmeyer, S., De Marco García, N.
V., Cardin, J. A., Voytek, B., & Muotri, A. R. (2021). The logic of developing
neocortical circuits in health and disease. The Journal of Neuroscience.
Society for Neuroscience. https://doi.org/10.1523/jneurosci.1655-20.2020
chicago: Hanganu-Opatz, Ileana L., Simon J. B. Butt, Simon Hippenmeyer, Natalia
V. De Marco García, Jessica A. Cardin, Bradley Voytek, and Alysson R. Muotri.
“The Logic of Developing Neocortical Circuits in Health and Disease.” The Journal
of Neuroscience. Society for Neuroscience, 2021. https://doi.org/10.1523/jneurosci.1655-20.2020.
ieee: I. L. Hanganu-Opatz et al., “The logic of developing neocortical circuits
in health and disease,” The Journal of Neuroscience, vol. 41, no. 5. Society
for Neuroscience, pp. 813–822, 2021.
ista: Hanganu-Opatz IL, Butt SJB, Hippenmeyer S, De Marco García NV, Cardin JA,
Voytek B, Muotri AR. 2021. The logic of developing neocortical circuits in health
and disease. The Journal of Neuroscience. 41(5), 813–822.
mla: Hanganu-Opatz, Ileana L., et al. “The Logic of Developing Neocortical Circuits
in Health and Disease.” The Journal of Neuroscience, vol. 41, no. 5, Society
for Neuroscience, 2021, pp. 813–22, doi:10.1523/jneurosci.1655-20.2020.
short: I.L. Hanganu-Opatz, S.J.B. Butt, S. Hippenmeyer, N.V. De Marco García, J.A.
Cardin, B. Voytek, A.R. Muotri, The Journal of Neuroscience 41 (2021) 813–822.
date_created: 2021-02-03T12:23:51Z
date_published: 2021-02-03T00:00:00Z
date_updated: 2023-09-05T14:03:17Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1523/jneurosci.1655-20.2020
ec_funded: 1
external_id:
isi:
- '000616763400002'
pmid:
- '33431633'
file:
- access_level: open_access
checksum: 578fd7ed1a0aef74bce61bea2d987b33
content_type: application/pdf
creator: dernst
date_created: 2022-05-27T06:59:55Z
date_updated: 2022-05-27T06:59:55Z
file_id: '11414'
file_name: 2021_JourNeuroscience_Hanganu.pdf
file_size: 1031150
relation: main_file
success: 1
file_date_updated: 2022-05-27T06:59:55Z
has_accepted_license: '1'
intvolume: ' 41'
isi: 1
issue: '5'
keyword:
- General Neuroscience
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
page: 813-822
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: The Journal of Neuroscience
publication_identifier:
eissn:
- 1529-2401
issn:
- 0270-6474
publication_status: published
publisher: Society for Neuroscience
quality_controlled: '1'
scopus_import: '1'
status: public
title: The logic of developing neocortical circuits in health and disease
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 41
year: '2021'
...
---
_id: '9793'
abstract:
- lang: eng
text: Astrocytes extensively infiltrate the neuropil to regulate critical aspects
of synaptic development and function. This process is regulated by transcellular
interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes
coordinate developmental processes among one another to parse out the synaptic
neuropil and form non-overlapping territories is unknown. Here we identify a molecular
mechanism regulating astrocyte-astrocyte interactions during development to coordinate
astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked,
astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for
territory and morphological complexity in the developing mouse cortex. Furthermore,
conditional deletion of Hepacam from developing astrocytes significantly impairs
gap junction coupling between astrocytes and disrupts the balance between synaptic
excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy
with subcortical cysts in humans. Therefore, our findings suggest that disruption
of astrocyte self-organization mechanisms could be an underlying cause of neural
pathology.
acknowledgement: This work was supported by the National Institutes of Health (R01
DA047258 and R01 NS102237 to C.E., F32 NS100392 to K.T.B.) and the Holland-Trice
Brain Research Award (to C.E.). K.T.B. was supported by postdoctoral fellowships
from the Foerster-Bernstein Family and The Hartwell Foundation. The Hippenmeyer
lab was supported by the European Research Council (ERC) under the European Union’s
Horizon 2020 research and innovations program (725780 LinPro) to S.H. R.E. was supported
by Ministerio de Ciencia y Tecnología (RTI2018-093493-B-I00). We thank the Duke
Light Microscopy Core Facility, the Duke Transgenic Mouse Facility, Dr. U. Schulte
for assistance with proteomic experiments, and Dr. D. Silver for critical review
of the manuscript. Cartoon elements of figure panels were created using BioRender.com.
article_processing_charge: No
article_type: original
author:
- first_name: Katherine T.
full_name: Baldwin, Katherine T.
last_name: Baldwin
- first_name: Christabel X.
full_name: Tan, Christabel X.
last_name: Tan
- first_name: Samuel T.
full_name: Strader, Samuel T.
last_name: Strader
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
- first_name: Justin T.
full_name: Savage, Justin T.
last_name: Savage
- first_name: Xabier
full_name: Elorza-Vidal, Xabier
last_name: Elorza-Vidal
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Raúl
full_name: Estévez, Raúl
last_name: Estévez
- first_name: Ru-Rong
full_name: Ji, Ru-Rong
last_name: Ji
- first_name: Cagla
full_name: Eroglu, Cagla
last_name: Eroglu
citation:
ama: Baldwin KT, Tan CX, Strader ST, et al. HepaCAM controls astrocyte self-organization
and coupling. Neuron. 2021;109(15):2427-2442.e10. doi:10.1016/j.neuron.2021.05.025
apa: Baldwin, K. T., Tan, C. X., Strader, S. T., Jiang, C., Savage, J. T., Elorza-Vidal,
X., … Eroglu, C. (2021). HepaCAM controls astrocyte self-organization and coupling.
Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2021.05.025
chicago: Baldwin, Katherine T., Christabel X. Tan, Samuel T. Strader, Changyu Jiang,
Justin T. Savage, Xabier Elorza-Vidal, Ximena Contreras, et al. “HepaCAM Controls
Astrocyte Self-Organization and Coupling.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2021.05.025.
ieee: K. T. Baldwin et al., “HepaCAM controls astrocyte self-organization
and coupling,” Neuron, vol. 109, no. 15. Elsevier, p. 2427–2442.e10, 2021.
ista: Baldwin KT, Tan CX, Strader ST, Jiang C, Savage JT, Elorza-Vidal X, Contreras
X, Rülicke T, Hippenmeyer S, Estévez R, Ji R-R, Eroglu C. 2021. HepaCAM controls
astrocyte self-organization and coupling. Neuron. 109(15), 2427–2442.e10.
mla: Baldwin, Katherine T., et al. “HepaCAM Controls Astrocyte Self-Organization
and Coupling.” Neuron, vol. 109, no. 15, Elsevier, 2021, p. 2427–2442.e10,
doi:10.1016/j.neuron.2021.05.025.
short: K.T. Baldwin, C.X. Tan, S.T. Strader, C. Jiang, J.T. Savage, X. Elorza-Vidal,
X. Contreras, T. Rülicke, S. Hippenmeyer, R. Estévez, R.-R. Ji, C. Eroglu, Neuron
109 (2021) 2427–2442.e10.
date_created: 2021-08-06T09:08:25Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2023-09-27T07:46:09Z
day: '04'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2021.05.025
ec_funded: 1
external_id:
isi:
- '000692851900010'
pmid:
- '34171291'
intvolume: ' 109'
isi: 1
issue: '15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2021.05.025
month: '08'
oa: 1
oa_version: Published Version
page: 2427-2442.e10
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: HepaCAM controls astrocyte self-organization and coupling
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2021'
...
---
_id: '10321'
abstract:
- lang: eng
text: Mosaic analysis with double markers (MADM) technology enables the generation
of genetic mosaic tissue in mice. MADM enables concomitant fluorescent cell labeling
and introduction of a mutation of a gene of interest with single-cell resolution.
This protocol highlights major steps for the generation of genetic mosaic tissue
and the isolation and processing of respective tissues for downstream histological
analysis. For complete details on the use and execution of this protocol, please
refer to Contreras et al. (2021).
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical
Facilities (PCF). We particularly thank Mohammad Goudarzi for assistance with photography
of mouse perfusion and dissection. N.A. received support from FWF Firnberg-Programm
(T 1031). This work was also supported by IST Austria institutional funds; FWF SFB
F78 to S.H.; and the European Research Council (ERC) under the European Union’s
Horizon 2020 research and innovation programme (grant agreement no. 725780 LinPro)
to S.H.
article_number: '100939'
article_processing_charge: Yes
article_type: original
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Hippenmeyer S. Genetic mosaic dissection of candidate genes in mice
using mosaic analysis with double markers. STAR Protocols. 2021;2(4). doi:10.1016/j.xpro.2021.100939
apa: Amberg, N., & Hippenmeyer, S. (2021). Genetic mosaic dissection of candidate
genes in mice using mosaic analysis with double markers. STAR Protocols.
Cell Press. https://doi.org/10.1016/j.xpro.2021.100939
chicago: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate
Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols.
Cell Press, 2021. https://doi.org/10.1016/j.xpro.2021.100939.
ieee: N. Amberg and S. Hippenmeyer, “Genetic mosaic dissection of candidate genes
in mice using mosaic analysis with double markers,” STAR Protocols, vol.
2, no. 4. Cell Press, 2021.
ista: Amberg N, Hippenmeyer S. 2021. Genetic mosaic dissection of candidate genes
in mice using mosaic analysis with double markers. STAR Protocols. 2(4), 100939.
mla: Amberg, Nicole, and Simon Hippenmeyer. “Genetic Mosaic Dissection of Candidate
Genes in Mice Using Mosaic Analysis with Double Markers.” STAR Protocols,
vol. 2, no. 4, 100939, Cell Press, 2021, doi:10.1016/j.xpro.2021.100939.
short: N. Amberg, S. Hippenmeyer, STAR Protocols 2 (2021).
date_created: 2021-11-21T23:01:28Z
date_published: 2021-11-10T00:00:00Z
date_updated: 2023-11-16T13:08:03Z
day: '10'
ddc:
- '573'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2021.100939
ec_funded: 1
file:
- access_level: open_access
checksum: 9e3f6d06bf583e7a8b6a9e9a60500a28
content_type: application/pdf
creator: cchlebak
date_created: 2021-11-22T08:23:58Z
date_updated: 2021-11-22T08:23:58Z
file_id: '10329'
file_name: 2021_STARProtocols_Amberg.pdf
file_size: 7309464
relation: main_file
success: 1
file_date_updated: 2021-11-22T08:23:58Z
has_accepted_license: '1'
intvolume: ' 2'
issue: '4'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
publication: STAR Protocols
publication_identifier:
eissn:
- 2666-1667
publication_status: published
publisher: Cell Press
quality_controlled: '1'
scopus_import: '1'
status: public
title: Genetic mosaic dissection of candidate genes in mice using mosaic analysis
with double markers
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 2
year: '2021'
...
---
_id: '8544'
abstract:
- lang: eng
text: The synaptotrophic hypothesis posits that synapse formation stabilizes dendritic
branches, yet this hypothesis has not been causally tested in vivo in the mammalian
brain. Presynaptic ligand cerebellin-1 (Cbln1) and postsynaptic receptor GluD2
mediate synaptogenesis between granule cells and Purkinje cells in the molecular
layer of the cerebellar cortex. Here we show that sparse but not global knockout
of GluD2 causes under-elaboration of Purkinje cell dendrites in the deep molecular
layer and overelaboration in the superficial molecular layer. Developmental, overexpression,
structure-function, and genetic epistasis analyses indicate that dendrite morphogenesis
defects result from competitive synaptogenesis in a Cbln1/GluD2-dependent manner.
A generative model of dendritic growth based on competitive synaptogenesis largely
recapitulates GluD2 sparse and global knockout phenotypes. Our results support
the synaptotrophic hypothesis at initial stages of dendrite development, suggest
a second mode in which cumulative synapse formation inhibits further dendrite
growth, and highlight the importance of competition in dendrite morphogenesis.
acknowledgement: We thank M. Mishina for GluD2fl frozen embryos, T.C. Südhof and J.I.
Morgan for Cbln1fl mice, L. Anderson for help in generating the MADM alleles, W.
Joo for a previously unpublished construct, M. Yuzaki, K. Shen, J. Ding, and members
of the Luo lab, including J.M. Kebschull, H. Li, J. Li, T. Li, C.M. McLaughlin,
D. Pederick, J. Ren, D.C. Wang and C. Xu for discussions and critiques of the manuscript,
and M. Yuzaki for supporting Y.H.T. during the final phase of this project. Y.H.T.
was supported by a JSPS fellowship; S.A.S. was supported by a Stanford Graduate
Fellowship and an NSF Predoctoral Fellowship; L.J. is supported by a Stanford Graduate
Fellowship and an NSF Predoctoral Fellowship; M.J.W. is supported by a Burroughs
Wellcome Fund CASI Award. This work was supported by an NIH grant (R01-NS050538)
to L.L.; the European Research Council (ERC) under the European Union's Horizon
2020 research and innovations programme (No. 725780 LinPro) to S.H.; and Simons
and James S. McDonnell Foundations and an NSF CAREER award to S.G.; L.L. is an HHMI
investigator.
article_processing_charge: No
article_type: original
author:
- first_name: Yukari H.
full_name: Takeo, Yukari H.
last_name: Takeo
- first_name: S. Andrew
full_name: Shuster, S. Andrew
last_name: Shuster
- first_name: Linnie
full_name: Jiang, Linnie
last_name: Jiang
- first_name: Miley
full_name: Hu, Miley
last_name: Hu
- first_name: David J.
full_name: Luginbuhl, David J.
last_name: Luginbuhl
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Mark J.
full_name: Wagner, Mark J.
last_name: Wagner
- first_name: Surya
full_name: Ganguli, Surya
last_name: Ganguli
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Takeo YH, Shuster SA, Jiang L, et al. GluD2- and Cbln1-mediated competitive
synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron.
2021;109(4):P629-644.E8. doi:10.1016/j.neuron.2020.11.028
apa: Takeo, Y. H., Shuster, S. A., Jiang, L., Hu, M., Luginbuhl, D. J., Rülicke,
T., … Luo, L. (2021). GluD2- and Cbln1-mediated competitive synaptogenesis shapes
the dendritic arbors of cerebellar Purkinje cells. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.11.028
chicago: Takeo, Yukari H., S. Andrew Shuster, Linnie Jiang, Miley Hu, David J. Luginbuhl,
Thomas Rülicke, Ximena Contreras, et al. “GluD2- and Cbln1-Mediated Competitive
Synaptogenesis Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron.
Elsevier, 2021. https://doi.org/10.1016/j.neuron.2020.11.028.
ieee: Y. H. Takeo et al., “GluD2- and Cbln1-mediated competitive synaptogenesis
shapes the dendritic arbors of cerebellar Purkinje cells,” Neuron, vol.
109, no. 4. Elsevier, p. P629–644.E8, 2021.
ista: Takeo YH, Shuster SA, Jiang L, Hu M, Luginbuhl DJ, Rülicke T, Contreras X,
Hippenmeyer S, Wagner MJ, Ganguli S, Luo L. 2021. GluD2- and Cbln1-mediated competitive
synaptogenesis shapes the dendritic arbors of cerebellar Purkinje cells. Neuron.
109(4), P629–644.E8.
mla: Takeo, Yukari H., et al. “GluD2- and Cbln1-Mediated Competitive Synaptogenesis
Shapes the Dendritic Arbors of Cerebellar Purkinje Cells.” Neuron, vol.
109, no. 4, Elsevier, 2021, p. P629–644.E8, doi:10.1016/j.neuron.2020.11.028.
short: Y.H. Takeo, S.A. Shuster, L. Jiang, M. Hu, D.J. Luginbuhl, T. Rülicke, X.
Contreras, S. Hippenmeyer, M.J. Wagner, S. Ganguli, L. Luo, Neuron 109 (2021)
P629–644.E8.
date_created: 2020-09-21T11:59:47Z
date_published: 2021-02-17T00:00:00Z
date_updated: 2024-03-06T12:12:48Z
day: '17'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2020.11.028
ec_funded: 1
intvolume: ' 109'
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.06.14.151258
month: '02'
oa: 1
oa_version: Preprint
page: P629-644.E8
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: GluD2- and Cbln1-mediated competitive synaptogenesis shapes the dendritic arbors
of cerebellar Purkinje cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2021'
...
---
_id: '7814'
abstract:
- lang: eng
text: 'Scientific research is to date largely restricted to wealthy laboratories
in developed nations due to the necessity of complex and expensive equipment.
This inequality limits the capacity of science to be used as a diplomatic channel.
Maker movements use open-source technologies including additive manufacturing
(3D printing) and laser cutting, together with low-cost computers for developing
novel products. This movement is setting the groundwork for a revolution, allowing
scientific equipment to be sourced at a fraction of the cost and has the potential
to increase the availability of equipment for scientists around the world. Science
education is increasingly recognized as another channel for science diplomacy.
In this perspective, we introduce the idea that the Maker movement and open-source
technologies have the potential to revolutionize science, technology, engineering
and mathematics (STEM) education worldwide. We present an open-source STEM didactic
tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education
and Science). SCOPES is self-contained, independent of local resources, and cost-effective.
SCOPES can be adapted to communicate complex subjects from genetics to neurobiology,
perform real-world biological experiments and explore digitized scientific samples.
We envision such platforms will enhance science diplomacy by providing a means
for scientists to share their findings with classrooms and for educators to incorporate
didactic concepts into STEM lessons. By providing students the opportunity to
design, perform, and share scientific experiments, students also experience firsthand
the benefits of a multinational scientific community. We provide instructions
on how to build and use SCOPES on our webpage: http://scopeseducation.org.'
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
- _id: EM-Fac
article_number: '48'
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
citation:
ama: 'Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source
platforms in education and science. Frontiers in Education. 2020;5. doi:10.3389/feduc.2020.00048'
apa: 'Beattie, R. J., Hippenmeyer, S., & Pauler, F. (2020). SCOPES: Sparking
curiosity through Open-Source platforms in education and science. Frontiers
in Education. Frontiers Media. https://doi.org/10.3389/feduc.2020.00048'
chicago: 'Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking
Curiosity through Open-Source Platforms in Education and Science.” Frontiers
in Education. Frontiers Media, 2020. https://doi.org/10.3389/feduc.2020.00048.'
ieee: 'R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity
through Open-Source platforms in education and science,” Frontiers in Education,
vol. 5. Frontiers Media, 2020.'
ista: 'Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through
Open-Source platforms in education and science. Frontiers in Education. 5, 48.'
mla: 'Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source
Platforms in Education and Science.” Frontiers in Education, vol. 5, 48,
Frontiers Media, 2020, doi:10.3389/feduc.2020.00048.'
short: R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020).
date_created: 2020-05-11T08:18:48Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2021-01-12T08:15:42Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/feduc.2020.00048
ec_funded: 1
file:
- access_level: open_access
checksum: a24ec24e38d843341ae620ec76c53688
content_type: application/pdf
creator: dernst
date_created: 2020-05-11T11:34:08Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7818'
file_name: 2020_FrontiersEduc_Beattie.pdf
file_size: 1402146
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
intvolume: ' 5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Frontiers in Education
publication_identifier:
issn:
- 2504-284X
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
status: public
title: 'SCOPES: Sparking curiosity through Open-Source platforms in education and
science'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2020'
...
---
_id: '8616'
abstract:
- lang: eng
text: The brain vasculature supplies neurons with glucose and oxygen, but little
is known about how vascular plasticity contributes to brain function. Using longitudinal
in vivo imaging, we reported that a substantial proportion
of blood vessels in the adult brain sporadically occluded and regressed. Their
regression proceeded through sequential stages of blood-flow occlusion, endothelial
cell collapse, relocation or loss of pericytes, and retraction of glial endfeet.
Regressing vessels were found to be widespread in mouse, monkey and human brains.
Both brief occlusions of the middle cerebral artery and lipopolysaccharide-mediated
inflammation induced an increase of vessel regression. Blockage of leukocyte adhesion
to endothelial cells alleviated LPS-induced vessel regression. We further revealed
that blood vessel regression caused a reduction of neuronal activity due to a
dysfunction in mitochondrial metabolism and glutamate production. Our results
elucidate the mechanism of vessel regression and its role in neuronal function
in the adult brain.
acknowledgement: 'The project was initiated in the Jan lab at UCSF. We thank Lily
Jan and Yuh-Nung Jan’s generous support. We thank Liqun Luo’s lab for providing
MADM-7 mice and Rolf A Brekken for VEGF-antibodies. Drs. Yuanquan Song (UPenn),
Zhaozhu Hu (JHU), Ji Hu (ShanghaiTech), Yang Xiang (U. Mass), Hao Wang (Zhejiang
U.) and Ruikang Wang (U. Washington) for critical input, colleagues at Children’s
Research Institute, Departments of Neuroscience, Neurology and Neurotherapeutics,
Pediatrics from UT Southwestern, and colleagues from the Jan lab for discussion.
Dr. Bridget Samuels, Sean Morrison (UT Southwestern), and Nannan Lu (Zhejiang U.)
for critical reading. We acknowledge the assistance of the CIBR Imaging core. We
also thank UT Southwestern Live Cell Imaging Facility, a Shared Resource of the
Harold C. Simmons Cancer Center, supported in part by an NCI Cancer Center Support
Grant, P30 CA142543K. This work is supported by CIBR funds and the American Heart
Association AWRP Summer 2016 Innovative Research Grant (17IRG33410377) to W-P.G.;
National Natural Science Foundation of China (No.81370031) to Z.Z.;National Key
Research and Development Program of China (2016YFE0125400)to F.H.;National Natural
Science Foundations of China (No. 81473202) to Y.L.; National Natural Science Foundation
of China (No.31600839) and Shenzhen Science and Technology Research Program (JCYJ20170818163320865)
to B.P.; National Natural Science Foundation of China (No. 31800864) and Westlake
University start-up funds to J-M. J. NIH R01NS088627 to W.L.J.; NIH: R01 AG020670
and RF1AG054111 to H.Z.; R01 NS088555 to A.M.S., and European Research Council No.725780
to S.H.;W-P.G. was a recipient of Bugher-American Heart Association Dan Adams Thinking
Outside the Box Award.'
article_processing_charge: No
author:
- first_name: Xiaofei
full_name: Gao, Xiaofei
last_name: Gao
- first_name: Jun-Liszt
full_name: Li, Jun-Liszt
last_name: Li
- first_name: Xingjun
full_name: Chen, Xingjun
last_name: Chen
- first_name: Bo
full_name: Ci, Bo
last_name: Ci
- first_name: Fei
full_name: Chen, Fei
last_name: Chen
- first_name: Nannan
full_name: Lu, Nannan
last_name: Lu
- first_name: Bo
full_name: Shen, Bo
last_name: Shen
- first_name: Lijun
full_name: Zheng, Lijun
last_name: Zheng
- first_name: Jie-Min
full_name: Jia, Jie-Min
last_name: Jia
- first_name: Yating
full_name: Yi, Yating
last_name: Yi
- first_name: Shiwen
full_name: Zhang, Shiwen
last_name: Zhang
- first_name: Ying-Chao
full_name: Shi, Ying-Chao
last_name: Shi
- first_name: Kaibin
full_name: Shi, Kaibin
last_name: Shi
- first_name: Nicholas E
full_name: Propson, Nicholas E
last_name: Propson
- first_name: Yubin
full_name: Huang, Yubin
last_name: Huang
- first_name: Katherine
full_name: Poinsatte, Katherine
last_name: Poinsatte
- first_name: Zhaohuan
full_name: Zhang, Zhaohuan
last_name: Zhang
- first_name: Yuanlei
full_name: Yue, Yuanlei
last_name: Yue
- first_name: Dale B
full_name: Bosco, Dale B
last_name: Bosco
- first_name: Ying-mei
full_name: Lu, Ying-mei
last_name: Lu
- first_name: Shi-bing
full_name: Yang, Shi-bing
last_name: Yang
- first_name: Ralf H.
full_name: Adams, Ralf H.
last_name: Adams
- first_name: Volkhard
full_name: Lindner, Volkhard
last_name: Lindner
- first_name: Fen
full_name: Huang, Fen
last_name: Huang
- first_name: Long-Jun
full_name: Wu, Long-Jun
last_name: Wu
- first_name: Hui
full_name: Zheng, Hui
last_name: Zheng
- first_name: Feng
full_name: Han, Feng
last_name: Han
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ann M.
full_name: Stowe, Ann M.
last_name: Stowe
- first_name: Bo
full_name: Peng, Bo
last_name: Peng
- first_name: Marta
full_name: Margeta, Marta
last_name: Margeta
- first_name: Xiaoqun
full_name: Wang, Xiaoqun
last_name: Wang
- first_name: Qiang
full_name: Liu, Qiang
last_name: Liu
- first_name: Jakob
full_name: Körbelin, Jakob
last_name: Körbelin
- first_name: Martin
full_name: Trepel, Martin
last_name: Trepel
- first_name: Hui
full_name: Lu, Hui
last_name: Lu
- first_name: Bo O.
full_name: Zhou, Bo O.
last_name: Zhou
- first_name: Hu
full_name: Zhao, Hu
last_name: Zhao
- first_name: Wenzhi
full_name: Su, Wenzhi
last_name: Su
- first_name: Robert M.
full_name: Bachoo, Robert M.
last_name: Bachoo
- first_name: Woo-ping
full_name: Ge, Woo-ping
last_name: Ge
citation:
ama: Gao X, Li J-L, Chen X, et al. Reduction of neuronal activity mediated by blood-vessel
regression in the brain. bioRxiv. doi:10.1101/2020.09.15.262782
apa: Gao, X., Li, J.-L., Chen, X., Ci, B., Chen, F., Lu, N., … Ge, W. (n.d.). Reduction
of neuronal activity mediated by blood-vessel regression in the brain. bioRxiv.
Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.09.15.262782
chicago: Gao, Xiaofei, Jun-Liszt Li, Xingjun Chen, Bo Ci, Fei Chen, Nannan Lu, Bo
Shen, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel Regression
in the Brain.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2020.09.15.262782.
ieee: X. Gao et al., “Reduction of neuronal activity mediated by blood-vessel
regression in the brain,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Gao X, Li J-L, Chen X, Ci B, Chen F, Lu N, Shen B, Zheng L, Jia J-M, Yi Y,
Zhang S, Shi Y-C, Shi K, Propson NE, Huang Y, Poinsatte K, Zhang Z, Yue Y, Bosco
DB, Lu Y, Yang S, Adams RH, Lindner V, Huang F, Wu L-J, Zheng H, Han F, Hippenmeyer
S, Stowe AM, Peng B, Margeta M, Wang X, Liu Q, Körbelin J, Trepel M, Lu H, Zhou
BO, Zhao H, Su W, Bachoo RM, Ge W. Reduction of neuronal activity mediated by
blood-vessel regression in the brain. bioRxiv, 10.1101/2020.09.15.262782.
mla: Gao, Xiaofei, et al. “Reduction of Neuronal Activity Mediated by Blood-Vessel
Regression in the Brain.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.09.15.262782.
short: X. Gao, J.-L. Li, X. Chen, B. Ci, F. Chen, N. Lu, B. Shen, L. Zheng, J.-M.
Jia, Y. Yi, S. Zhang, Y.-C. Shi, K. Shi, N.E. Propson, Y. Huang, K. Poinsatte,
Z. Zhang, Y. Yue, D.B. Bosco, Y. Lu, S. Yang, R.H. Adams, V. Lindner, F. Huang,
L.-J. Wu, H. Zheng, F. Han, S. Hippenmeyer, A.M. Stowe, B. Peng, M. Margeta, X.
Wang, Q. Liu, J. Körbelin, M. Trepel, H. Lu, B.O. Zhou, H. Zhao, W. Su, R.M. Bachoo,
W. Ge, BioRxiv (n.d.).
date_created: 2020-10-06T08:58:59Z
date_published: 2020-09-15T00:00:00Z
date_updated: 2021-01-12T08:20:19Z
day: '15'
department:
- _id: SiHi
doi: 10.1101/2020.09.15.262782
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.09.15.262782
month: '09'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Reduction of neuronal activity mediated by blood-vessel regression in the brain
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8978'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables concomitant
fluorescent cell labeling and induction of uniparental chromosome disomy (UPD)
with single-cell resolution. In UPD, imprinted genes are either overexpressed
2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting
phenotypes at the transcriptional level. This protocol highlights major steps
for the generation and isolation of projection neurons and astrocytes with MADM-induced
UPD from mouse cerebral cortex for downstream single-cell and low-input sample
RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution
of this protocol, please refer to Laukoter et al. (2020b)."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical
Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031).
This work was also supported by IST Austria institutional funds; FWF SFB F78 to
S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the
European Research Council (ERC) under the European Union’s Horizon 2020 research
and innovation programme (grant agreement no. 725780 LinPro) to S.H.
article_number: '100215'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of
single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 2020;1(3). doi:10.1016/j.xpro.2020.100215
apa: Laukoter, S., Amberg, N., Pauler, F., & Hippenmeyer, S. (2020). Generation
and isolation of single cells from mouse brain with mosaic analysis with double
markers-induced uniparental chromosome disomy. STAR Protocols. Elsevier.
https://doi.org/10.1016/j.xpro.2020.100215
chicago: Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer.
“Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis
with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols.
Elsevier, 2020. https://doi.org/10.1016/j.xpro.2020.100215.
ieee: S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy,” STAR Protocols, vol. 1, no. 3. Elsevier,
2020.
ista: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 1(3), 100215.
mla: Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse
Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome
Disomy.” STAR Protocols, vol. 1, no. 3, 100215, Elsevier, 2020, doi:10.1016/j.xpro.2020.100215.
short: S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020).
date_created: 2020-12-30T10:17:07Z
date_published: 2020-12-18T00:00:00Z
date_updated: 2021-01-12T08:21:36Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2020.100215
ec_funded: 1
external_id:
pmid:
- '33377108'
file:
- access_level: open_access
checksum: f1e9a433e9cb0f41f7b6df6b76db1f6e
content_type: application/pdf
creator: dernst
date_created: 2021-01-07T15:57:27Z
date_updated: 2021-01-07T15:57:27Z
file_id: '8996'
file_name: 2020_STARProtocols_Laukoter.pdf
file_size: 4031449
relation: main_file
success: 1
file_date_updated: 2021-01-07T15:57:27Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '3'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F07805
name: Molecular Mechanisms of Neural Stem Cell Lineage Progression
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: published
publisher: Elsevier
quality_controlled: '1'
status: public
title: Generation and isolation of single cells from mouse brain with mosaic analysis
with double markers-induced uniparental chromosome disomy
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2020'
...
---
_id: '7253'
abstract:
- lang: eng
text: The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted
Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex
development. How Cdkn1c regulates corticogenesis is however not clear. To this
end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically
dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find
that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous
one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous
Cdkn1c function which at the mechanistic level mediates radial glial progenitor
cell and nascent projection neuron survival. Strikingly, the growth-promoting
function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting.
Collectively, our results suggest that the Cdkn1c locus regulates cortical development
through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally,
our study highlights the importance to probe the relative contributions of cell
intrinsic gene function and tissue-wide mechanisms to the overall phenotype.
acknowledged_ssus:
- _id: PreCl
article_number: '195'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Keiichi I.
full_name: Nakayama, Keiichi I.
last_name: Nakayama
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted
Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex
development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2
apa: Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., &
Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes
cell survival in cerebral cortex development. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-019-14077-2
chicago: Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi
I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2.
ieee: S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer,
“Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development,” Nature Communications, vol. 11. Springer Nature, 2020.
ista: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020.
Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development. Nature Communications. 11, 195.
mla: Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications,
vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2.
short: S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer,
Nature Communications 11 (2020).
date_created: 2020-01-11T10:42:48Z
date_published: 2020-01-10T00:00:00Z
date_updated: 2023-08-17T14:23:41Z
day: '10'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1038/s41467-019-14077-2
ec_funded: 1
external_id:
isi:
- '000551459000005'
file:
- access_level: open_access
checksum: ebf1ed522f4e0be8d94c939c1806a709
content_type: application/pdf
creator: dernst
date_created: 2020-01-13T07:42:31Z
date_updated: 2020-07-14T12:47:54Z
file_id: '7261'
file_name: 2020_NatureComm_Laukoter.pdf
file_size: 8063333
relation: main_file
file_date_updated: 2020-07-14T12:47:54Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/
scopus_import: '1'
status: public
title: Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in
cerebral cortex development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2020'
...
---
_id: '7593'
abstract:
- lang: eng
text: Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption
of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability
and dynein motor function/localization that alters mitotic spindle orientation,
chromosomal segregation, and nuclear migration. Recently, human induced pluripotent
stem cell (iPSC) models revealed an important role for LIS1 in controlling the
length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting
cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter
cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse
embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient
neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with
mislocalization of furrow-associated markers, associated with actomyosin dysfunction
and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular
link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility
is tightly controlled to execute proper daughter cell separation.
article_number: '51512'
article_processing_charge: No
article_type: original
author:
- first_name: Hyang Mi
full_name: Moon, Hyang Mi
last_name: Moon
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Anthony
full_name: Wynshaw-Boris, Anthony
last_name: Wynshaw-Boris
citation:
ama: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane
positioning by regulating actomyosin-mediated cell membrane contractility. eLife.
2020;9. doi:10.7554/elife.51512
apa: Moon, H. M., Hippenmeyer, S., Luo, L., & Wynshaw-Boris, A. (2020). LIS1
determines cleavage plane positioning by regulating actomyosin-mediated cell membrane
contractility. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.51512
chicago: Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris.
“LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated
Cell Membrane Contractility.” ELife. eLife Sciences Publications, 2020.
https://doi.org/10.7554/elife.51512.
ieee: H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines
cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,”
eLife, vol. 9. eLife Sciences Publications, 2020.
ista: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage
plane positioning by regulating actomyosin-mediated cell membrane contractility.
eLife. 9, 51512.
mla: Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating
Actomyosin-Mediated Cell Membrane Contractility.” ELife, vol. 9, 51512,
eLife Sciences Publications, 2020, doi:10.7554/elife.51512.
short: H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020).
date_created: 2020-03-20T13:16:41Z
date_published: 2020-03-11T00:00:00Z
date_updated: 2023-08-18T07:06:31Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/elife.51512
external_id:
isi:
- '000522835800001'
pmid:
- '32159512'
file:
- access_level: open_access
checksum: 396ceb2dd10b102ef4e699666b9342c3
content_type: application/pdf
creator: dernst
date_created: 2020-09-24T07:03:20Z
date_updated: 2020-09-24T07:03:20Z
file_id: '8567'
file_name: 2020_elife_Moon.pdf
file_size: 15089438
relation: main_file
success: 1
file_date_updated: 2020-09-24T07:03:20Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/751958
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: LIS1 determines cleavage plane positioning by regulating actomyosin-mediated
cell membrane contractility
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '8162'
abstract:
- lang: eng
text: In mammalian genomes, a subset of genes is regulated by genomic imprinting,
resulting in silencing of one parental allele. Imprinting is essential for cerebral
cortex development, but prevalence and functional impact in individual cells is
unclear. Here, we determined allelic expression in cortical cell types and established
a quantitative platform to interrogate imprinting in single cells. We created
cells with uniparental chromosome disomy (UPD) containing two copies of either
the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold
overexpressed or not expressed. By genetic labeling of UPD, we determined cellular
phenotypes and transcriptional responses to deregulated imprinted gene expression
at unprecedented single-cell resolution. We discovered an unexpected degree of
cell-type specificity and a novel function of imprinting in the regulation of
cortical astrocyte survival. More generally, our results suggest functional relevance
of imprinted gene expression in glial astrocyte lineage and thus for generating
cortical cell-type diversity.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and
C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical
support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen
for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of
the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo
for comments on earlier versions of the manuscript. This research was supported
by the Scientific Service Units (SSU) of IST Austria through resources provided
by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical
Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian
Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031).
R.B. received support from the FWF Meitner-Programm (M 2416). This work was also
supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b]
life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers
Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions)
of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant
agreement 618444 to S.H.; and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro)
to S.H.
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Thomas
full_name: Penz, Thomas
last_name: Penz
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
orcid: 0000-0001-6091-3088
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting
in cerebral cortex. Neuron. 2020;107(6):1160-1179.e9. doi:10.1016/j.neuron.2020.06.031
apa: Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher,
C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.06.031
chicago: Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi
H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer.
“Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron.
Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.06.031.
ieee: S. Laukoter et al., “Cell-type specificity of genomic imprinting in
cerebral cortex,” Neuron, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020.
ista: Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T,
Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. 107(6), 1160–1179.e9.
mla: Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral
Cortex.” Neuron, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:10.1016/j.neuron.2020.06.031.
short: S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher,
T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9.
date_created: 2020-07-23T16:03:12Z
date_published: 2020-09-23T00:00:00Z
date_updated: 2023-08-22T08:20:11Z
day: '23'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2020.06.031
ec_funded: 1
external_id:
isi:
- '000579698700006'
file:
- access_level: open_access
checksum: 7becdc16a6317304304631087ae7dd7f
content_type: application/pdf
creator: dernst
date_created: 2020-12-02T09:26:46Z
date_updated: 2020-12-02T09:26:46Z
file_id: '8828'
file_name: 2020_Neuron_Laukoter.pdf
file_size: 8911830
relation: main_file
success: 1
file_date_updated: 2020-12-02T09:26:46Z
has_accepted_license: '1'
intvolume: ' 107'
isi: 1
issue: '6'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 1160-1179.e9
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Website
relation: press_release
url: https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/
scopus_import: '1'
status: public
title: Cell-type specificity of genomic imprinting in cerebral cortex
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 107
year: '2020'
...
---
_id: '8592'
abstract:
- lang: eng
text: Glioblastoma is the most malignant cancer in the brain and currently incurable.
It is urgent to identify effective targets for this lethal disease. Inhibition
of such targets should suppress the growth of cancer cells and, ideally also precancerous
cells for early prevention, but minimally affect their normal counterparts. Using
genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor
cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility
of cells within the development hierarchy of glioma to the knockout of insulin‐like
growth factor I receptor (IGF1R) is determined not only by their oncogenic states,
but also by their cell identities/states. Knockout of IGF1R selectively disrupts
the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable
outcome of IGF1R knockout on cell growth requires the mutant cells to commit to
the OPC identity regardless of its development hierarchical status. At the molecular
level, oncogenic mutations reprogram the cellular network of OPCs and force them
to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally
available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed.
The findings reveal the cellular window of IGF1R targeting and establish IGF1R
as an effective target for the prevention and treatment of glioblastoma.
acknowledgement: The authors thank Drs. J. Eisen, QR. Lu, S. Duan, Z‐H. Li, W. Mo,
and Q. Wu for their critical comments on the manuscript. They also thank Dr. H.
Zong for providing the CKO_NG2‐CreER model. This work is supported by the National
Key Research and Development Program of China, Stem Cell and Translational Research
(2016YFA0101201 to C.L., 2016YFA0100303 to Y.J.W.), the National Natural Science
Foundation of China (81673035 and 81972915 to C.L., 81472722 to Y.J.W.), the Science
Foundation for Distinguished Young Scientists of Zhejiang Province (LR17H160001
to C.L.), Fundamental Research Funds for the Central Universities (2016QNA7023 and
2017QNA7028 to C.L.) and the Thousand Talent Program for Young Outstanding Scientists,
China (to C.L.), IST Austria institutional funds (to S.H.), European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation programme
(725780 LinPro to S.H.). C.L. is a scholar of K. C. Wong Education Foundation.
article_number: '2001724'
article_processing_charge: No
article_type: original
author:
- first_name: Anhao
full_name: Tian, Anhao
last_name: Tian
- first_name: Bo
full_name: Kang, Bo
last_name: Kang
- first_name: Baizhou
full_name: Li, Baizhou
last_name: Li
- first_name: Biying
full_name: Qiu, Biying
last_name: Qiu
- first_name: Wenhong
full_name: Jiang, Wenhong
last_name: Jiang
- first_name: Fangjie
full_name: Shao, Fangjie
last_name: Shao
- first_name: Qingqing
full_name: Gao, Qingqing
last_name: Gao
- first_name: Rui
full_name: Liu, Rui
last_name: Liu
- first_name: Chengwei
full_name: Cai, Chengwei
last_name: Cai
- first_name: Rui
full_name: Jing, Rui
last_name: Jing
- first_name: Wei
full_name: Wang, Wei
last_name: Wang
- first_name: Pengxiang
full_name: Chen, Pengxiang
last_name: Chen
- first_name: Qinghui
full_name: Liang, Qinghui
last_name: Liang
- first_name: Lili
full_name: Bao, Lili
last_name: Bao
- first_name: Jianghong
full_name: Man, Jianghong
last_name: Man
- first_name: Yan
full_name: Wang, Yan
last_name: Wang
- first_name: Yu
full_name: Shi, Yu
last_name: Shi
- first_name: Jin
full_name: Li, Jin
last_name: Li
- first_name: Minmin
full_name: Yang, Minmin
last_name: Yang
- first_name: Lisha
full_name: Wang, Lisha
last_name: Wang
- first_name: Jianmin
full_name: Zhang, Jianmin
last_name: Zhang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Junming
full_name: Zhu, Junming
last_name: Zhu
- first_name: Xiuwu
full_name: Bian, Xiuwu
last_name: Bian
- first_name: Ying‐Jie
full_name: Wang, Ying‐Jie
last_name: Wang
- first_name: Chong
full_name: Liu, Chong
last_name: Liu
citation:
ama: Tian A, Kang B, Li B, et al. Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting. Advanced Science. 2020;7(21). doi:10.1002/advs.202001724
apa: Tian, A., Kang, B., Li, B., Qiu, B., Jiang, W., Shao, F., … Liu, C. (2020).
Oncogenic state and cell identity combinatorially dictate the susceptibility of
cells within glioma development hierarchy to IGF1R targeting. Advanced Science.
Wiley. https://doi.org/10.1002/advs.202001724
chicago: Tian, Anhao, Bo Kang, Baizhou Li, Biying Qiu, Wenhong Jiang, Fangjie Shao,
Qingqing Gao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science. Wiley, 2020. https://doi.org/10.1002/advs.202001724.
ieee: A. Tian et al., “Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting,” Advanced Science, vol. 7, no. 21. Wiley, 2020.
ista: Tian A, Kang B, Li B, Qiu B, Jiang W, Shao F, Gao Q, Liu R, Cai C, Jing R,
Wang W, Chen P, Liang Q, Bao L, Man J, Wang Y, Shi Y, Li J, Yang M, Wang L, Zhang
J, Hippenmeyer S, Zhu J, Bian X, Wang Y, Liu C. 2020. Oncogenic state and cell
identity combinatorially dictate the susceptibility of cells within glioma development
hierarchy to IGF1R targeting. Advanced Science. 7(21), 2001724.
mla: Tian, Anhao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science, vol. 7, no. 21, 2001724, Wiley, 2020, doi:10.1002/advs.202001724.
short: A. Tian, B. Kang, B. Li, B. Qiu, W. Jiang, F. Shao, Q. Gao, R. Liu, C. Cai,
R. Jing, W. Wang, P. Chen, Q. Liang, L. Bao, J. Man, Y. Wang, Y. Shi, J. Li, M.
Yang, L. Wang, J. Zhang, S. Hippenmeyer, J. Zhu, X. Bian, Y. Wang, C. Liu, Advanced
Science 7 (2020).
date_created: 2020-10-01T09:44:13Z
date_published: 2020-11-04T00:00:00Z
date_updated: 2023-08-22T09:53:01Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1002/advs.202001724
ec_funded: 1
external_id:
isi:
- '000573860700001'
file:
- access_level: open_access
checksum: 92818c23ecc70e35acfa671f3cfb9909
content_type: application/pdf
creator: dernst
date_created: 2020-12-10T14:07:24Z
date_updated: 2020-12-10T14:07:24Z
file_id: '8938'
file_name: 2020_AdvScience_Tian.pdf
file_size: 7835833
relation: main_file
success: 1
file_date_updated: 2020-12-10T14:07:24Z
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
issue: '21'
keyword:
- General Engineering
- General Physics and Astronomy
- General Materials Science
- Medicine (miscellaneous)
- General Chemical Engineering
- Biochemistry
- Genetics and Molecular Biology (miscellaneous)
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Advanced Science
publication_identifier:
issn:
- 2198-3844
publication_status: published
publisher: Wiley
quality_controlled: '1'
status: public
title: Oncogenic state and cell identity combinatorially dictate the susceptibility
of cells within glioma development hierarchy to IGF1R targeting
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 7
year: '2020'
...
---
_id: '8949'
abstract:
- lang: eng
text: Development of the nervous system undergoes important transitions,
including one from neurogenesis to gliogenesis which occurs late during embryonic
gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic
Analysis with Double Markers (MADM) with quantitative and computational methods.
Results reveal that developmental gliogenesis in the cerebral cortex occurs in
a fraction of earlier neurogenic clones, accelerating around E16.5, and giving
rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion
of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that
Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices.
A broad range in the proliferation capacity, symmetry of clones, and competitive
advantage of MADM cells was evident in clones that contained one cellular lineage
with double dosage of Egfr relative to their environment, while their sibling
Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia
in MADM clones balance out regardless of significant alterations in clonal symmetries.
The variability in glial clones shows stochastic patterns that we define mathematically,
which are different from the deterministic patterns in neuronal clones. This study
sets a foundation for studying the biological significance of stochastic and deterministic
clonal principles underlying tissue development, and identifying mechanisms that
differentiate between neurogenesis and gliogenesis.
acknowledgement: This research was funded by grants from the National Institutes of
Health to H.T.G. (R01NS098370 and R01NS089795). C.V.M. was supported by a National
Science Foundation Graduate Research Fellowship (DGE-1746939). R.B. was supported
by the FWF Lise-Meitner program (M 2416), and S.H. was supported by the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
programme (grant agreement No 725780 LinPro).The authors thank members of the Ghashghaei
lab for discussions, technical support, and help with preparation of the manuscript.
article_number: '2662'
article_processing_charge: No
article_type: original
author:
- first_name: Xuying
full_name: Zhang, Xuying
last_name: Zhang
- first_name: Christine V.
full_name: Mennicke, Christine V.
last_name: Mennicke
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Mansoor
full_name: Haider, Mansoor
last_name: Haider
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H. Troy
full_name: Ghashghaei, H. Troy
last_name: Ghashghaei
citation:
ama: Zhang X, Mennicke CV, Xiao G, et al. Clonal analysis of gliogenesis in the
cerebral cortex reveals stochastic expansion of glia and cell autonomous responses
to Egfr dosage. Cells. 2020;9(12). doi:10.3390/cells9122662
apa: Zhang, X., Mennicke, C. V., Xiao, G., Beattie, R. J., Haider, M., Hippenmeyer,
S., & Ghashghaei, H. T. (2020). Clonal analysis of gliogenesis in the cerebral
cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr
dosage. Cells. MDPI. https://doi.org/10.3390/cells9122662
chicago: Zhang, Xuying, Christine V. Mennicke, Guanxi Xiao, Robert J Beattie, Mansoor
Haider, Simon Hippenmeyer, and H. Troy Ghashghaei. “Clonal Analysis of Gliogenesis
in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous
Responses to Egfr Dosage.” Cells. MDPI, 2020. https://doi.org/10.3390/cells9122662.
ieee: X. Zhang et al., “Clonal analysis of gliogenesis in the cerebral cortex
reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage,”
Cells, vol. 9, no. 12. MDPI, 2020.
ista: Zhang X, Mennicke CV, Xiao G, Beattie RJ, Haider M, Hippenmeyer S, Ghashghaei
HT. 2020. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic
expansion of glia and cell autonomous responses to Egfr dosage. Cells. 9(12),
2662.
mla: Zhang, Xuying, et al. “Clonal Analysis of Gliogenesis in the Cerebral Cortex
Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.”
Cells, vol. 9, no. 12, 2662, MDPI, 2020, doi:10.3390/cells9122662.
short: X. Zhang, C.V. Mennicke, G. Xiao, R.J. Beattie, M. Haider, S. Hippenmeyer,
H.T. Ghashghaei, Cells 9 (2020).
date_created: 2020-12-14T08:04:03Z
date_published: 2020-12-11T00:00:00Z
date_updated: 2023-08-24T10:57:48Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/cells9122662
ec_funded: 1
external_id:
isi:
- '000601787300001'
file:
- access_level: open_access
checksum: 5095cbdc728c9a510c5761cf60a8861c
content_type: application/pdf
creator: dernst
date_created: 2020-12-14T08:09:43Z
date_updated: 2020-12-14T08:09:43Z
file_id: '8950'
file_name: 2020_Cells_Zhang.pdf
file_size: 3504525
relation: main_file
success: 1
file_date_updated: 2020-12-14T08:09:43Z
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Cells
publication_identifier:
issn:
- 2073-4409
publication_status: published
publisher: MDPI
quality_controlled: '1'
status: public
title: Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion
of glia and cell autonomous responses to Egfr dosage
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '8813'
abstract:
- lang: eng
text: 'In mammals, chromatin marks at imprinted genes are asymmetrically inherited
to control parentally-biased gene expression. This control is thought predominantly
to involve parent-specific differentially methylated regions (DMR) in genomic
DNA. However, neither parent-of-origin-specific transcription nor DMRs have been
comprehensively mapped. We here address this by integrating transcriptomic and
epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis
identified 71 genes expressed with previously unknown parent-of-origin-specific
expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental
expression of nBiX genes disappeared soon after implantation. Micro-whole-genome
bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859
DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated
with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated
imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted
gene, and five novel clusters contained exclusively nBiX-genes. These data suggest
a complex program of stage-specific imprinting involving different tiers of regulation.'
article_processing_charge: No
author:
- first_name: Laura
full_name: Santini, Laura
last_name: Santini
- first_name: Florian
full_name: Halbritter, Florian
last_name: Halbritter
- first_name: Fabian
full_name: Titz-Teixeira, Fabian
last_name: Titz-Teixeira
- first_name: Toru
full_name: Suzuki, Toru
last_name: Suzuki
- first_name: Maki
full_name: Asami, Maki
last_name: Asami
- first_name: Julia
full_name: Ramesmayer, Julia
last_name: Ramesmayer
- first_name: Xiaoyan
full_name: Ma, Xiaoyan
last_name: Ma
- first_name: Andreas
full_name: Lackner, Andreas
last_name: Lackner
- first_name: Nick
full_name: Warr, Nick
last_name: Warr
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ernest
full_name: Laue, Ernest
last_name: Laue
- first_name: Matthias
full_name: Farlik, Matthias
last_name: Farlik
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Andreas
full_name: Beyer, Andreas
last_name: Beyer
- first_name: Anthony C. F.
full_name: Perry, Anthony C. F.
last_name: Perry
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
citation:
ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts
are predominantly DNA methylation independent. bioRxiv. doi:10.1101/2020.11.03.366948
apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer,
J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2020.11.03.366948
chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki,
Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts
Are Predominantly DNA Methylation Independent.” BioRxiv. Cold Spring Harbor
Laboratory, n.d. https://doi.org/10.1101/2020.11.03.366948.
ieee: L. Santini et al., “Novel imprints in mouse blastocysts are predominantly
DNA methylation independent,” bioRxiv. Cold Spring Harbor Laboratory.
ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J,
Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer
A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv, 10.1101/2020.11.03.366948.
mla: Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly
DNA Methylation Independent.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2020.11.03.366948.
short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer,
X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C.
Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.).
date_created: 2020-11-26T07:17:19Z
date_published: 2020-11-05T00:00:00Z
date_updated: 2023-09-12T11:05:28Z
day: '05'
department:
- _id: SiHi
doi: 10.1101/2020.11.03.366948
external_id:
pmid:
- 'PPR234457 '
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.11.03.366948
month: '11'
oa: 1
oa_version: Preprint
pmid: 1
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Novel imprints in mouse blastocysts are predominantly DNA methylation independent
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '8569'
abstract:
- lang: eng
text: Concerted radial migration of newly born cortical projection neurons, from
their birthplace to their final target lamina, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating the specific
sequential steps of radial neuronal migration in vivo are however still unclear,
let alone the effects and interactions with the extracellular environment. In
any in vivo context, cells will always be exposed to a complex extracellular environment
consisting of (1) secreted factors acting as potential signaling cues, (2) the
extracellular matrix, and (3) other cells providing cell–cell interaction through
receptors and/or direct physical stimuli. Most studies so far have described and
focused mainly on intrinsic cell-autonomous gene functions in neuronal migration
but there is accumulating evidence that non-cell-autonomous-, local-, systemic-,
and/or whole tissue-wide effects substantially contribute to the regulation of
radial neuronal migration. These non-cell-autonomous effects may differentially
affect cortical neuron migration in distinct cellular environments. However, the
cellular and molecular natures of such non-cell-autonomous mechanisms are mostly
unknown. Furthermore, physical forces due to collective migration and/or community
effects (i.e., interactions with surrounding cells) may play important roles in
neocortical projection neuron migration. In this concise review, we first outline
distinct models of non-cell-autonomous interactions of cortical projection neurons
along their radial migration trajectory during development. We then summarize
experimental assays and platforms that can be utilized to visualize and potentially
probe non-cell-autonomous mechanisms. Lastly, we define key questions to address
in the future.
acknowledgement: AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy
of Sciences. This work also received support from IST Austria institutional funds;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH.
article_number: '574382'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 2020;8(9). doi:10.3389/fcell.2020.574382
apa: Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms
in radial projection neuron migration in the developing cerebral cortex. Frontiers
in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms
in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382.
ieee: A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial
projection neuron migration in the developing cerebral cortex,” Frontiers in
Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020.
ista: Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 8(9), 574382.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in
Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020,
doi:10.3389/fcell.2020.574382.
short: A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology
8 (2020).
date_created: 2020-09-26T06:11:07Z
date_published: 2020-09-25T00:00:00Z
date_updated: 2024-03-28T23:30:41Z
day: '25'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/fcell.2020.574382
ec_funded: 1
external_id:
isi:
- '000577915900001'
pmid:
- '33102480'
file:
- access_level: open_access
checksum: 01f731824194c94c81a5da360d997073
content_type: application/pdf
creator: dernst
date_created: 2020-09-28T13:11:17Z
date_updated: 2020-09-28T13:11:17Z
file_id: '8584'
file_name: 2020_Frontiers_Hansen.pdf
file_size: 5527139
relation: main_file
success: 1
file_date_updated: 2020-09-28T13:11:17Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
issn:
- 2296-634X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Non-cell-autonomous mechanisms in radial projection neuron migration in the
developing cerebral cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2020'
...
---
_id: '7815'
abstract:
- lang: eng
text: Beginning from a limited pool of progenitors, the mammalian cerebral cortex
forms highly organized functional neural circuits. However, the underlying cellular
and molecular mechanisms regulating lineage transitions of neural stem cells (NSCs)
and eventual production of neurons and glia in the developing neuroepithelium
remains unclear. Methods to trace NSC division patterns and map the lineage of
clonally related cells have advanced dramatically. However, many contemporary
lineage tracing techniques suffer from the lack of cellular resolution of progeny
cell fate, which is essential for deciphering progenitor cell division patterns.
Presented is a protocol using mosaic analysis with double markers (MADM) to perform
in vivo clonal analysis. MADM concomitantly manipulates individual progenitor
cells and visualizes precise division patterns and lineage progression at unprecedented
single cell resolution. MADM-based interchromosomal recombination events during
the G2-X phase of mitosis, together with temporally inducible CreERT2, provide
exact information on the birth dates of clones and their division patterns. Thus,
MADM lineage tracing provides unprecedented qualitative and quantitative optical
readouts of the proliferation mode of stem cell progenitors at the single cell
level. MADM also allows for examination of the mechanisms and functional requirements
of candidate genes in NSC lineage progression. This method is unique in that comparative
analysis of control and mutant subclones can be performed in the same tissue environment
in vivo. Here, the protocol is described in detail, and experimental paradigms
to employ MADM for clonal analysis and lineage tracing in the developing cerebral
cortex are demonstrated. Importantly, this protocol can be adapted to perform
MADM clonal analysis in any murine stem cell niche, as long as the CreERT2 driver
is present.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
article_number: e61147
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Streicher C, Amberg N, et al. Lineage tracing and clonal analysis
in developing cerebral cortex using mosaic analysis with double markers (MADM).
Journal of Visual Experiments. 2020;(159). doi:10.3791/61147
apa: Beattie, R. J., Streicher, C., Amberg, N., Cheung, G. T., Contreras, X., Hansen,
A. H., & Hippenmeyer, S. (2020). Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM). Journal of
Visual Experiments. MyJove Corporation. https://doi.org/10.3791/61147
chicago: Beattie, Robert J, Carmen Streicher, Nicole Amberg, Giselle T Cheung, Ximena
Contreras, Andi H Hansen, and Simon Hippenmeyer. “Lineage Tracing and Clonal Analysis
in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).”
Journal of Visual Experiments. MyJove Corporation, 2020. https://doi.org/10.3791/61147.
ieee: R. J. Beattie et al., “Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM),” Journal
of Visual Experiments, no. 159. MyJove Corporation, 2020.
ista: Beattie RJ, Streicher C, Amberg N, Cheung GT, Contreras X, Hansen AH, Hippenmeyer
S. 2020. Lineage tracing and clonal analysis in developing cerebral cortex using
mosaic analysis with double markers (MADM). Journal of Visual Experiments. (159),
e61147.
mla: Beattie, Robert J., et al. “Lineage Tracing and Clonal Analysis in Developing
Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal
of Visual Experiments, no. 159, e61147, MyJove Corporation, 2020, doi:10.3791/61147.
short: R.J. Beattie, C. Streicher, N. Amberg, G.T. Cheung, X. Contreras, A.H. Hansen,
S. Hippenmeyer, Journal of Visual Experiments (2020).
date_created: 2020-05-11T08:31:20Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2024-03-28T23:30:42Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3791/61147
ec_funded: 1
external_id:
isi:
- '000546406600043'
file:
- access_level: open_access
checksum: 3154ea7f90b9fb45e084cd1c2770597d
content_type: application/pdf
creator: rbeattie
date_created: 2020-05-11T08:28:38Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7816'
file_name: jove-protocol-61147-lineage-tracing-clonal-analysis-developing-cerebral-cortex-using.pdf
file_size: 1352186
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
isi: 1
issue: '159'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular Mechanisms of Radial Neuronal Migration
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Visual Experiments
publication_identifier:
issn:
- 1940-087X
publication_status: published
publisher: MyJove Corporation
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Lineage tracing and clonal analysis in developing cerebral cortex using mosaic
analysis with double markers (MADM)
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '6091'
abstract:
- lang: eng
text: Cortical networks are characterized by sparse connectivity, with synapses
found at only a subset of axo-dendritic contacts. Yet within these networks, neurons
can exhibit high connection probabilities, suggesting that cell-intrinsic factors,
not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a
factor that determines synapse density by mediating a cell-cell competition that
requires ephrin-B-EphB signaling. In a microisland culture system designed to
isolate cell-cell competition, we find that eB3 determines winning and losing
neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM)
genetic mouse model system in vivo the relative levels of eB3 control spine density
in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls
synapse density independently of action potential-driven activity. Our findings
illustrate a new class of competitive mechanism mediated by trans-synaptic organizing
proteins which control the number of synapses neurons receive relative to neighboring
neurons.
article_number: e41563
article_processing_charge: No
author:
- first_name: Nathan T.
full_name: Henderson, Nathan T.
last_name: Henderson
- first_name: Sylvain J.
full_name: Le Marchand, Sylvain J.
last_name: Le Marchand
- first_name: Martin
full_name: Hruska, Martin
last_name: Hruska
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Matthew B.
full_name: Dalva, Matthew B.
last_name: Dalva
citation:
ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3
controls excitatory synapse density through cell-cell competition for EphBs. eLife.
2019;8. doi:10.7554/eLife.41563
apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L.,
& Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through
cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563
chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer,
Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.41563.
ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and
M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell
competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019.
Ephrin-B3 controls excitatory synapse density through cell-cell competition for
EphBs. eLife. 8, e41563.
mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife
Sciences Publications, 2019, doi:10.7554/eLife.41563.
short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B.
Dalva, ELife 8 (2019).
date_created: 2019-03-10T22:59:20Z
date_published: 2019-02-21T00:00:00Z
date_updated: 2023-08-24T14:50:50Z
day: '21'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.41563
external_id:
isi:
- '000459380600001'
pmid:
- '30789343'
file:
- access_level: open_access
checksum: 7b0800d003f14cd06b1802dea0c52941
content_type: application/pdf
creator: dernst
date_created: 2019-03-11T16:15:37Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6098'
file_name: 2019_eLife_Henderson.pdf
file_size: 7260753
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ephrin-B3 controls excitatory synapse density through cell-cell competition
for EphBs
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6844'
abstract:
- lang: eng
text: Studying the progression of the proliferative and differentiative patterns
of neural stem cells at the individual cell level is crucial to the understanding
of cortex development and how the disruption of such patterns can lead to malformations
and neurodevelopmental diseases. However, our understanding of the precise lineage
progression programme at single-cell resolution is still incomplete due to the
technical variations in lineage- tracing approaches. One of the key challenges
involves developing a robust theoretical framework in which we can integrate experimental
observations and introduce correction factors to obtain a reliable and representative
description of the temporal modulation of proliferation and differentiation. In
order to obtain more conclusive insights, we carry out virtual clonal analysis
using mathematical modelling and compare our results against experimental data.
Using a dataset obtained with Mosaic Analysis with Double Markers, we illustrate
how the theoretical description can be exploited to interpret and reconcile the
disparity between virtual and experimental results.
article_processing_charge: No
article_type: original
author:
- first_name: Noemi
full_name: Picco, Noemi
last_name: Picco
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Julio
full_name: Rodarte, Julio
id: 3C70A038-F248-11E8-B48F-1D18A9856A87
last_name: Rodarte
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Zoltán
full_name: Molnár, Zoltán
last_name: Molnár
- first_name: Philip K.
full_name: Maini, Philip K.
last_name: Maini
- first_name: Thomas E.
full_name: Woolley, Thomas E.
last_name: Woolley
citation:
ama: Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell
labelling experiments for clonal analysis. Journal of Anatomy. 2019;235(3):686-696.
doi:10.1111/joa.13001
apa: Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini,
P. K., & Woolley, T. E. (2019). A mathematical insight into cell labelling
experiments for clonal analysis. Journal of Anatomy. Wiley. https://doi.org/10.1111/joa.13001
chicago: Picco, Noemi, Simon Hippenmeyer, Julio Rodarte, Carmen Streicher, Zoltán
Molnár, Philip K. Maini, and Thomas E. Woolley. “A Mathematical Insight into Cell
Labelling Experiments for Clonal Analysis.” Journal of Anatomy. Wiley,
2019. https://doi.org/10.1111/joa.13001.
ieee: N. Picco et al., “A mathematical insight into cell labelling experiments
for clonal analysis,” Journal of Anatomy, vol. 235, no. 3. Wiley, pp. 686–696,
2019.
ista: Picco N, Hippenmeyer S, Rodarte J, Streicher C, Molnár Z, Maini PK, Woolley
TE. 2019. A mathematical insight into cell labelling experiments for clonal analysis.
Journal of Anatomy. 235(3), 686–696.
mla: Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments
for Clonal Analysis.” Journal of Anatomy, vol. 235, no. 3, Wiley, 2019,
pp. 686–96, doi:10.1111/joa.13001.
short: N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini,
T.E. Woolley, Journal of Anatomy 235 (2019) 686–696.
date_created: 2019-09-02T11:57:28Z
date_published: 2019-09-01T00:00:00Z
date_updated: 2023-08-29T07:19:39Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/joa.13001
ec_funded: 1
external_id:
isi:
- '000482426800017'
file:
- access_level: open_access
checksum: 160f960844b204057f20896e0e1f8ee7
content_type: application/pdf
creator: dernst
date_created: 2019-09-02T12:05:18Z
date_updated: 2020-07-14T12:47:42Z
file_id: '6845'
file_name: 2019_JournalAnatomy_Picco.pdf
file_size: 1192994
relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: ' 235'
isi: 1
issue: '3'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 686-696
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Anatomy
publication_identifier:
eissn:
- 1469-7580
issn:
- 0021-8782
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: A mathematical insight into cell labelling experiments for clonal analysis
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 235
year: '2019'
...
---
_id: '6455'
abstract:
- lang: eng
text: During corticogenesis, distinct subtypes of neurons are sequentially born
from ventricular zone progenitors. How these cells are molecularly temporally
patterned is poorly understood. We used single-cell RNA sequencing at high temporal
resolution to trace the lineage of the molecular identities of successive generations
of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified
a core set of evolutionarily conserved, temporally patterned genes that drive
APs from internally driven to more exteroceptive states. We found that the Polycomb
repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic
age–dependent AP molecular states are transmitted to their progeny as successive
ground states, onto which essentially conserved early postmitotic differentiation
programs are applied, and are complemented by later-occurring environment-dependent
signals. Thus, epigenetically regulated temporal molecular birthmarks present
in progenitors act in their postmitotic progeny to seed adult neuronal diversity.
article_number: eaav2522
article_processing_charge: No
article_type: original
author:
- first_name: L
full_name: Telley, L
last_name: Telley
- first_name: G
full_name: Agirman, G
last_name: Agirman
- first_name: J
full_name: Prados, J
last_name: Prados
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: S
full_name: Fièvre, S
last_name: Fièvre
- first_name: P
full_name: Oberst, P
last_name: Oberst
- first_name: G
full_name: Bartolini, G
last_name: Bartolini
- first_name: I
full_name: Vitali, I
last_name: Vitali
- first_name: C
full_name: Cadilhac, C
last_name: Cadilhac
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: L
full_name: Nguyen, L
last_name: Nguyen
- first_name: A
full_name: Dayer, A
last_name: Dayer
- first_name: D
full_name: Jabaudon, D
last_name: Jabaudon
citation:
ama: Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors
and their daughter neurons in the developing neocortex. Science. 2019;364(6440).
doi:10.1126/science.aav2522
apa: Telley, L., Agirman, G., Prados, J., Amberg, N., Fièvre, S., Oberst, P., …
Jabaudon, D. (2019). Temporal patterning of apical progenitors and their daughter
neurons in the developing neocortex. Science. AAAS. https://doi.org/10.1126/science.aav2522
chicago: Telley, L, G Agirman, J Prados, Nicole Amberg, S Fièvre, P Oberst, G Bartolini,
et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in
the Developing Neocortex.” Science. AAAS, 2019. https://doi.org/10.1126/science.aav2522.
ieee: L. Telley et al., “Temporal patterning of apical progenitors and their
daughter neurons in the developing neocortex,” Science, vol. 364, no. 6440.
AAAS, 2019.
ista: Telley L, Agirman G, Prados J, Amberg N, Fièvre S, Oberst P, Bartolini G,
Vitali I, Cadilhac C, Hippenmeyer S, Nguyen L, Dayer A, Jabaudon D. 2019. Temporal
patterning of apical progenitors and their daughter neurons in the developing
neocortex. Science. 364(6440), eaav2522.
mla: Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter
Neurons in the Developing Neocortex.” Science, vol. 364, no. 6440, eaav2522,
AAAS, 2019, doi:10.1126/science.aav2522.
short: L. Telley, G. Agirman, J. Prados, N. Amberg, S. Fièvre, P. Oberst, G. Bartolini,
I. Vitali, C. Cadilhac, S. Hippenmeyer, L. Nguyen, A. Dayer, D. Jabaudon, Science
364 (2019).
date_created: 2019-05-14T13:07:47Z
date_published: 2019-05-10T00:00:00Z
date_updated: 2023-09-05T11:51:09Z
day: '10'
department:
- _id: SiHi
doi: 10.1126/science.aav2522
ec_funded: 1
external_id:
isi:
- '000467631800034'
pmid:
- '31073041'
intvolume: ' 364'
isi: 1
issue: '6440'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T0101031
name: Role of Eed in neural stem cell lineage progression
publication: Science
publication_identifier:
eissn:
- 1095-9203
issn:
- 0036-8075
publication_status: published
publisher: AAAS
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/
scopus_import: '1'
status: public
title: Temporal patterning of apical progenitors and their daughter neurons in the
developing neocortex
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 364
year: '2019'
...
---
_id: '6454'
abstract:
- lang: eng
text: 'Adult neural stem cells and multiciliated ependymalcells are glial cells
essential for neurological func-tions. Together, they make up the adult neurogenicniche.
Using both high-throughput clonal analysisand single-cell resolution of progenitor
division pat-terns and fate, we show that these two componentsof the neurogenic
niche are lineally related: adult neu-ral stem cells are sister cells to ependymal
cells,whereas most ependymal cells arise from the termi-nal symmetric divisions
of the lineage. Unexpectedly,we found that the antagonist regulators of DNA repli-cation,
GemC1 and Geminin, can tune the proportionof neural stem cells and ependymal cells.
Our find-ings reveal the controlled dynamic of the neurogenicniche ontogeny and
identify the Geminin familymembers as key regulators of the initial pool of adultneural
stem cells.'
article_processing_charge: No
author:
- first_name: G
full_name: Ortiz-Álvarez, G
last_name: Ortiz-Álvarez
- first_name: M
full_name: Daclin, M
last_name: Daclin
- first_name: A
full_name: Shihavuddin, A
last_name: Shihavuddin
- first_name: P
full_name: Lansade, P
last_name: Lansade
- first_name: A
full_name: Fortoul, A
last_name: Fortoul
- first_name: M
full_name: Faucourt, M
last_name: Faucourt
- first_name: S
full_name: Clavreul, S
last_name: Clavreul
- first_name: ME
full_name: Lalioti, ME
last_name: Lalioti
- first_name: S
full_name: Taraviras, S
last_name: Taraviras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: J
full_name: Livet, J
last_name: Livet
- first_name: A
full_name: Meunier, A
last_name: Meunier
- first_name: A
full_name: Genovesio, A
last_name: Genovesio
- first_name: N
full_name: Spassky, N
last_name: Spassky
citation:
ama: Ortiz-Álvarez G, Daclin M, Shihavuddin A, et al. Adult neural stem cells and
multiciliated ependymal cells share a common lineage regulated by the Geminin
family members. Neuron. 2019;102(1):159-172.e7. doi:10.1016/j.neuron.2019.01.051
apa: Ortiz-Álvarez, G., Daclin, M., Shihavuddin, A., Lansade, P., Fortoul, A., Faucourt,
M., … Spassky, N. (2019). Adult neural stem cells and multiciliated ependymal
cells share a common lineage regulated by the Geminin family members. Neuron.
Elsevier. https://doi.org/10.1016/j.neuron.2019.01.051
chicago: Ortiz-Álvarez, G, M Daclin, A Shihavuddin, P Lansade, A Fortoul, M Faucourt,
S Clavreul, et al. “Adult Neural Stem Cells and Multiciliated Ependymal Cells
Share a Common Lineage Regulated by the Geminin Family Members.” Neuron.
Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.01.051.
ieee: G. Ortiz-Álvarez et al., “Adult neural stem cells and multiciliated
ependymal cells share a common lineage regulated by the Geminin family members,”
Neuron, vol. 102, no. 1. Elsevier, p. 159–172.e7, 2019.
ista: Ortiz-Álvarez G, Daclin M, Shihavuddin A, Lansade P, Fortoul A, Faucourt M,
Clavreul S, Lalioti M, Taraviras S, Hippenmeyer S, Livet J, Meunier A, Genovesio
A, Spassky N. 2019. Adult neural stem cells and multiciliated ependymal cells
share a common lineage regulated by the Geminin family members. Neuron. 102(1),
159–172.e7.
mla: Ortiz-Álvarez, G., et al. “Adult Neural Stem Cells and Multiciliated Ependymal
Cells Share a Common Lineage Regulated by the Geminin Family Members.” Neuron,
vol. 102, no. 1, Elsevier, 2019, p. 159–172.e7, doi:10.1016/j.neuron.2019.01.051.
short: G. Ortiz-Álvarez, M. Daclin, A. Shihavuddin, P. Lansade, A. Fortoul, M. Faucourt,
S. Clavreul, M. Lalioti, S. Taraviras, S. Hippenmeyer, J. Livet, A. Meunier, A.
Genovesio, N. Spassky, Neuron 102 (2019) 159–172.e7.
date_created: 2019-05-14T13:06:30Z
date_published: 2019-04-03T00:00:00Z
date_updated: 2023-09-05T13:02:21Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.01.051
ec_funded: 1
external_id:
isi:
- '000463337900018'
pmid:
- '30824354'
file:
- access_level: open_access
checksum: 1fb6e195c583eb0c5cabf26f69ff6675
content_type: application/pdf
creator: dernst
date_created: 2019-05-15T09:28:41Z
date_updated: 2020-07-14T12:47:30Z
file_id: '6457'
file_name: 2019_Neuron_Ortiz.pdf
file_size: 7288572
relation: main_file
file_date_updated: 2020-07-14T12:47:30Z
has_accepted_license: '1'
intvolume: ' 102'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 159-172.e7
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Adult neural stem cells and multiciliated ependymal cells share a common lineage
regulated by the Geminin family members
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 102
year: '2019'
...
---
_id: '7202'
abstract:
- lang: eng
text: The cerebral cortex contains multiple areas with distinctive cytoarchitectonical
patterns, but the cellular mechanisms underlying the emergence of this diversity
remain unclear. Here, we have investigated the neuronal output of individual progenitor
cells in the developing mouse neocortex using a combination of methods that together
circumvent the biases and limitations of individual approaches. Our experimental
results indicate that progenitor cells generate pyramidal cell lineages with a
wide range of sizes and laminar configurations. Mathematical modelling indicates
that these outcomes are compatible with a stochastic model of cortical neurogenesis
in which progenitor cells undergo a series of probabilistic decisions that lead
to the specification of very heterogeneous progenies. Our findings support a mechanism
for cortical neurogenesis whose flexibility would make it capable to generate
the diverse cytoarchitectures that characterize distinct neocortical areas.
article_number: e51381
article_processing_charge: No
article_type: original
author:
- first_name: Alfredo
full_name: Llorca, Alfredo
last_name: Llorca
- first_name: Gabriele
full_name: Ciceri, Gabriele
last_name: Ciceri
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Fong Kuan
full_name: Wong, Fong Kuan
last_name: Wong
- first_name: Giovanni
full_name: Diana, Giovanni
last_name: Diana
- first_name: Eleni
full_name: Serafeimidou-Pouliou, Eleni
last_name: Serafeimidou-Pouliou
- first_name: Marian
full_name: Fernández-Otero, Marian
last_name: Fernández-Otero
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Sebastian J.
full_name: Arnold, Sebastian J.
last_name: Arnold
- first_name: Martin
full_name: Meyer, Martin
last_name: Meyer
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Miguel
full_name: Maravall, Miguel
last_name: Maravall
- first_name: Oscar
full_name: Marín, Oscar
last_name: Marín
citation:
ama: Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis
underlies the assembly of neocortical cytoarchitecture. eLife. 2019;8.
doi:10.7554/eLife.51381
apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou-Pouliou,
E., … Marín, O. (2019). A stochastic framework of neurogenesis underlies the assembly
of neocortical cytoarchitecture. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51381
chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong Kuan Wong, Giovanni
Diana, Eleni Serafeimidou-Pouliou, Marian Fernández-Otero, et al. “A Stochastic
Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.”
ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/eLife.51381.
ieee: A. Llorca et al., “A stochastic framework of neurogenesis underlies
the assembly of neocortical cytoarchitecture,” eLife, vol. 8. eLife Sciences
Publications, 2019.
ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou-Pouliou E,
Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M,
Marín O. 2019. A stochastic framework of neurogenesis underlies the assembly of
neocortical cytoarchitecture. eLife. 8, e51381.
mla: Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the
Assembly of Neocortical Cytoarchitecture.” ELife, vol. 8, e51381, eLife
Sciences Publications, 2019, doi:10.7554/eLife.51381.
short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou-Pouliou,
M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
O. Marín, ELife 8 (2019).
date_created: 2019-12-22T23:00:42Z
date_published: 2019-11-18T00:00:00Z
date_updated: 2023-09-06T14:38:39Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.51381
ec_funded: 1
external_id:
isi:
- '000508156800001'
pmid:
- '31736464'
file:
- access_level: open_access
checksum: b460ecc33e1a68265e7adea775021f3a
content_type: application/pdf
creator: dernst
date_created: 2020-02-18T15:19:26Z
date_updated: 2020-07-14T12:47:53Z
file_id: '7503'
file_name: 2019_eLife_Llorca.pdf
file_size: 2960543
relation: main_file
file_date_updated: 2020-07-14T12:47:53Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
publication: eLife
publication_identifier:
eissn:
- 2050084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: A stochastic framework of neurogenesis underlies the assembly of neocortical
cytoarchitecture
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 8
year: '2019'
...
---
_id: '27'
abstract:
- lang: eng
text: The cerebral cortex is composed of a large variety of distinct cell-types
including projection neurons, interneurons and glial cells which emerge from distinct
neural stem cell (NSC) lineages. The vast majority of cortical projection neurons
and certain classes of glial cells are generated by radial glial progenitor cells
(RGPs) in a highly orchestrated manner. Recent studies employing single cell analysis
and clonal lineage tracing suggest that NSC and RGP lineage progression are regulated
in a profound deterministic manner. In this review we focus on recent advances
based mainly on correlative phenotypic data emerging from functional genetic studies
in mice. We establish hypotheses to test in future research and outline a conceptual
framework how epigenetic cues modulate the generation of cell-type diversity during
cortical development. This article is protected by copyright. All rights reserved.
acknowledgement: " This work was supported by IST Austria institutional funds; NÖ
Forschung und Bildung \r\nn[f+b] (C13-002) to SH; a program grant from
\ the Human Frontiers Science Program (RGP0053/2014) to SH; the People
\ Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement No 618444 to SH, and the European
\ Research Council (ERC) under the European Union’s Horizon 2020 research
\ and innovation programme (grant agreement No 725780 LinPro)to SH.\r\n"
article_processing_charge: Yes (via OA deal)
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Laukoter S, Hippenmeyer S. Epigenetic cues modulating the generation
of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
2019;149(1):12-26. doi:10.1111/jnc.14601
apa: Amberg, N., Laukoter, S., & Hippenmeyer, S. (2019). Epigenetic cues modulating
the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
Wiley. https://doi.org/10.1111/jnc.14601
chicago: Amberg, Nicole, Susanne Laukoter, and Simon Hippenmeyer. “Epigenetic Cues
Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” Journal
of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14601.
ieee: N. Amberg, S. Laukoter, and S. Hippenmeyer, “Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex,” Journal of Neurochemistry,
vol. 149, no. 1. Wiley, pp. 12–26, 2019.
ista: Amberg N, Laukoter S, Hippenmeyer S. 2019. Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
149(1), 12–26.
mla: Amberg, Nicole, et al. “Epigenetic Cues Modulating the Generation of Cell Type
Diversity in the Cerebral Cortex.” Journal of Neurochemistry, vol. 149,
no. 1, Wiley, 2019, pp. 12–26, doi:10.1111/jnc.14601.
short: N. Amberg, S. Laukoter, S. Hippenmeyer, Journal of Neurochemistry 149 (2019)
12–26.
date_created: 2018-12-11T11:44:14Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2023-09-11T13:40:26Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/jnc.14601
ec_funded: 1
external_id:
isi:
- '000462680200002'
file:
- access_level: open_access
checksum: db027721a95d36f5de36aadcd0bdf7e6
content_type: application/pdf
creator: kschuh
date_created: 2020-01-07T13:35:52Z
date_updated: 2020-07-14T12:45:45Z
file_id: '7239'
file_name: 2019_Wiley_Amberg.pdf
file_size: 889709
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 12-26
project:
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Neurochemistry
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Epigenetic cues modulating the generation of cell type diversity in the cerebral
cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 149
year: '2019'
...
---
_id: '6830'
article_processing_charge: No
article_type: letter_note
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Hippenmeyer S. Memo1 tiles the radial glial cell grid. Neuron.
2019;103(5):750-752. doi:10.1016/j.neuron.2019.08.021
apa: Contreras, X., & Hippenmeyer, S. (2019). Memo1 tiles the radial glial cell
grid. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2019.08.021
chicago: Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial
Cell Grid.” Neuron. Elsevier, 2019. https://doi.org/10.1016/j.neuron.2019.08.021.
ieee: X. Contreras and S. Hippenmeyer, “Memo1 tiles the radial glial cell grid,”
Neuron, vol. 103, no. 5. Elsevier, pp. 750–752, 2019.
ista: Contreras X, Hippenmeyer S. 2019. Memo1 tiles the radial glial cell grid.
Neuron. 103(5), 750–752.
mla: Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial Cell
Grid.” Neuron, vol. 103, no. 5, Elsevier, 2019, pp. 750–52, doi:10.1016/j.neuron.2019.08.021.
short: X. Contreras, S. Hippenmeyer, Neuron 103 (2019) 750–752.
date_created: 2019-08-25T22:00:50Z
date_published: 2019-09-04T00:00:00Z
date_updated: 2024-03-28T23:30:42Z
day: '04'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.08.021
external_id:
isi:
- '000484400200002'
pmid:
- '31487522'
intvolume: ' 103'
isi: 1
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2019.08.021
month: '09'
oa: 1
oa_version: Published Version
page: 750-752
pmid: 1
publication: Neuron
publication_identifier:
eissn:
- '10974199'
issn:
- '08966273'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Memo1 tiles the radial glial cell grid
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 103
year: '2019'
...
---
_id: '8547'
abstract:
- lang: eng
text: The cerebral cortex contains multiple hierarchically organized areas with
distinctive cytoarchitectonical patterns, but the cellular mechanisms underlying
the emergence of this diversity remain unclear. Here, we have quantitatively investigated
the neuronal output of individual progenitor cells in the ventricular zone of
the developing mouse neocortex using a combination of methods that together circumvent
the biases and limitations of individual approaches. We found that individual
cortical progenitor cells show a high degree of stochasticity and generate pyramidal
cell lineages that adopt a wide range of laminar configurations. Mathematical
modelling these lineage data suggests that a small number of progenitor cell populations,
each generating pyramidal cells following different stochastic developmental programs,
suffice to generate the heterogenous complement of pyramidal cell lineages that
collectively build the complex cytoarchitecture of the neocortex.
acknowledgement: We thank I. Andrew and S.E. Bae for excellent technical assistance,
F. Gage for plasmids, and K. Nave (Nex-Cre) for mouse colonies. We thank members
of the Marín and Rico laboratories for stimulating discussions and ideas. Our research
on this topic is supported by grants from the European Research Council (ERC-2017-AdG
787355 to O.M and ERC2016-CoG 725780 to S.H.) and Wellcome Trust (103714MA) to O.M.
L.L. was the recipient of an EMBO long-term postdoctoral fellowship, R.B. received
support from FWF Lise-Meitner program (M 2416) and F.K.W. was supported by an EMBO
postdoctoral fellowship and is currently a Marie Skłodowska-Curie Fellow from the
European Commission under the H2020 Programme.
article_processing_charge: No
author:
- first_name: Alfredo
full_name: Llorca, Alfredo
last_name: Llorca
- first_name: Gabriele
full_name: Ciceri, Gabriele
last_name: Ciceri
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Fong K.
full_name: Wong, Fong K.
last_name: Wong
- first_name: Giovanni
full_name: Diana, Giovanni
last_name: Diana
- first_name: Eleni
full_name: Serafeimidou, Eleni
last_name: Serafeimidou
- first_name: Marian
full_name: Fernández-Otero, Marian
last_name: Fernández-Otero
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Sebastian J.
full_name: Arnold, Sebastian J.
last_name: Arnold
- first_name: Martin
full_name: Meyer, Martin
last_name: Meyer
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Miguel
full_name: Maravall, Miguel
last_name: Maravall
- first_name: Oscar
full_name: Marín, Oscar
last_name: Marín
citation:
ama: Llorca A, Ciceri G, Beattie RJ, et al. Heterogeneous progenitor cell behaviors
underlie the assembly of neocortical cytoarchitecture. bioRxiv. doi:10.1101/494088
apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou,
E., … Marín, O. (n.d.). Heterogeneous progenitor cell behaviors underlie the assembly
of neocortical cytoarchitecture. bioRxiv. Cold Spring Harbor Laboratory.
https://doi.org/10.1101/494088
chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong K. Wong, Giovanni
Diana, Eleni Serafeimidou, Marian Fernández-Otero, et al. “Heterogeneous Progenitor
Cell Behaviors Underlie the Assembly of Neocortical Cytoarchitecture.” BioRxiv.
Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/494088.
ieee: A. Llorca et al., “Heterogeneous progenitor cell behaviors underlie
the assembly of neocortical cytoarchitecture,” bioRxiv. Cold Spring Harbor
Laboratory.
ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou E, Fernández-Otero
M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M, Marín O. Heterogeneous
progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture.
bioRxiv, 10.1101/494088.
mla: Llorca, Alfredo, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the
Assembly of Neocortical Cytoarchitecture.” BioRxiv, Cold Spring Harbor
Laboratory, doi:10.1101/494088.
short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou,
M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
O. Marín, BioRxiv (n.d.).
date_created: 2020-09-21T12:01:50Z
date_published: 2018-12-13T00:00:00Z
date_updated: 2021-01-12T08:20:00Z
day: '13'
department:
- _id: SiHi
doi: 10.1101/494088
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/494088
month: '12'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Cerebral Cortex
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Heterogeneous progenitor cell behaviors underlie the assembly of neocortical
cytoarchitecture
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
_id: '28'
abstract:
- lang: eng
text: 'This scientific commentary refers to ‘NEGR1 and FGFR2 cooperatively regulate
cortical development and core behaviours related to autism disorders in mice’
by Szczurkowska et al. '
article_processing_charge: No
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Contreras X, Hippenmeyer S. Incorrect trafficking route leads to autism. Brain
a journal of neurology. 2018;141(9):2542-2544. doi:10.1093/brain/awy218
apa: Contreras, X., & Hippenmeyer, S. (2018). Incorrect trafficking route leads
to autism. Brain a Journal of Neurology. Oxford University Press. https://doi.org/10.1093/brain/awy218
chicago: Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route
Leads to Autism.” Brain a Journal of Neurology. Oxford University Press,
2018. https://doi.org/10.1093/brain/awy218.
ieee: X. Contreras and S. Hippenmeyer, “Incorrect trafficking route leads to autism,”
Brain a journal of neurology, vol. 141, no. 9. Oxford University Press,
pp. 2542–2544, 2018.
ista: Contreras X, Hippenmeyer S. 2018. Incorrect trafficking route leads to autism.
Brain a journal of neurology. 141(9), 2542–2544.
mla: Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route Leads
to Autism.” Brain a Journal of Neurology, vol. 141, no. 9, Oxford University
Press, 2018, pp. 2542–44, doi:10.1093/brain/awy218.
short: X. Contreras, S. Hippenmeyer, Brain a Journal of Neurology 141 (2018) 2542–2544.
date_created: 2018-12-11T11:44:14Z
date_published: 2018-09-01T00:00:00Z
date_updated: 2024-03-28T23:30:42Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/brain/awy218
external_id:
isi:
- '000446548100012'
intvolume: ' 141'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa_version: None
page: 2542 - 2544
publication: Brain a journal of neurology
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Incorrect trafficking route leads to autism
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 141
year: '2018'
...
---
_id: '9707'
abstract:
- lang: eng
text: Branching morphogenesis of the epithelial ureteric bud forms the renal collecting
duct system and is critical for normal nephron number, while low nephron number
is implicated in hypertension and renal disease. Ureteric bud growth and branching
requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric
bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling
up-regulates transcription factors Etv4 and Etv5, which are also critical for
branching. Despite extensive knowledge of the genetic control of these events,
it is not understood, at the cellular level, how renal branching morphogenesis
is achieved or how Ret signaling influences epithelial cell behaviors to promote
this process. Analysis of chimeric embryos previously suggested a role for Ret
signaling in promoting cell rearrangements in the nephric duct, but this method
was unsuited to study individual cell behaviors during ureteric bud branching.
Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture
and time-lapse imaging, to trace the movements and divisions of individual ureteric
bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type
clones in which the mutant and wild-type sister cells are differentially and heritably
marked by green and red fluorescent proteins. We find that, in normal kidneys,
most individual tip cells behave as self-renewing progenitors, some of whose progeny
remain at the tips while others populate the growing UB trunks. In Ret or Etv4
MADM clones, the wild-type cells generated at a UB tip are much more likely to
remain at, or move to, the new tips during branching and elongation, while their
Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks.
By tracking successive mitoses in a cell lineage, we find that Ret signaling has
little effect on proliferation, in contrast to its effects on cell movement. Our
results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric
bud tips, and suggest a model in which these cell movements mediate branching
morphogenesis.
article_processing_charge: No
author:
- first_name: Paul
full_name: Riccio, Paul
last_name: Riccio
- first_name: Christina
full_name: Cebrián, Christina
last_name: Cebrián
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Frank
full_name: Costantini, Frank
last_name: Costantini
citation:
ama: 'Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Data from: Ret and
Etv4 promote directed movements of progenitor cells during renal branching morphogenesis.
2017. doi:10.5061/dryad.pk16b'
apa: 'Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2017).
Data from: Ret and Etv4 promote directed movements of progenitor cells during
renal branching morphogenesis. Dryad. https://doi.org/10.5061/dryad.pk16b'
chicago: 'Riccio, Paul, Christina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank
Costantini. “Data from: Ret and Etv4 Promote Directed Movements of Progenitor
Cells during Renal Branching Morphogenesis.” Dryad, 2017. https://doi.org/10.5061/dryad.pk16b.'
ieee: 'P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Data
from: Ret and Etv4 promote directed movements of progenitor cells during renal
branching morphogenesis.” Dryad, 2017.'
ista: 'Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2017. Data from:
Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis, Dryad, 10.5061/dryad.pk16b.'
mla: 'Riccio, Paul, et al. Data from: Ret and Etv4 Promote Directed Movements
of Progenitor Cells during Renal Branching Morphogenesis. Dryad, 2017, doi:10.5061/dryad.pk16b.'
short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, (2017).
date_created: 2021-07-23T09:39:34Z
date_published: 2017-01-14T00:00:00Z
date_updated: 2022-08-25T13:34:55Z
day: '14'
department:
- _id: SiHi
doi: 10.5061/dryad.pk16b
main_file_link:
- open_access: '1'
url: https://doi.org/10.5061/dryad.pk16b
month: '01'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
record:
- id: '9702'
relation: used_in_publication
status: deleted
status: public
title: 'Data from: Ret and Etv4 promote directed movements of progenitor cells during
renal branching morphogenesis'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '944'
abstract:
- lang: eng
text: The concerted production of neurons and glia by neural stem cells (NSCs) is
essential for neural circuit assembly. In the developing cerebral cortex, radial
glia progenitors (RGPs) generate nearly all neocortical neurons and certain glia
lineages. RGP proliferation behavior shows a high degree of non-stochasticity,
thus a deterministic characteristic of neuron and glia production. However, the
cellular and molecular mechanisms controlling RGP behavior and proliferation dynamics
in neurogenesis and glia generation remain unknown. By using mosaic analysis with
double markers (MADM)-based genetic paradigms enabling the sparse and global knockout
with unprecedented single-cell resolution, we identified Lgl1 as a critical regulatory
component. We uncover Lgl1-dependent tissue-wide community effects required for
embryonic cortical neurogenesis and novel cell-autonomous Lgl1 functions controlling
RGP-mediated glia genesis and postnatal NSC behavior. These results suggest that
NSC-mediated neuron and glia production is tightly regulated through the concerted
interplay of sequential Lgl1-dependent global and cell intrinsic mechanisms.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
article_processing_charge: No
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Laura
full_name: Burnett, Laura
id: 3B717F68-F248-11E8-B48F-1D18A9856A87
last_name: Burnett
orcid: 0000-0002-8937-410X
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Olga
full_name: Klezovitch, Olga
last_name: Klezovitch
- first_name: Valeri
full_name: Vasioukhin, Valeri
last_name: Vasioukhin
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Postiglione MP, Burnett L, et al. Mosaic analysis with double markers
reveals distinct sequential functions of Lgl1 in neural stem cells. Neuron.
2017;94(3):517-533.e3. doi:10.1016/j.neuron.2017.04.012
apa: Beattie, R. J., Postiglione, M. P., Burnett, L., Laukoter, S., Streicher, C.,
Pauler, F., … Hippenmeyer, S. (2017). Mosaic analysis with double markers reveals
distinct sequential functions of Lgl1 in neural stem cells. Neuron. Cell
Press. https://doi.org/10.1016/j.neuron.2017.04.012
chicago: Beattie, Robert J, Maria P Postiglione, Laura Burnett, Susanne Laukoter,
Carmen Streicher, Florian Pauler, Guanxi Xiao, et al. “Mosaic Analysis with Double
Markers Reveals Distinct Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron.
Cell Press, 2017. https://doi.org/10.1016/j.neuron.2017.04.012.
ieee: R. J. Beattie et al., “Mosaic analysis with double markers reveals
distinct sequential functions of Lgl1 in neural stem cells,” Neuron, vol.
94, no. 3. Cell Press, p. 517–533.e3, 2017.
ista: Beattie RJ, Postiglione MP, Burnett L, Laukoter S, Streicher C, Pauler F,
Xiao G, Klezovitch O, Vasioukhin V, Ghashghaei T, Hippenmeyer S. 2017. Mosaic
analysis with double markers reveals distinct sequential functions of Lgl1 in
neural stem cells. Neuron. 94(3), 517–533.e3.
mla: Beattie, Robert J., et al. “Mosaic Analysis with Double Markers Reveals Distinct
Sequential Functions of Lgl1 in Neural Stem Cells.” Neuron, vol. 94, no.
3, Cell Press, 2017, p. 517–533.e3, doi:10.1016/j.neuron.2017.04.012.
short: R.J. Beattie, M.P. Postiglione, L. Burnett, S. Laukoter, C. Streicher, F.
Pauler, G. Xiao, O. Klezovitch, V. Vasioukhin, T. Ghashghaei, S. Hippenmeyer,
Neuron 94 (2017) 517–533.e3.
date_created: 2018-12-11T11:49:20Z
date_published: 2017-05-03T00:00:00Z
date_updated: 2023-09-26T15:37:02Z
day: '03'
department:
- _id: SiHi
- _id: MaJö
doi: 10.1016/j.neuron.2017.04.012
ec_funded: 1
external_id:
isi:
- '000400466700011'
intvolume: ' 94'
isi: 1
issue: '3'
language:
- iso: eng
month: '05'
oa_version: None
page: 517 - 533.e3
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Neuron
publication_identifier:
issn:
- '08966273'
publication_status: published
publisher: Cell Press
publist_id: '6473'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mosaic analysis with double markers reveals distinct sequential functions of
Lgl1 in neural stem cells
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 94
year: '2017'
...
---
_id: '621'
abstract:
- lang: eng
text: The mammalian cerebral cortex is responsible for higher cognitive functions
such as perception, consciousness, and acquiring and processing information. The
neocortex is organized into six distinct laminae, each composed of a rich diversity
of cell types which assemble into highly complex cortical circuits. Radial glia
progenitors (RGPs) are responsible for producing all neocortical neurons and certain
glia lineages. Here, we discuss recent discoveries emerging from clonal lineage
analysis at the single RGP cell level that provide us with an inaugural quantitative
framework of RGP lineage progression. We further discuss the importance of the
relative contribution of intrinsic gene functions and non-cell-autonomous or community
effects in regulating RGP proliferation behavior and lineage progression.
article_processing_charge: Yes (in subscription journal)
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Hippenmeyer S. Mechanisms of radial glia progenitor cell lineage
progression. FEBS letters. 2017;591(24):3993-4008. doi:10.1002/1873-3468.12906
apa: Beattie, R. J., & Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor
cell lineage progression. FEBS Letters. Wiley-Blackwell. https://doi.org/10.1002/1873-3468.12906
chicago: Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor
Cell Lineage Progression.” FEBS Letters. Wiley-Blackwell, 2017. https://doi.org/10.1002/1873-3468.12906.
ieee: R. J. Beattie and S. Hippenmeyer, “Mechanisms of radial glia progenitor cell
lineage progression,” FEBS letters, vol. 591, no. 24. Wiley-Blackwell,
pp. 3993–4008, 2017.
ista: Beattie RJ, Hippenmeyer S. 2017. Mechanisms of radial glia progenitor cell
lineage progression. FEBS letters. 591(24), 3993–4008.
mla: Beattie, Robert J., and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor
Cell Lineage Progression.” FEBS Letters, vol. 591, no. 24, Wiley-Blackwell,
2017, pp. 3993–4008, doi:10.1002/1873-3468.12906.
short: R.J. Beattie, S. Hippenmeyer, FEBS Letters 591 (2017) 3993–4008.
date_created: 2018-12-11T11:47:32Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2024-02-14T12:02:08Z
day: '01'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1002/1873-3468.12906
ec_funded: 1
external_id:
pmid:
- '29121403'
file:
- access_level: open_access
checksum: a46dadc84e0c28d389dd3e9e954464db
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:24Z
date_updated: 2020-07-14T12:47:24Z
file_id: '5211'
file_name: IST-2018-928-v1+1_Beattie_et_al-2017-FEBS_Letters.pdf
file_size: 644149
relation: main_file
file_date_updated: 2020-07-14T12:47:24Z
has_accepted_license: '1'
intvolume: ' 591'
issue: '24'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 3993 - 4008
pmid: 1
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: FEBS letters
publication_identifier:
issn:
- '00145793'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '7183'
pubrep_id: '928'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanisms of radial glia progenitor cell lineage progression
tmp:
image: /images/cc_by_nc.png
legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
short: CC BY-NC (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 591
year: '2017'
...
---
_id: '960'
abstract:
- lang: eng
text: The human cerebral cortex is the seat of our cognitive abilities and composed
of an extraordinary number of neurons, organized in six distinct layers. The establishment
of specific morphological and physiological features in individual neurons needs
to be regulated with high precision. Impairments in the sequential developmental
programs instructing corticogenesis lead to alterations in the cortical cytoarchitecture
which is thought to represent the major underlying cause for several neurological
disorders including neurodevelopmental and psychiatric diseases. In this review
we discuss the role of cell polarity at sequential stages during cortex development.
We first provide an overview of morphological cell polarity features in cortical
neural stem cells and newly-born postmitotic neurons. We then synthesize a conceptual
molecular and biochemical framework how cell polarity is established at the cellular
level through a break in symmetry in nascent cortical projection neurons. Lastly
we provide a perspective how the molecular mechanisms applying to single cells
could be probed and integrated in an in vivo and tissue-wide context.
article_number: '176'
article_processing_charge: Yes
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Christian F
full_name: Düllberg, Christian F
id: 459064DC-F248-11E8-B48F-1D18A9856A87
last_name: Düllberg
orcid: 0000-0001-6335-9748
- first_name: Christine
full_name: Mieck, Christine
id: 34CAE85C-F248-11E8-B48F-1D18A9856A87
last_name: Mieck
orcid: 0000-0003-1919-7416
- first_name: Martin
full_name: Loose, Martin
id: 462D4284-F248-11E8-B48F-1D18A9856A87
last_name: Loose
orcid: 0000-0001-7309-9724
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. Cell polarity in cerebral
cortex development - cellular architecture shaped by biochemical networks. Frontiers
in Cellular Neuroscience. 2017;11. doi:10.3389/fncel.2017.00176
apa: Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., & Hippenmeyer, S.
(2017). Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks. Frontiers in Cellular Neuroscience. Frontiers
Research Foundation. https://doi.org/10.3389/fncel.2017.00176
chicago: Hansen, Andi H, Christian F Düllberg, Christine Mieck, Martin Loose, and
Simon Hippenmeyer. “Cell Polarity in Cerebral Cortex Development - Cellular Architecture
Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience. Frontiers
Research Foundation, 2017. https://doi.org/10.3389/fncel.2017.00176.
ieee: A. H. Hansen, C. F. Düllberg, C. Mieck, M. Loose, and S. Hippenmeyer, “Cell
polarity in cerebral cortex development - cellular architecture shaped by biochemical
networks,” Frontiers in Cellular Neuroscience, vol. 11. Frontiers Research
Foundation, 2017.
ista: Hansen AH, Düllberg CF, Mieck C, Loose M, Hippenmeyer S. 2017. Cell polarity
in cerebral cortex development - cellular architecture shaped by biochemical networks.
Frontiers in Cellular Neuroscience. 11, 176.
mla: Hansen, Andi H., et al. “Cell Polarity in Cerebral Cortex Development - Cellular
Architecture Shaped by Biochemical Networks.” Frontiers in Cellular Neuroscience,
vol. 11, 176, Frontiers Research Foundation, 2017, doi:10.3389/fncel.2017.00176.
short: A.H. Hansen, C.F. Düllberg, C. Mieck, M. Loose, S. Hippenmeyer, Frontiers
in Cellular Neuroscience 11 (2017).
date_created: 2018-12-11T11:49:25Z
date_published: 2017-06-28T00:00:00Z
date_updated: 2024-03-28T23:30:41Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
isi:
- '000404486700001'
file:
- access_level: open_access
checksum: dc1f5a475b918d09a0f9f587400b1626
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:40Z
date_updated: 2020-07-14T12:48:16Z
file_id: '4764'
file_name: IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf
file_size: 2153858
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
publication: Frontiers in Cellular Neuroscience
publication_identifier:
issn:
- '16625102'
publication_status: published
publisher: Frontiers Research Foundation
publist_id: '6445'
pubrep_id: '830'
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Cell polarity in cerebral cortex development - cellular architecture shaped
by biochemical networks
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 11
year: '2017'
...
---
_id: '1181'
abstract:
- lang: eng
text: 'This review accompanies a 2016 SFN mini-symposium presenting examples of
current studies that address a central question: How do neural stem cells (NSCs)
divide in different ways to produce heterogeneous daughter types at the right
time and in proper numbers to build a cerebral cortex with the appropriate size
and structure? We will focus on four aspects of corticogenesis: cytokinesis events
that follow apical mitoses of NSCs; coordinating abscission with delamination
from the apical membrane; timing of neurogenesis and its indirect regulation through
emergence of intermediate progenitors; and capacity of single NSCs to generate
the correct number and laminar fate of cortical neurons. Defects in these mechanisms
can cause microcephaly and other brain malformations, and understanding them is
critical to designing diagnostic tools and preventive and corrective therapies.'
acknowledgement: This work was supported by National Institutes of Health Grants R01NS089795
and R01NS098370 to H.T.G., R01NS076640 to N.D.D., and R01MH094589 and R01NS089777
to B.C., Academia Sinica AS-104-TPB09-2 to S.-J.C, European Union FP7-CIG618444
and Human Frontiers Science Program RGP0053 to S.H., and Fonds Léon Fredericq, from
the Fondation Médicale Reine Elisabeth, and from the Fonation Simone et Pierre Clerdent
to L.N. The authors apologize to colleagues whose work could not be cited due to
space limitations.
author:
- first_name: Noelle
full_name: Dwyer, Noelle
last_name: Dwyer
- first_name: Bin
full_name: Chen, Bin
last_name: Chen
- first_name: Shen
full_name: Chou, Shen
last_name: Chou
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. Neural stem
cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior and
productivity. Journal of Neuroscience. 2016;36(45):11394-11401. doi:10.1523/JNEUROSCI.2359-16.2016'
apa: 'Dwyer, N., Chen, B., Chou, S., Hippenmeyer, S., Nguyen, L., & Ghashghaei,
T. (2016). Neural stem cells to cerebral cortex: Emerging mechanisms regulating
progenitor behavior and productivity. Journal of Neuroscience. Society
for Neuroscience. https://doi.org/10.1523/JNEUROSCI.2359-16.2016'
chicago: 'Dwyer, Noelle, Bin Chen, Shen Chou, Simon Hippenmeyer, Laurent Nguyen,
and Troy Ghashghaei. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience.
Society for Neuroscience, 2016. https://doi.org/10.1523/JNEUROSCI.2359-16.2016.'
ieee: 'N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, and T. Ghashghaei,
“Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity,” Journal of Neuroscience, vol. 36, no. 45. Society
for Neuroscience, pp. 11394–11401, 2016.'
ista: 'Dwyer N, Chen B, Chou S, Hippenmeyer S, Nguyen L, Ghashghaei T. 2016. Neural
stem cells to cerebral cortex: Emerging mechanisms regulating progenitor behavior
and productivity. Journal of Neuroscience. 36(45), 11394–11401.'
mla: 'Dwyer, Noelle, et al. “Neural Stem Cells to Cerebral Cortex: Emerging Mechanisms
Regulating Progenitor Behavior and Productivity.” Journal of Neuroscience,
vol. 36, no. 45, Society for Neuroscience, 2016, pp. 11394–401, doi:10.1523/JNEUROSCI.2359-16.2016.'
short: N. Dwyer, B. Chen, S. Chou, S. Hippenmeyer, L. Nguyen, T. Ghashghaei, Journal
of Neuroscience 36 (2016) 11394–11401.
date_created: 2018-12-11T11:50:35Z
date_published: 2016-11-09T00:00:00Z
date_updated: 2021-01-12T06:48:54Z
day: '09'
department:
- _id: SiHi
doi: 10.1523/JNEUROSCI.2359-16.2016
intvolume: ' 36'
issue: '45'
language:
- iso: eng
month: '11'
oa_version: None
page: 11394 - 11401
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Journal of Neuroscience
publication_status: published
publisher: Society for Neuroscience
publist_id: '6172'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Neural stem cells to cerebral cortex: Emerging mechanisms regulating progenitor
behavior and productivity'
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 36
year: '2016'
...
---
_id: '1488'
abstract:
- lang: eng
text: Branching morphogenesis of the epithelial ureteric bud forms the renal collecting
duct system and is critical for normal nephron number, while low nephron number
is implicated in hypertension and renal disease. Ureteric bud growth and branching
requires GDNF signaling from the surrounding mesenchyme to cells at the ureteric
bud tips, via the Ret receptor tyrosine kinase and coreceptor Gfrα1; Ret signaling
up-regulates transcription factors Etv4 and Etv5, which are also critical for
branching. Despite extensive knowledge of the genetic control of these events,
it is not understood, at the cellular level, how renal branching morphogenesis
is achieved or how Ret signaling influences epithelial cell behaviors to promote
this process. Analysis of chimeric embryos previously suggested a role for Ret
signaling in promoting cell rearrangements in the nephric duct, but this method
was unsuited to study individual cell behaviors during ureteric bud branching.
Here, we use Mosaic Analysis with Double Markers (MADM), combined with organ culture
and time-lapse imaging, to trace the movements and divisions of individual ureteric
bud tip cells. We first examine wild-type clones and then Ret or Etv4 mutant/wild-type
clones in which the mutant and wild-type sister cells are differentially and heritably
marked by green and red fluorescent proteins. We find that, in normal kidneys,
most individual tip cells behave as self-renewing progenitors, some of whose progeny
remain at the tips while others populate the growing UB trunks. In Ret or Etv4
MADM clones, the wild-type cells generated at a UB tip are much more likely to
remain at, or move to, the new tips during branching and elongation, while their
Ret−/− or Etv4−/− sister cells tend to lag behind and contribute only to the trunks.
By tracking successive mitoses in a cell lineage, we find that Ret signaling has
little effect on proliferation, in contrast to its effects on cell movement. Our
results show that Ret/Etv4 signaling promotes directed cell movements in the ureteric
bud tips, and suggest a model in which these cell movements mediate branching
morphogenesis.
acknowledgement: We thank Silvia Arber, Thomas Jessell, Kenneth M. Murphy, Carlton
Bates, Hideki Enomoto, Liqun Luo and Andrew McMahon for mouse strains; Thomas Jessell
for antibodies; and Laura Martinez Prat for experimental assistance.
article_number: e1002382
author:
- first_name: Paul
full_name: Riccio, Paul
last_name: Riccio
- first_name: Cristina
full_name: Cebrián, Cristina
last_name: Cebrián
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Frank
full_name: Costantini, Frank
last_name: Costantini
citation:
ama: Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. Ret and Etv4 promote
directed movements of progenitor cells during renal branching morphogenesis. PLoS
Biology. 2016;14(2). doi:10.1371/journal.pbio.1002382
apa: Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., & Costantini, F. (2016).
Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis. PLoS Biology. Public Library of Science. https://doi.org/10.1371/journal.pbio.1002382
chicago: Riccio, Paul, Cristina Cebrián, Hui Zong, Simon Hippenmeyer, and Frank
Costantini. “Ret and Etv4 Promote Directed Movements of Progenitor Cells during
Renal Branching Morphogenesis.” PLoS Biology. Public Library of Science,
2016. https://doi.org/10.1371/journal.pbio.1002382.
ieee: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, and F. Costantini, “Ret and
Etv4 promote directed movements of progenitor cells during renal branching morphogenesis,”
PLoS Biology, vol. 14, no. 2. Public Library of Science, 2016.
ista: Riccio P, Cebrián C, Zong H, Hippenmeyer S, Costantini F. 2016. Ret and Etv4
promote directed movements of progenitor cells during renal branching morphogenesis.
PLoS Biology. 14(2), e1002382.
mla: Riccio, Paul, et al. “Ret and Etv4 Promote Directed Movements of Progenitor
Cells during Renal Branching Morphogenesis.” PLoS Biology, vol. 14, no.
2, e1002382, Public Library of Science, 2016, doi:10.1371/journal.pbio.1002382.
short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, PLoS Biology
14 (2016).
date_created: 2018-12-11T11:52:19Z
date_published: 2016-02-19T00:00:00Z
date_updated: 2023-02-23T10:01:08Z
day: '19'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pbio.1002382
file:
- access_level: open_access
checksum: 7f8fa1b3a29f94c0a14dd4465278cdbc
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:42Z
date_updated: 2020-07-14T12:44:57Z
file_id: '5027'
file_name: IST-2016-517-v1+1_journal.pbio.1002382_1_.PDF
file_size: 5904773
relation: main_file
file_date_updated: 2020-07-14T12:44:57Z
has_accepted_license: '1'
intvolume: ' 14'
issue: '2'
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '5699'
pubrep_id: '517'
quality_controlled: '1'
related_material:
record:
- id: '9703'
relation: research_data
status: deleted
scopus_import: 1
status: public
title: Ret and Etv4 promote directed movements of progenitor cells during renal branching
morphogenesis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 14
year: '2016'
...
---
_id: '1550'
abstract:
- lang: eng
text: The medial ganglionic eminence (MGE) gives rise to the majority of mouse forebrain
interneurons. Here, we examine the lineage relationship among MGE-derived interneurons
using a replication-defective retroviral library containing a highly diverse set
of DNA barcodes. Recovering the barcodes from the mature progeny of infected progenitor
cells enabled us to unambiguously determine their respective lineal relationship.
We found that clonal dispersion occurs across large areas of the brain and is
not restricted by anatomical divisions. As such, sibling interneurons can populate
the cortex, hippocampus striatum, and globus pallidus. The majority of interneurons
appeared to be generated from asymmetric divisions of MGE progenitor cells, followed
by symmetric divisions within the subventricular zone. Altogether, our findings
uncover that lineage relationships do not appear to determine interneuron allocation
to particular regions. As such, it is likely that clonally related interneurons
have considerable flexibility as to the particular forebrain circuits to which
they can contribute.
acknowledgement: "Research in the G.F. laboratory is supported by NIH (NS 081297,
MH095147, and P01NS074972) and the Simons Foundation. Research in the S.H. laboratory
is supported by the European Union (FP7-CIG618444). C.M. is supported by EMBO ALTF
(1295-2012). X.H.J. is supported by EMBO (ALTF 303-2010) and HFSP (LT000078/2011-L).\r\n\r\n"
author:
- first_name: Christian
full_name: Mayer, Christian
last_name: Mayer
- first_name: Xavier
full_name: Jaglin, Xavier
last_name: Jaglin
- first_name: Lucy
full_name: Cobbs, Lucy
last_name: Cobbs
- first_name: Rachel
full_name: Bandler, Rachel
last_name: Bandler
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Constance
full_name: Cepko, Constance
last_name: Cepko
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Gord
full_name: Fishell, Gord
last_name: Fishell
citation:
ama: Mayer C, Jaglin X, Cobbs L, et al. Clonally related forebrain interneurons
disperse broadly across both functional areas and structural boundaries. Neuron.
2015;87(5):989-998. doi:10.1016/j.neuron.2015.07.011
apa: Mayer, C., Jaglin, X., Cobbs, L., Bandler, R., Streicher, C., Cepko, C., …
Fishell, G. (2015). Clonally related forebrain interneurons disperse broadly across
both functional areas and structural boundaries. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.07.011
chicago: Mayer, Christian, Xavier Jaglin, Lucy Cobbs, Rachel Bandler, Carmen Streicher,
Constance Cepko, Simon Hippenmeyer, and Gord Fishell. “Clonally Related Forebrain
Interneurons Disperse Broadly across Both Functional Areas and Structural Boundaries.”
Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.07.011.
ieee: C. Mayer et al., “Clonally related forebrain interneurons disperse
broadly across both functional areas and structural boundaries,” Neuron,
vol. 87, no. 5. Elsevier, pp. 989–998, 2015.
ista: Mayer C, Jaglin X, Cobbs L, Bandler R, Streicher C, Cepko C, Hippenmeyer S,
Fishell G. 2015. Clonally related forebrain interneurons disperse broadly across
both functional areas and structural boundaries. Neuron. 87(5), 989–998.
mla: Mayer, Christian, et al. “Clonally Related Forebrain Interneurons Disperse
Broadly across Both Functional Areas and Structural Boundaries.” Neuron,
vol. 87, no. 5, Elsevier, 2015, pp. 989–98, doi:10.1016/j.neuron.2015.07.011.
short: C. Mayer, X. Jaglin, L. Cobbs, R. Bandler, C. Streicher, C. Cepko, S. Hippenmeyer,
G. Fishell, Neuron 87 (2015) 989–998.
date_created: 2018-12-11T11:52:40Z
date_published: 2015-09-02T00:00:00Z
date_updated: 2021-01-12T06:51:32Z
day: '02'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2015.07.011
external_id:
pmid:
- '26299473'
intvolume: ' 87'
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4560602/
month: '09'
oa: 1
oa_version: Submitted Version
page: 989 - 998
pmid: 1
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '5621'
quality_controlled: '1'
scopus_import: 1
status: public
title: Clonally related forebrain interneurons disperse broadly across both functional
areas and structural boundaries
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 87
year: '2015'
...
---
_id: '2022'
abstract:
- lang: eng
text: Radial glial progenitors (RGPs) are responsible for producing nearly all neocortical
neurons. To gain insight into the patterns of RGP division and neuron production,
we quantitatively analyzed excitatory neuron genesis in the mouse neocortex using
Mosaic Analysis with Double Markers, which provides single-cell resolution of
progenitor division patterns and potential in vivo. We found that RGPs progress
through a coherent program in which their proliferative potential diminishes in
a predictable manner. Upon entry into the neurogenic phase, individual RGPs produce
∼8–9 neurons distributed in both deep and superficial layers, indicating a unitary
output in neuronal production. Removal of OTX1, a transcription factor transiently
expressed in RGPs, results in both deep- and superficial-layer neuron loss and
a reduction in neuronal unit size. Moreover, ∼1/6 of neurogenic RGPs proceed to
produce glia. These results suggest that progenitor behavior and histogenesis
in the mammalian neocortex conform to a remarkably orderly and deterministic program.
author:
- first_name: Peng
full_name: Gao, Peng
last_name: Gao
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Teresa
full_name: Krieger, Teresa
last_name: Krieger
- first_name: Luisirene
full_name: Hernandez, Luisirene
last_name: Hernandez
- first_name: Chao
full_name: Wang, Chao
last_name: Wang
- first_name: Zhi
full_name: Han, Zhi
last_name: Han
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Ryan
full_name: Insolera, Ryan
last_name: Insolera
- first_name: Kritika
full_name: Chugh, Kritika
last_name: Chugh
- first_name: Oren
full_name: Kodish, Oren
last_name: Kodish
- first_name: Kun
full_name: Huang, Kun
last_name: Huang
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Song
full_name: Shi, Song
last_name: Shi
citation:
ama: Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior
and unitary production of neurons in the neocortex. Cell. 2014;159(4):775-788.
doi:10.1016/j.cell.2014.10.027
apa: Gao, P., Postiglione, M. P., Krieger, T., Hernandez, L., Wang, C., Han, Z.,
… Shi, S. (2014). Deterministic progenitor behavior and unitary production of
neurons in the neocortex. Cell. Cell Press. https://doi.org/10.1016/j.cell.2014.10.027
chicago: Gao, Peng, Maria P Postiglione, Teresa Krieger, Luisirene Hernandez, Chao
Wang, Zhi Han, Carmen Streicher, et al. “Deterministic Progenitor Behavior and
Unitary Production of Neurons in the Neocortex.” Cell. Cell Press, 2014.
https://doi.org/10.1016/j.cell.2014.10.027.
ieee: P. Gao et al., “Deterministic progenitor behavior and unitary production
of neurons in the neocortex,” Cell, vol. 159, no. 4. Cell Press, pp. 775–788,
2014.
ista: Gao P, Postiglione MP, Krieger T, Hernandez L, Wang C, Han Z, Streicher C,
Papusheva E, Insolera R, Chugh K, Kodish O, Huang K, Simons B, Luo L, Hippenmeyer
S, Shi S. 2014. Deterministic progenitor behavior and unitary production of neurons
in the neocortex. Cell. 159(4), 775–788.
mla: Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production
of Neurons in the Neocortex.” Cell, vol. 159, no. 4, Cell Press, 2014,
pp. 775–88, doi:10.1016/j.cell.2014.10.027.
short: P. Gao, M.P. Postiglione, T. Krieger, L. Hernandez, C. Wang, Z. Han, C. Streicher,
E. Papusheva, R. Insolera, K. Chugh, O. Kodish, K. Huang, B. Simons, L. Luo, S.
Hippenmeyer, S. Shi, Cell 159 (2014) 775–788.
date_created: 2018-12-11T11:55:16Z
date_published: 2014-11-06T00:00:00Z
date_updated: 2021-01-12T06:54:47Z
day: '06'
ddc:
- '570'
department:
- _id: SiHi
- _id: Bio
doi: 10.1016/j.cell.2014.10.027
ec_funded: 1
file:
- access_level: open_access
checksum: 6c5de8329bb2ffa71cba9fda750f14ce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:47Z
date_updated: 2020-07-14T12:45:25Z
file_id: '4709'
file_name: IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf
file_size: 4435787
relation: main_file
file_date_updated: 2020-07-14T12:45:25Z
has_accepted_license: '1'
intvolume: ' 159'
issue: '4'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 775 - 788
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5050'
pubrep_id: '423'
quality_controlled: '1'
scopus_import: 1
status: public
title: Deterministic progenitor behavior and unitary production of neurons in the
neocortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 159
year: '2014'
...
---
_id: '2020'
abstract:
- lang: eng
text: The mammalian heart has long been considered a postmitotic organ, implying
that the total number of cardiomyocytes is set at birth. Analysis of cell division
in the mammalian heart is complicated by cardiomyocyte binucleation shortly after
birth, which makes it challenging to interpret traditional assays of cell turnover
[Laflamme MA, Murray CE (2011) Nature 473(7347):326–335; Bergmann O, et al. (2009)
Science 324(5923):98–102]. An elegant multi-isotope imaging-mass spectrometry
technique recently calculated the low, discrete rate of cardiomyocyte generation
in mice [Senyo SE, et al. (2013) Nature 493(7432):433–436], yet our cellular-level
understanding of postnatal cardiomyogenesis remains limited. Herein, we provide
a new line of evidence for the differentiated α-myosin heavy chain-expressing
cardiomyocyte as the cell of origin of postnatal cardiomyogenesis using the “mosaic
analysis with double markers” mouse model. We show limited, life-long, symmetric
division of cardiomyocytes as a rare event that is evident in utero but significantly
diminishes after the first month of life in mice; daughter cardiomyocytes divide
very seldom, which this study is the first to demonstrate, to our knowledge. Furthermore,
ligation of the left anterior descending coronary artery, which causes a myocardial
infarction in the mosaic analysis with double-marker mice, did not increase the
rate of cardiomyocyte division above the basal level for up to 4 wk after the
injury. The clonal analysis described here provides direct evidence of postnatal
mammalian cardiomyogenesis.
author:
- first_name: Shah
full_name: Ali, Shah
last_name: Ali
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Lily
full_name: Saadat, Lily
last_name: Saadat
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Irving
full_name: Weissman, Irving
last_name: Weissman
- first_name: Reza
full_name: Ardehali, Reza
last_name: Ardehali
citation:
ama: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. Existing cardiomyocytes
generate cardiomyocytes at a low rate after birth in mice. PNAS. 2014;111(24):8850-8855.
doi:10.1073/pnas.1408233111
apa: Ali, S., Hippenmeyer, S., Saadat, L., Luo, L., Weissman, I., & Ardehali,
R. (2014). Existing cardiomyocytes generate cardiomyocytes at a low rate after
birth in mice. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1408233111
chicago: Ali, Shah, Simon Hippenmeyer, Lily Saadat, Liqun Luo, Irving Weissman,
and Reza Ardehali. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate
after Birth in Mice.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1408233111.
ieee: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, and R. Ardehali, “Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice,” PNAS,
vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014.
ista: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. 2014. Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS.
111(24), 8850–8855.
mla: Ali, Shah, et al. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low
Rate after Birth in Mice.” PNAS, vol. 111, no. 24, National Academy of
Sciences, 2014, pp. 8850–55, doi:10.1073/pnas.1408233111.
short: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS
111 (2014) 8850–8855.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-06-17T00:00:00Z
date_updated: 2021-01-12T06:54:46Z
day: '17'
department:
- _id: SiHi
doi: 10.1073/pnas.1408233111
intvolume: ' 111'
issue: '24'
language:
- iso: eng
month: '06'
oa_version: None
page: 8850 - 8855
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5052'
quality_controlled: '1'
scopus_import: 1
status: public
title: Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in
mice
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 111
year: '2014'
...
---
_id: '2021'
abstract:
- lang: eng
text: Neurotrophins regulate diverse aspects of neuronal development and plasticity,
but their precise in vivo functions during neural circuit assembly in the central
brain remain unclear. We show that the neurotrophin receptor tropomyosin-related
kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar
Purkinje cells. Sparse TrkC knockout reduced dendrite complexity, but global Purkinje
cell knockout had no effect. Removal of the TrkC ligand neurotrophin-3 (NT-3)
from cerebellar granule cells, which provide major afferent input to developing
Purkinje cell dendrites, rescued the dendrite defects caused by sparse TrkC disruption
in Purkinje cells. Our data demonstrate that NT-3 from presynaptic neurons (granule
cells) is required for TrkC-dependent competitive dendrite morphogenesis in postsynaptic
neurons (Purkinje cells)—a previously unknown mechanism of neural circuit development.
author:
- first_name: Joo
full_name: William, Joo
last_name: William
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 2014;346(6209):626-629. doi:10.1126/science.1258996
apa: William, J., Hippenmeyer, S., & Luo, L. (2014). Dendrite morphogenesis
depends on relative levels of NT-3/TrkC signaling. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.1258996
chicago: William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis
Depends on Relative Levels of NT-3/TrkC Signaling.” Science. American Association
for the Advancement of Science, 2014. https://doi.org/10.1126/science.1258996.
ieee: J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on
relative levels of NT-3/TrkC signaling,” Science, vol. 346, no. 6209. American
Association for the Advancement of Science, pp. 626–629, 2014.
ista: William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 346(6209), 626–629.
mla: William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of
NT-3/TrkC Signaling.” Science, vol. 346, no. 6209, American Association
for the Advancement of Science, 2014, pp. 626–29, doi:10.1126/science.1258996.
short: J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-10-31T00:00:00Z
date_updated: 2021-01-12T06:54:47Z
day: '31'
department:
- _id: SiHi
doi: 10.1126/science.1258996
intvolume: ' 346'
issue: '6209'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/
month: '10'
oa: 1
oa_version: Submitted Version
page: 626 - 629
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5051'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 346
year: '2014'
...
---
_id: '2261'
abstract:
- lang: eng
text: To reveal the full potential of human pluripotent stem cells, new methods
for rapid, site-specific genomic engineering are needed. Here, we describe a system
for precise genetic modification of human embryonic stem cells (ESCs) and induced
pluripotent stem cells (iPSCs). We identified a novel human locus, H11, located
in a safe, intergenic, transcriptionally active region of chromosome 22, as the
recipient site, to provide robust, ubiquitous expression of inserted genes. Recipient
cell lines were established by site-specific placement of a ‘landing pad’ cassette
carrying attP sites for phiC31 and Bxb1 integrases at the H11 locus by spontaneous
or TALEN-assisted homologous recombination. Dual integrase cassette exchange (DICE)
mediated by phiC31 and Bxb1 integrases was used to insert genes of interest flanked
by phiC31 and Bxb1 attB sites at the H11 locus, replacing the landing pad. This
system provided complete control over content, direction and copy number of inserted
genes, with a specificity of 100%. A series of genes, including mCherry and various
combinations of the neural transcription factors LMX1a, FOXA2 and OTX2, were inserted
in recipient cell lines derived from H9 ESC, as well as iPSC lines derived from
a Parkinson’s disease patient and a normal sibling control. The DICE system offers
rapid, efficient and precise gene insertion in ESC and iPSC and is particularly
well suited for repeated modifications of the same locus.
acknowledgement: "California Institute for Regenerative Medicine [RT2-01880 and TR2-01756].
Funding for open access charge: California Institute for Regenerative Medicine [RT2-01880
and TR2-01756]\r\nCC BY 3,0"
article_number: e34
author:
- first_name: Fangfang
full_name: Zhu, Fangfang
last_name: Zhu
- first_name: Matthew
full_name: Gamboa, Matthew
last_name: Gamboa
- first_name: Alfonso
full_name: Farruggio, Alfonso
last_name: Farruggio
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Bosiljka
full_name: Tasic, Bosiljka
last_name: Tasic
- first_name: Birgitt
full_name: Schüle, Birgitt
last_name: Schüle
- first_name: Yanru
full_name: Chen Tsai, Yanru
last_name: Chen Tsai
- first_name: Michele
full_name: Calos, Michele
last_name: Calos
citation:
ama: Zhu F, Gamboa M, Farruggio A, et al. DICE, an efficient system for iterative
genomic editing in human pluripotent stem cells. Nucleic Acids Research.
2014;42(5). doi:10.1093/nar/gkt1290
apa: Zhu, F., Gamboa, M., Farruggio, A., Hippenmeyer, S., Tasic, B., Schüle, B.,
… Calos, M. (2014). DICE, an efficient system for iterative genomic editing in
human pluripotent stem cells. Nucleic Acids Research. Oxford University
Press. https://doi.org/10.1093/nar/gkt1290
chicago: Zhu, Fangfang, Matthew Gamboa, Alfonso Farruggio, Simon Hippenmeyer, Bosiljka
Tasic, Birgitt Schüle, Yanru Chen Tsai, and Michele Calos. “DICE, an Efficient
System for Iterative Genomic Editing in Human Pluripotent Stem Cells.” Nucleic
Acids Research. Oxford University Press, 2014. https://doi.org/10.1093/nar/gkt1290.
ieee: F. Zhu et al., “DICE, an efficient system for iterative genomic editing
in human pluripotent stem cells,” Nucleic Acids Research, vol. 42, no.
5. Oxford University Press, 2014.
ista: Zhu F, Gamboa M, Farruggio A, Hippenmeyer S, Tasic B, Schüle B, Chen Tsai
Y, Calos M. 2014. DICE, an efficient system for iterative genomic editing in human
pluripotent stem cells. Nucleic Acids Research. 42(5), e34.
mla: Zhu, Fangfang, et al. “DICE, an Efficient System for Iterative Genomic Editing
in Human Pluripotent Stem Cells.” Nucleic Acids Research, vol. 42, no.
5, e34, Oxford University Press, 2014, doi:10.1093/nar/gkt1290.
short: F. Zhu, M. Gamboa, A. Farruggio, S. Hippenmeyer, B. Tasic, B. Schüle, Y.
Chen Tsai, M. Calos, Nucleic Acids Research 42 (2014).
date_created: 2018-12-11T11:56:38Z
date_published: 2014-03-05T00:00:00Z
date_updated: 2021-01-12T06:56:22Z
day: '05'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1093/nar/gkt1290
file:
- access_level: open_access
checksum: e9268f5f96a820f04d7ebbf85927c3cb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:15Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4738'
file_name: IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf
file_size: 11044478
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 42'
issue: '5'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Preprint
publication: Nucleic Acids Research
publication_status: published
publisher: Oxford University Press
publist_id: '4684'
pubrep_id: '961'
quality_controlled: '1'
scopus_import: 1
status: public
title: DICE, an efficient system for iterative genomic editing in human pluripotent
stem cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 42
year: '2014'
...
---
_id: '2265'
abstract:
- lang: eng
text: Coordinated migration of newly-born neurons to their target territories is
essential for correct neuronal circuit assembly in the developing brain. Although
a cohort of signaling pathways has been implicated in the regulation of cortical
projection neuron migration, the precise molecular mechanisms and how a balanced
interplay of cell-autonomous and non-autonomous functions of candidate signaling
molecules controls the discrete steps in the migration process, are just being
revealed. In this chapter, I will focally review recent advances that improved
our understanding of the cell-autonomous and possible cell-nonautonomous functions
of the evolutionarily conserved LIS1/NDEL1-complex in regulating the sequential
steps of cortical projection neuron migration. I will then elaborate on the emerging
concept that the Reelin signaling pathway, acts exactly at precise stages in the
course of cortical projection neuron migration. Lastly, I will discuss how finely
tuned transcriptional programs and downstream effectors govern particular aspects
in driving radial migration at discrete stages and how they regulate the precise
positioning of cortical projection neurons in the developing cerebral cortex.
alternative_title:
- Advances in Experimental Medicine and Biology
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical
projection neuron migration. In: Nguyen L, ed. Cellular and Molecular Control
of Neuronal Migration. Vol 800. Springer; 2014:1-24. doi:10.1007/978-94-007-7687-6_1'
apa: Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps
of cortical projection neuron migration. In L. Nguyen (Ed.), Cellular and
Molecular Control of Neuronal Migration (Vol. 800, pp. 1–24). Springer. https://doi.org/10.1007/978-94-007-7687-6_1
chicago: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps
of Cortical Projection Neuron Migration.” In Cellular and Molecular Control
of Neuronal Migration, edited by Laurent Nguyen, 800:1–24. Springer, 2014.
https://doi.org/10.1007/978-94-007-7687-6_1.
ieee: S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical
projection neuron migration,” in Cellular and Molecular Control of Neuronal
Migration, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24.
ista: 'Hippenmeyer S. 2014.Molecular pathways controlling the sequential steps of
cortical projection neuron migration. In: Cellular and Molecular Control of Neuronal
Migration. Advances in Experimental Medicine and Biology, vol. 800, 1–24.'
mla: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of
Cortical Projection Neuron Migration.” Cellular and Molecular Control of Neuronal
Migration, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:10.1007/978-94-007-7687-6_1.
short: S. Hippenmeyer, in:, L. Nguyen (Ed.), Cellular and Molecular Control of
Neuronal Migration, Springer, 2014, pp. 1–24.
date_created: 2018-12-11T11:56:39Z
date_published: 2014-01-01T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '01'
department:
- _id: SiHi
doi: 10.1007/978-94-007-7687-6_1
editor:
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
intvolume: ' 800'
language:
- iso: eng
month: '01'
oa_version: None
page: 1 - 24
publication: ' Cellular and Molecular Control of Neuronal Migration'
publication_status: published
publisher: Springer
publist_id: '4679'
quality_controlled: '1'
scopus_import: 1
status: public
title: Molecular pathways controlling the sequential steps of cortical projection
neuron migration
type: book_chapter
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 800
year: '2014'
...
---
_id: '2175'
abstract:
- lang: eng
text: The cerebral cortex, the seat of our cognitive abilities, is composed of an
intricate network of billions of excitatory projection and inhibitory interneurons.
Postmitotic cortical neurons are generated by a diverse set of neural stem cell
progenitors within dedicated zones and defined periods of neurogenesis during
embryonic development. Disruptions in neurogenesis can lead to alterations in
the neuronal cytoarchitecture, which is thought to represent a major underlying
cause for several neurological disorders, including microcephaly, autism and epilepsy.
Although a number of signaling pathways regulating neurogenesis have been described,
the precise cellular and molecular mechanisms regulating the functional neural
stem cell properties in cortical neurogenesis remain unclear. Here, we discuss
the most up-to-date strategies to monitor the fundamental mechanistic parameters
of neuronal progenitor proliferation, and recent advances deciphering the logic
and dynamics of neurogenesis.
article_processing_charge: No
author:
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex:
an update. Future Neurology. 2014;9(3):323-340. doi:10.2217/fnl.14.18'
apa: 'Postiglione, M. P., & Hippenmeyer, S. (2014). Monitoring neurogenesis
in the cerebral cortex: an update. Future Neurology. Future Science Group.
https://doi.org/10.2217/fnl.14.18'
chicago: 'Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis
in the Cerebral Cortex: An Update.” Future Neurology. Future Science Group,
2014. https://doi.org/10.2217/fnl.14.18.'
ieee: 'M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral
cortex: an update,” Future Neurology, vol. 9, no. 3. Future Science Group,
pp. 323–340, 2014.'
ista: 'Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral
cortex: an update. Future Neurology. 9(3), 323–340.'
mla: 'Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in
the Cerebral Cortex: An Update.” Future Neurology, vol. 9, no. 3, Future
Science Group, 2014, pp. 323–40, doi:10.2217/fnl.14.18.'
short: M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340.
date_created: 2018-12-11T11:56:09Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2023-10-17T08:34:27Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.2217/fnl.14.18
ec_funded: 1
file:
- access_level: open_access
checksum: ba06659ecadabceec9a37dd8c4586dce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:25Z
date_updated: 2020-07-14T12:45:31Z
file_id: '4812'
file_name: IST-2016-528-v1+1_fnl.14.18.pdf
file_size: 3848424
relation: main_file
file_date_updated: 2020-07-14T12:45:31Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '3'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 323 - 340
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Future Neurology
publication_identifier:
eissn:
- 1748-6971
issn:
- 1479-6708
publication_status: published
publisher: Future Science Group
publist_id: '4806'
pubrep_id: '528'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Monitoring neurogenesis in the cerebral cortex: an update'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '2264'
abstract:
- lang: eng
text: Faithful progression through the cell cycle is crucial to the maintenance
and developmental potential of stem cells. Here, we demonstrate that neural stem
cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger
transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in
two temporally and spatially distinct progenitor domains. Differential conditional
deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal
olfactory bulb progenitors disrupted transitions through G1, G2 and M phases,
whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified
by deletion of Sp2 using mosaic analysis with double markers, which clearly established
that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly,
conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons
in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms
as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis
in the embryonic and postnatal brain.
article_processing_charge: No
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Haifeng
full_name: Yin, Haifeng
last_name: Yin
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Jonathan
full_name: Horowitz, Jonathan
last_name: Horowitz
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development
is dependent on the function of specificity protein 2 in cell cycle progression.
Development. 2013;140(3):552-561. doi:10.1242/dev.085621
apa: Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., & Ghashghaei,
T. (2013). Neural development is dependent on the function of specificity protein
2 in cell cycle progression. Development. Company of Biologists. https://doi.org/10.1242/dev.085621
chicago: Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz,
and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity
Protein 2 in Cell Cycle Progression.” Development. Company of Biologists,
2013. https://doi.org/10.1242/dev.085621.
ieee: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei,
“Neural development is dependent on the function of specificity protein 2 in cell
cycle progression,” Development, vol. 140, no. 3. Company of Biologists,
pp. 552–561, 2013.
ista: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural
development is dependent on the function of specificity protein 2 in cell cycle
progression. Development. 140(3), 552–561.
mla: Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of
Specificity Protein 2 in Cell Cycle Progression.” Development, vol. 140,
no. 3, Company of Biologists, 2013, pp. 552–61, doi:10.1242/dev.085621.
short: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development
140 (2013) 552–561.
date_created: 2018-12-11T11:56:39Z
date_published: 2013-02-01T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '01'
department:
- _id: SiHi
doi: 10.1242/dev.085621
external_id:
pmid:
- '23293287'
intvolume: ' 140'
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/
month: '02'
oa: 1
oa_version: Submitted Version
page: 552 - 561
pmid: 1
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '4681'
quality_controlled: '1'
scopus_import: 1
status: public
title: Neural development is dependent on the function of specificity protein 2 in
cell cycle progression
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 140
year: '2013'
...
---
_id: '2303'
abstract:
- lang: eng
text: MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach
in mice to visualize and concomitantly manipulate genetically defined cells at
clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent
interchromosomal mitotic recombination to reconstitute two split marker genes—green
GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in
one color and wild-type cells in the other color in an otherwise unlabeled background.
At present, major MADM applications include lineage tracing, single cell labeling,
conditional knockouts in small populations of cells and induction of uniparental
chromosome disomy to assess effects of genomic imprinting. MADM can be applied
universally in the mouse with the sole limitation being the specificity of the
promoter controlling Cre recombinase expression. Here I review recent developments
and extensions of the MADM technique and give an overview of the major discoveries
and progresses enabled by the implementation of the novel genetic MADM tools.
acknowledgement: This work was supported by IST Austria institutional funds.
article_type: review
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis
with double markers. Frontiers in Biology. 2013;8(6):557-568. doi:10.1007/s11515-013-1279-6
apa: Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. Springer. https://doi.org/10.1007/s11515-013-1279-6
chicago: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using
Mosaic Analysis with Double Markers.” Frontiers in Biology. Springer, 2013.
https://doi.org/10.1007/s11515-013-1279-6.
ieee: S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic
analysis with double markers,” Frontiers in Biology, vol. 8, no. 6. Springer,
pp. 557–568, 2013.
ista: Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. 8(6), 557–568.
mla: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic
Analysis with Double Markers.” Frontiers in Biology, vol. 8, no. 6, Springer,
2013, pp. 557–68, doi:10.1007/s11515-013-1279-6.
short: S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568.
date_created: 2018-12-11T11:56:52Z
date_published: 2013-09-03T00:00:00Z
date_updated: 2021-01-12T06:56:39Z
day: '03'
department:
- _id: SiHi
doi: 10.1007/s11515-013-1279-6
intvolume: ' 8'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
page: 557 - 568
publication: Frontiers in Biology
publication_status: published
publisher: Springer
publist_id: '4624'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dissection of gene function at clonal level using mosaic analysis with double
markers
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2013'
...
---
_id: '2855'
abstract:
- lang: eng
text: Genomic imprinting leads to preferred expression of either the maternal or
paternal alleles of a subset of genes. Imprinting is essential for mammalian development,
and its deregulation causes many diseases. However, the functional relevance of
imprinting at the cellular level is poorly understood for most imprinted genes.
We used mosaic analysis with double markers (MADM) in mice to create uniparental
disomies (UPDs) and to visualize imprinting effects with single-cell resolution.
Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7
UPD caused highly significant paternal growth dominance in the liver and lung,
but not in the brain or heart. A single gene on chromosome 7, encoding the secreted
insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance
effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting
cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and
cell-type specificity of genomic imprinting effects.
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Randy
full_name: Johnson, Randy
last_name: Johnson
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals
cell type specific paternal growth dominance. Cell Reports. 2013;3(3):960-967.
doi:10.1016/j.celrep.2013.02.002
apa: Hippenmeyer, S., Johnson, R., & Luo, L. (2013). Mosaic analysis with double
markers reveals cell type specific paternal growth dominance. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2013.02.002
chicago: Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with
Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell
Reports. Cell Press, 2013. https://doi.org/10.1016/j.celrep.2013.02.002.
ieee: S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers
reveals cell type specific paternal growth dominance,” Cell Reports, vol.
3, no. 3. Cell Press, pp. 960–967, 2013.
ista: Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers
reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967.
mla: Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell
Type Specific Paternal Growth Dominance.” Cell Reports, vol. 3, no. 3,
Cell Press, 2013, pp. 960–67, doi:10.1016/j.celrep.2013.02.002.
short: S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967.
date_created: 2018-12-11T11:59:57Z
date_published: 2013-03-28T00:00:00Z
date_updated: 2021-01-12T07:00:16Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2013.02.002
file:
- access_level: open_access
checksum: 6e977b918e81384cd571ec5a9d812289
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:20Z
date_updated: 2020-07-14T12:45:51Z
file_id: '5274'
file_name: IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf
file_size: 1907211
relation: main_file
file_date_updated: 2020-07-14T12:45:51Z
has_accepted_license: '1'
intvolume: ' 3'
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 960 - 967
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '3937'
pubrep_id: '405'
quality_controlled: '1'
scopus_import: 1
status: public
title: Mosaic analysis with double markers reveals cell type specific paternal growth
dominance
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 3
year: '2013'
...
---
_id: '2263'
abstract:
- lang: eng
text: Nestin-cre transgenic mice have been widely used to direct recombination to
neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here
we report that a readily utilized, and the only commercially available, Nestin-cre
line is insufficient for directing recombination in early embryonic NSCs and NPCs.
Analysis of recombination efficiency in multiple cre-dependent reporters and a
genetic mosaic line revealed consistent temporal and spatial patterns of recombination
in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found
robust recombination in NSCs and NPCs in ventricular and subventricular zones
of the cerebral cortices as early as embryonic day 12.5. In addition we found
that the rate of Nestin-cre driven recombination only reaches sufficiently high
levels in NSCs and NPCs during late embryonic and early postnatal periods. These
findings are important when commercially available cre lines are considered for
directing recombination to embryonic NSCs and NPCs.
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H.
full_name: Ghashghaei, H.
last_name: Ghashghaei
citation:
ama: Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient
for recombination in early embryonic neural progenitors. Biology open.
2012;1(12):1200-1203. doi:10.1242/bio.20122287
apa: Liang, H., Hippenmeyer, S., & Ghashghaei, H. (2012). A Nestin-cre transgenic
mouse is insufficient for recombination in early embryonic neural progenitors.
Biology Open. The Company of Biologists. https://doi.org/10.1242/bio.20122287
chicago: Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic
Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.”
Biology Open. The Company of Biologists, 2012. https://doi.org/10.1242/bio.20122287.
ieee: H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors,” Biology
open, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012.
ista: Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors. Biology
open. 1(12), 1200–1203.
mla: Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination
in Early Embryonic Neural Progenitors.” Biology Open, vol. 1, no. 12, The
Company of Biologists, 2012, pp. 1200–03, doi:10.1242/bio.20122287.
short: H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203.
date_created: 2018-12-11T11:56:38Z
date_published: 2012-12-15T00:00:00Z
date_updated: 2021-01-12T06:56:23Z
day: '15'
ddc:
- '576'
department:
- _id: SiHi
doi: 10.1242/bio.20122287
file:
- access_level: open_access
checksum: 605a1800b81227848c361fd6ba7d22ba
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:09Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4990'
file_name: IST-2015-387-v1+1_1200.full.pdf
file_size: 726695
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 1'
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 1200 - 1203
publication: Biology open
publication_status: published
publisher: The Company of Biologists
publist_id: '4682'
pubrep_id: '387'
quality_controlled: '1'
scopus_import: 1
status: public
title: A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic
neural progenitors
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2012'
...
---
_id: '2262'
abstract:
- lang: eng
text: 'Mosaic Analysis with Double Markers (MADM) is a method for generating genetically
mosaic mice, in which sibling mutant and wild-type cells are labeled with different
fluorescent markers. It is a powerful tool that enables analysis of gene function
at the single cell level in vivo. It requires transgenic cassettes to be located
between the centromere and the mutation in the gene of interest on the same chromosome.
Here we compare procedures for introduction of MADM cassettes into new loci in
the mouse genome, and describe new approaches for expanding the utility of MADM.
We show that: 1) Targeted homologous recombination outperforms random transgenesis
in generation of reliably expressed MADM cassettes, 2) MADM cassettes in new genomic
loci need to be validated for biallelic and ubiquitous expression, 3) Recombination
between MADM cassettes on different chromosomes can be used to study reciprocal
chromosomal deletions/duplications, and 4) MADM can be modified to permit transgene
expression by combining it with a binary expression system. The advances described
in this study expand current, and enable new and more versatile applications of
MADM.'
acknowledgement: This work was supported by a National Institutes of Health grant
to LL (R01-NS050835). BT was a Damon Runyon Fellow and was supported by the Damon
Runyon Cancer Research Foundation Grant DRG-1819-04. KM was supported by the Japan
Society for the Promotion of Science program for Research Abroad and Human Frontier
Science Program Organization (LT00300/2007-L). SH was supported by postdoctoral
fellowships from the European Molecular Biology Organization (ALTF 851-2005), Human
Frontier Science Program Organization (LT00805/2006-L), and Swiss National Science
Foundation (PA00P3_124160 and PA00P3_136482). HZ is a Pew Scholar in Biomedical
Sciences, supported by The Pew Charitable Trusts. LL is an investigator of the Howard
Hughes Medical Institute. The funders had no role in study design, data collection
and analysis, decision to publish, or preparation of the manuscript.
author:
- first_name: Bosiljka
full_name: Tasic, Bosiljka
last_name: Tasic
- first_name: Kazunari
full_name: Miyamichi, Kazunari
last_name: Miyamichi
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Vardhan
full_name: Dani, Vardhan S.
last_name: Dani
- first_name: H.
full_name: Zeng, H.
last_name: Zeng
- first_name: William
full_name: Joo, William
last_name: Joo
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Yanru
full_name: Chen-Tsai, Yanru
last_name: Chen Tsai
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Tasic B, Miyamichi K, Hippenmeyer S, et al. Extensions of MADM (Mosaic Analysis
with Double Markers) in Mice . PLoS One. 2012;7(3). doi:10.1371/journal.pone.0033332
apa: Tasic, B., Miyamichi, K., Hippenmeyer, S., Dani, V., Zeng, H., Joo, W., … Luo,
L. (2012). Extensions of MADM (Mosaic Analysis with Double Markers) in Mice .
PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0033332
chicago: Tasic, Bosiljka, Kazunari Miyamichi, Simon Hippenmeyer, Vardhan Dani, H.
Zeng, William Joo, Hui Zong, Yanru Chen Tsai, and Liqun Luo. “Extensions of MADM
(Mosaic Analysis with Double Markers) in Mice .” PLoS One. Public Library
of Science, 2012. https://doi.org/10.1371/journal.pone.0033332.
ieee: B. Tasic et al., “Extensions of MADM (Mosaic Analysis with Double Markers)
in Mice ,” PLoS One, vol. 7, no. 3. Public Library of Science, 2012.
ista: Tasic B, Miyamichi K, Hippenmeyer S, Dani V, Zeng H, Joo W, Zong H, Chen Tsai
Y, Luo L. 2012. Extensions of MADM (Mosaic Analysis with Double Markers) in Mice
. PLoS One. 7(3).
mla: Tasic, Bosiljka, et al. “Extensions of MADM (Mosaic Analysis with Double Markers)
in Mice .” PLoS One, vol. 7, no. 3, Public Library of Science, 2012, doi:10.1371/journal.pone.0033332.
short: B. Tasic, K. Miyamichi, S. Hippenmeyer, V. Dani, H. Zeng, W. Joo, H. Zong,
Y. Chen Tsai, L. Luo, PLoS One 7 (2012).
date_created: 2018-12-11T11:56:38Z
date_published: 2012-03-27T00:00:00Z
date_updated: 2021-01-12T06:56:22Z
day: '27'
doi: 10.1371/journal.pone.0033332
extern: 1
intvolume: ' 7'
issue: '3'
month: '03'
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '4683'
quality_controlled: 0
status: public
title: 'Extensions of MADM (Mosaic Analysis with Double Markers) in Mice '
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
volume: 7
year: '2012'
...
---
_id: '3147'
abstract:
- lang: eng
text: Cancer cell of origin is difficult to identify by analyzing cells within terminal
stage tumors, whose identity could be concealed by the acquired plasticity. Thus,
an ideal approach to identify the cell of origin is to analyze proliferative abnormalities
in distinct lineages prior to malignancy. Here, we use mosaic analysis with double
markers (MADM) in mice to model gliomagenesis by initiating concurrent p53/Nf1
mutations sporadically in neural stem cells (NSCs). Surprisingly, MADM-based lineage
tracing revealed significant aberrant growth prior to malignancy only in oligodendrocyte
precursor cells (OPCs), but not in any other NSC-derived lineages or NSCs themselves.
Upon tumor formation, phenotypic and transcriptome analyses of tumor cells revealed
salient OPC features. Finally, introducing the same p53/Nf1 mutations directly
into OPCs consistently led to gliomagenesis. Our findings suggest OPCs as the
cell of origin in this model, even when initial mutations occur in NSCs, and highlight
the importance of analyzing premalignant stages to identify the cancer cell of
origin.
author:
- first_name: Chong
full_name: Liu, Chong
last_name: Liu
- first_name: Jonathan
full_name: Sage, Jonathan C
last_name: Sage
- first_name: Michael
full_name: Miller, Michael R
last_name: Miller
- first_name: Roel
full_name: Verhaak, Roel G
last_name: Verhaak
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Hannes
full_name: Vogel, Hannes
last_name: Vogel
- first_name: Oded
full_name: Foreman, Oded
last_name: Foreman
- first_name: Roderick
full_name: Bronson, Roderick T
last_name: Bronson
- first_name: Akiko
full_name: Nishiyama, Akiko
last_name: Nishiyama
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
citation:
ama: Liu C, Sage J, Miller M, et al. Mosaic analysis with double markers reveals
tumor cell of origin in glioma. Cell. 2011;146(2):209-221. doi:10.1016/j.cell.2011.06.014
apa: Liu, C., Sage, J., Miller, M., Verhaak, R., Hippenmeyer, S., Vogel, H., … Zong,
H. (2011). Mosaic analysis with double markers reveals tumor cell of origin in
glioma. Cell. Cell Press. https://doi.org/10.1016/j.cell.2011.06.014
chicago: Liu, Chong, Jonathan Sage, Michael Miller, Roel Verhaak, Simon Hippenmeyer,
Hannes Vogel, Oded Foreman, et al. “Mosaic Analysis with Double Markers Reveals
Tumor Cell of Origin in Glioma.” Cell. Cell Press, 2011. https://doi.org/10.1016/j.cell.2011.06.014.
ieee: C. Liu et al., “Mosaic analysis with double markers reveals tumor cell
of origin in glioma,” Cell, vol. 146, no. 2. Cell Press, pp. 209–221, 2011.
ista: Liu C, Sage J, Miller M, Verhaak R, Hippenmeyer S, Vogel H, Foreman O, Bronson
R, Nishiyama A, Luo L, Zong H. 2011. Mosaic analysis with double markers reveals
tumor cell of origin in glioma. Cell. 146(2), 209–221.
mla: Liu, Chong, et al. “Mosaic Analysis with Double Markers Reveals Tumor Cell
of Origin in Glioma.” Cell, vol. 146, no. 2, Cell Press, 2011, pp. 209–21,
doi:10.1016/j.cell.2011.06.014.
short: C. Liu, J. Sage, M. Miller, R. Verhaak, S. Hippenmeyer, H. Vogel, O. Foreman,
R. Bronson, A. Nishiyama, L. Luo, H. Zong, Cell 146 (2011) 209–221.
date_created: 2018-12-11T12:01:40Z
date_published: 2011-07-22T00:00:00Z
date_updated: 2021-01-12T07:41:23Z
day: '22'
doi: 10.1016/j.cell.2011.06.014
extern: 1
intvolume: ' 146'
issue: '2'
month: '07'
page: 209 - 221
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '3548'
quality_controlled: 0
status: public
title: Mosaic analysis with double markers reveals tumor cell of origin in glioma
type: journal_article
volume: 146
year: '2011'
...
---
_id: '3145'
abstract:
- lang: eng
text: Microinjection of recombinant DNA into zygotic pronuclei has been widely used
for producing transgenic mice. However, with this method, the insertion site,
integrity, and copy number of the transgene cannot be controlled. Here, we present
an integrase-based approach to produce transgenic mice via pronuclear injection,
whereby an intact single-copy transgene can be inserted into predetermined chromosomal
loci with high efficiency (up to 40%), and faithfully transmitted through generations.
We show that neighboring transgenic elements and bacterial DNA within the transgene
cause profound silencing and expression variability of the transgenic marker.
Removal of these undesirable elements leads to global high-level marker expression
from transgenes driven by a ubiquitous promoter. We also obtained faithful marker
expression from a tissue-specific promoter. The technique presented here will
greatly facilitate murine transgenesis and precise structure/function dissection
of mammalian gene function and regulation in vivo.
author:
- first_name: Bosiljka
full_name: Tasic, Bosiljka
last_name: Tasic
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Charlene
full_name: Wang, Charlene
last_name: Wang
- first_name: Matthew
full_name: Gamboa, Matthew
last_name: Gamboa
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Yanru
full_name: Chen-Tsai, Yanru
last_name: Chen Tsai
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Tasic B, Hippenmeyer S, Wang C, et al. Site specific integrase mediated transgenesis
in mice via pronuclear injection. PNAS. 2011;108(19):7902-7907. doi:10.1073/pnas.1019507108
apa: Tasic, B., Hippenmeyer, S., Wang, C., Gamboa, M., Zong, H., Chen Tsai, Y.,
& Luo, L. (2011). Site specific integrase mediated transgenesis in mice via
pronuclear injection. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1019507108
chicago: Tasic, Bosiljka, Simon Hippenmeyer, Charlene Wang, Matthew Gamboa, Hui
Zong, Yanru Chen Tsai, and Liqun Luo. “Site Specific Integrase Mediated Transgenesis
in Mice via Pronuclear Injection.” PNAS. National Academy of Sciences,
2011. https://doi.org/10.1073/pnas.1019507108.
ieee: B. Tasic et al., “Site specific integrase mediated transgenesis in
mice via pronuclear injection,” PNAS, vol. 108, no. 19. National Academy
of Sciences, pp. 7902–7907, 2011.
ista: Tasic B, Hippenmeyer S, Wang C, Gamboa M, Zong H, Chen Tsai Y, Luo L. 2011.
Site specific integrase mediated transgenesis in mice via pronuclear injection.
PNAS. 108(19), 7902–7907.
mla: Tasic, Bosiljka, et al. “Site Specific Integrase Mediated Transgenesis in Mice
via Pronuclear Injection.” PNAS, vol. 108, no. 19, National Academy of
Sciences, 2011, pp. 7902–07, doi:10.1073/pnas.1019507108.
short: B. Tasic, S. Hippenmeyer, C. Wang, M. Gamboa, H. Zong, Y. Chen Tsai, L. Luo,
PNAS 108 (2011) 7902–7907.
date_created: 2018-12-11T12:01:39Z
date_published: 2011-05-10T00:00:00Z
date_updated: 2021-01-12T07:41:22Z
day: '10'
doi: 10.1073/pnas.1019507108
extern: 1
intvolume: ' 108'
issue: '19'
month: '05'
page: 7902 - 7907
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '3549'
quality_controlled: 0
status: public
title: Site specific integrase mediated transgenesis in mice via pronuclear injection
type: journal_article
volume: 108
year: '2011'
...
---
_id: '3146'
abstract:
- lang: eng
text: 'Coordinated migration of newly born neurons to their prospective target laminae
is a prerequisite for neural circuit assembly in the developing brain. The evolutionarily
conserved LIS1/NDEL1 complex is essential for neuronal migration in the mammalian
cerebral cortex. The cytoplasmic nature of LIS1 and NDEL1 proteins suggest that
they regulate neuronal migration cell autonomously. Here, we extend mosaic analysis
with double markers (MADM) to mouse chromosome 11 where Lis1, Ndel1, and 14-3-3e{open}
(encoding a LIS1/NDEL1 signaling partner) are located. Analyses of sparse and
uniquely labeled mutant cells in mosaic animals reveal distinct cell-autonomous
functions for these three genes. Lis1 regulates neuronal migration efficiency
in a dose-dependent manner, while Ndel1 is essential for a specific, previously
uncharacterized, late step of neuronal migration: entry into the target lamina.
Comparisons with previous genetic perturbations of Lis1 and Ndel1 also suggest
a surprising degree of cell-nonautonomous function for these proteins in regulating
neuronal migration.'
author:
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Yong
full_name: Youn, Yong H
last_name: Youn
- first_name: Hyang
full_name: Moon, Hyang M
last_name: Moon
- first_name: Kazunari
full_name: Miyamichi, Kazunari
last_name: Miyamichi
- first_name: Hui
full_name: Zong, Hui
last_name: Zong
- first_name: Anthony
full_name: Wynshaw-Boris, Anthony
last_name: Wynshaw Boris
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Hippenmeyer S, Youn Y, Moon H, et al. Genetic mosaic dissection of Lis1 and
Ndel1 in neuronal migration. Neuron. 2010;68(4):695-709. doi:10.1016/j.neuron.2010.09.027
apa: Hippenmeyer, S., Youn, Y., Moon, H., Miyamichi, K., Zong, H., Wynshaw Boris,
A., & Luo, L. (2010). Genetic mosaic dissection of Lis1 and Ndel1 in neuronal
migration. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2010.09.027
chicago: Hippenmeyer, Simon, Yong Youn, Hyang Moon, Kazunari Miyamichi, Hui Zong,
Anthony Wynshaw Boris, and Liqun Luo. “Genetic Mosaic Dissection of Lis1 and Ndel1
in Neuronal Migration.” Neuron. Elsevier, 2010. https://doi.org/10.1016/j.neuron.2010.09.027.
ieee: S. Hippenmeyer et al., “Genetic mosaic dissection of Lis1 and Ndel1
in neuronal migration,” Neuron, vol. 68, no. 4. Elsevier, pp. 695–709,
2010.
ista: Hippenmeyer S, Youn Y, Moon H, Miyamichi K, Zong H, Wynshaw Boris A, Luo L.
2010. Genetic mosaic dissection of Lis1 and Ndel1 in neuronal migration. Neuron.
68(4), 695–709.
mla: Hippenmeyer, Simon, et al. “Genetic Mosaic Dissection of Lis1 and Ndel1 in
Neuronal Migration.” Neuron, vol. 68, no. 4, Elsevier, 2010, pp. 695–709,
doi:10.1016/j.neuron.2010.09.027.
short: S. Hippenmeyer, Y. Youn, H. Moon, K. Miyamichi, H. Zong, A. Wynshaw Boris,
L. Luo, Neuron 68 (2010) 695–709.
date_created: 2018-12-11T12:01:39Z
date_published: 2010-11-18T00:00:00Z
date_updated: 2021-01-12T07:41:22Z
day: '18'
doi: 10.1016/j.neuron.2010.09.027
extern: 1
intvolume: ' 68'
issue: '4'
month: '11'
page: 695 - 709
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '3550'
quality_controlled: 0
status: public
title: Genetic mosaic dissection of Lis1 and Ndel1 in neuronal migration
type: journal_article
volume: 68
year: '2010'
...
---
_id: '3144'
abstract:
- lang: eng
text: Accumulation of specific proteins at synaptic structures is essential for
synapse assembly and function, but mechanisms regulating local protein enrichment
remain poorly understood. At the neuromuscular junction (NMJ), subsynaptic nuclei
underlie motor axon terminals within extrafusal muscle fibers and are transcriptionally
distinct from neighboring nuclei. In this study, we show that expression of the
ETS transcription factor Erm is highly concentrated at subsynaptic nuclei, and
its mutation in mice leads to severe downregulation of many genes with normally
enriched subsynaptic expression. Erm mutant mice display an expansion of the muscle
central domain in which acetylcholine receptor (AChR) clusters accumulate, show
gradual fragmentation of AChR clusters, and exhibit symptoms of muscle weakness
mimicking congenital myasthenic syndrome (CMS). Together, our findings define
Erm as an upstream regulator of a transcriptional program selective to subsynaptic
nuclei at the NMJ and underscore the importance of transcriptional control of
local synaptic protein accumulation.
author:
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Roland
full_name: Huber, Roland M
last_name: Huber
- first_name: David
full_name: Ladle, David R
last_name: Ladle
- first_name: Kenneth
full_name: Murphy, Kenneth
last_name: Murphy
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Huber R, Ladle D, Murphy K, Arber S. ETS transcription factor
Erm controls subsynaptic gene expression in skeletal muscles. Neuron. 2007;55(5):726-740.
doi:10.1016/j.neuron.2007.07.028
apa: Hippenmeyer, S., Huber, R., Ladle, D., Murphy, K., & Arber, S. (2007).
ETS transcription factor Erm controls subsynaptic gene expression in skeletal
muscles. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2007.07.028
chicago: Hippenmeyer, Simon, Roland Huber, David Ladle, Kenneth Murphy, and Silvia
Arber. “ETS Transcription Factor Erm Controls Subsynaptic Gene Expression in Skeletal
Muscles.” Neuron. Elsevier, 2007. https://doi.org/10.1016/j.neuron.2007.07.028.
ieee: S. Hippenmeyer, R. Huber, D. Ladle, K. Murphy, and S. Arber, “ETS transcription
factor Erm controls subsynaptic gene expression in skeletal muscles,” Neuron,
vol. 55, no. 5. Elsevier, pp. 726–740, 2007.
ista: Hippenmeyer S, Huber R, Ladle D, Murphy K, Arber S. 2007. ETS transcription
factor Erm controls subsynaptic gene expression in skeletal muscles. Neuron. 55(5),
726–740.
mla: Hippenmeyer, Simon, et al. “ETS Transcription Factor Erm Controls Subsynaptic
Gene Expression in Skeletal Muscles.” Neuron, vol. 55, no. 5, Elsevier,
2007, pp. 726–40, doi:10.1016/j.neuron.2007.07.028.
short: S. Hippenmeyer, R. Huber, D. Ladle, K. Murphy, S. Arber, Neuron 55 (2007)
726–740.
date_created: 2018-12-11T12:01:39Z
date_published: 2007-09-06T00:00:00Z
date_updated: 2021-01-12T07:41:22Z
day: '06'
doi: 10.1016/j.neuron.2007.07.028
extern: 1
intvolume: ' 55'
issue: '5'
month: '09'
page: 726 - 740
publication: Neuron
publication_status: published
publisher: Elsevier
publist_id: '3551'
quality_controlled: 0
status: public
title: ETS transcription factor Erm controls subsynaptic gene expression in skeletal
muscles
type: journal_article
volume: 55
year: '2007'
...
---
_id: '3143'
abstract:
- lang: eng
text: Two ETS transcription factors of the Pea3 subfamily are induced in subpopulations
of dorsal root ganglion (DRG) sensory and spinal motor neurons by target-derived
factors. Their expression controls late aspects of neuronal differentiation such
as target invasion and branching. Here, we show that the late onset of ETS gene
expression is an essential requirement for normal sensory neuron differentiation.
We provide genetic evidence in the mouse that precocious ETS expression in DRG
sensory neurons perturbs axonal projections, the acquisition of terminal differentiation
markers, and their dependence on neurotrophic support. Together, our findings
indicate that DRG sensory neurons exhibit a temporal developmental switch that
can be revealed by distinct responses to ETS transcription factor signaling at
sequential steps of neuronal maturation.
author:
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Eline
full_name: Vrieseling, Eline
last_name: Vrieseling
- first_name: Markus
full_name: Sigrist, Markus
last_name: Sigrist
- first_name: Thomas
full_name: Portmann, Thomas
last_name: Portmann
- first_name: Celia
full_name: Laengle, Celia
last_name: Laengle
- first_name: David
full_name: Ladle, David R
last_name: Ladle
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Vrieseling E, Sigrist M, et al. A developmental switch in the
response of DRG neurons to ETS transcription factor signaling. PLoS Biology.
2005;3(5):0878-0890. doi:10.1371/journal.pbio.0030159
apa: Hippenmeyer, S., Vrieseling, E., Sigrist, M., Portmann, T., Laengle, C., Ladle,
D., & Arber, S. (2005). A developmental switch in the response of DRG neurons
to ETS transcription factor signaling. PLoS Biology. Public Library of
Science. https://doi.org/10.1371/journal.pbio.0030159
chicago: Hippenmeyer, Simon, Eline Vrieseling, Markus Sigrist, Thomas Portmann,
Celia Laengle, David Ladle, and Silvia Arber. “A Developmental Switch in the Response
of DRG Neurons to ETS Transcription Factor Signaling.” PLoS Biology. Public
Library of Science, 2005. https://doi.org/10.1371/journal.pbio.0030159.
ieee: S. Hippenmeyer et al., “A developmental switch in the response of DRG
neurons to ETS transcription factor signaling,” PLoS Biology, vol. 3, no.
5. Public Library of Science, pp. 0878–0890, 2005.
ista: Hippenmeyer S, Vrieseling E, Sigrist M, Portmann T, Laengle C, Ladle D, Arber
S. 2005. A developmental switch in the response of DRG neurons to ETS transcription
factor signaling. PLoS Biology. 3(5), 0878–0890.
mla: Hippenmeyer, Simon, et al. “A Developmental Switch in the Response of DRG Neurons
to ETS Transcription Factor Signaling.” PLoS Biology, vol. 3, no. 5, Public
Library of Science, 2005, pp. 0878–90, doi:10.1371/journal.pbio.0030159.
short: S. Hippenmeyer, E. Vrieseling, M. Sigrist, T. Portmann, C. Laengle, D. Ladle,
S. Arber, PLoS Biology 3 (2005) 0878–0890.
date_created: 2018-12-11T12:01:38Z
date_published: 2005-05-01T00:00:00Z
date_updated: 2021-01-12T07:41:21Z
day: '01'
doi: 10.1371/journal.pbio.0030159
extern: 1
intvolume: ' 3'
issue: '5'
month: '05'
page: 0878 - 0890
publication: PLoS Biology
publication_status: published
publisher: Public Library of Science
publist_id: '3552'
quality_controlled: 0
status: public
title: A developmental switch in the response of DRG neurons to ETS transcription
factor signaling
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
volume: 3
year: '2005'
...
---
_id: '3141'
abstract:
- lang: eng
text: The two actin-related subunits of the Arp2/3 complex, Arp2 and Arp3, are proposed
to form a pseudo actin dimer that nucleates actin polymerization. However, in
the crystal structure of the inactive complex, they are too far apart to form
such a nucleus. Here, we show using EM that yeast and bovine Arp2/3 complexes
exist in a distribution among open, intermediate and closed conformations. The
crystal structure docks well into the open conformation. The activator WASp binds
at the cleft between Arp2 and Arp3, and all WASp-bound complexes are closed. The
inhibitor coronin binds near the p35 subunit, and all coronin-bound complexes
are open. Activating and loss-of-function mutations in the p35 subunit skew conformational
distribution in opposite directions, closed and open, respectively. We conclude
that WASp stabilizes p35-dependent closure of the complex, holding Arp2 and Arp3
closer together to nucleate an actin filament.
author:
- first_name: Avital
full_name: Rodal, Avital A
last_name: Rodal
- first_name: Olga
full_name: Sokolova, Olga
last_name: Sokolova
- first_name: Deborah
full_name: Robins, Deborah B
last_name: Robins
- first_name: Karen
full_name: Daugherty, Karen M
last_name: Daugherty
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Howard
full_name: Riezman, Howard
last_name: Riezman
- first_name: Nikolaus
full_name: Grigorieff, Nikolaus
last_name: Grigorieff
- first_name: Bruce
full_name: Goode, Bruce L
last_name: Goode
citation:
ama: Rodal A, Sokolova O, Robins D, et al. Conformational changes in the Arp2 3
complex leading to actin nucleation. Nature Structural and Molecular Biology.
2005;12(1):26-31. doi:10.1038/nsmb870
apa: Rodal, A., Sokolova, O., Robins, D., Daugherty, K., Hippenmeyer, S., Riezman,
H., … Goode, B. (2005). Conformational changes in the Arp2 3 complex leading to
actin nucleation. Nature Structural and Molecular Biology. Nature Publishing
Group. https://doi.org/10.1038/nsmb870
chicago: Rodal, Avital, Olga Sokolova, Deborah Robins, Karen Daugherty, Simon Hippenmeyer,
Howard Riezman, Nikolaus Grigorieff, and Bruce Goode. “Conformational Changes
in the Arp2 3 Complex Leading to Actin Nucleation.” Nature Structural and Molecular
Biology. Nature Publishing Group, 2005. https://doi.org/10.1038/nsmb870.
ieee: A. Rodal et al., “Conformational changes in the Arp2 3 complex leading
to actin nucleation,” Nature Structural and Molecular Biology, vol. 12,
no. 1. Nature Publishing Group, pp. 26–31, 2005.
ista: Rodal A, Sokolova O, Robins D, Daugherty K, Hippenmeyer S, Riezman H, Grigorieff
N, Goode B. 2005. Conformational changes in the Arp2 3 complex leading to actin
nucleation. Nature Structural and Molecular Biology. 12(1), 26–31.
mla: Rodal, Avital, et al. “Conformational Changes in the Arp2 3 Complex Leading
to Actin Nucleation.” Nature Structural and Molecular Biology, vol. 12,
no. 1, Nature Publishing Group, 2005, pp. 26–31, doi:10.1038/nsmb870.
short: A. Rodal, O. Sokolova, D. Robins, K. Daugherty, S. Hippenmeyer, H. Riezman,
N. Grigorieff, B. Goode, Nature Structural and Molecular Biology 12 (2005) 26–31.
date_created: 2018-12-11T12:01:38Z
date_published: 2005-01-01T00:00:00Z
date_updated: 2021-01-12T07:41:21Z
day: '01'
doi: 10.1038/nsmb870
extern: 1
intvolume: ' 12'
issue: '1'
month: '01'
page: 26 - 31
publication: Nature Structural and Molecular Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '3554'
quality_controlled: 0
status: public
title: Conformational changes in the Arp2 3 complex leading to actin nucleation
type: journal_article
volume: 12
year: '2005'
...
---
_id: '3142'
abstract:
- lang: eng
text: Assembly of neuronal circuits is controlled by the sequential acquisition
of neuronal subpopulation-specific identities at progressive developmental steps.
Whereas neuronal features involved in initial phases of differentiation are already
established at cell-cycle exit, recent findings, based mainly on work in the peripheral
nervous system, suggest that the timely integration of signals encountered en
route to targets and from the target region itself is essential to control late
steps in connectivity. As neurons project towards their targets they require target-derived
signals to establish mature axonal projections and acquire neuronal traits such
as the expression of distinct combinations of neurotransmitters. Recent evidence
presented in this review shows that this principle, of a signaling interplay between
target-derived signals and neuronal cell bodies, is often mediated through transcriptional
events and is evolutionarily conserved.
author:
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ina
full_name: Kramer, Ina
last_name: Kramer
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: 'Hippenmeyer S, Kramer I, Arber S. Control of neuronal phenotype: What targets
tell the cell bodies. Trends in Neurosciences. 2004;27(8):482-488. doi:10.1016/j.tins.2004.05.012'
apa: 'Hippenmeyer, S., Kramer, I., & Arber, S. (2004). Control of neuronal phenotype:
What targets tell the cell bodies. Trends in Neurosciences. Elsevier. https://doi.org/10.1016/j.tins.2004.05.012'
chicago: 'Hippenmeyer, Simon, Ina Kramer, and Silvia Arber. “Control of Neuronal
Phenotype: What Targets Tell the Cell Bodies.” Trends in Neurosciences.
Elsevier, 2004. https://doi.org/10.1016/j.tins.2004.05.012.'
ieee: 'S. Hippenmeyer, I. Kramer, and S. Arber, “Control of neuronal phenotype:
What targets tell the cell bodies,” Trends in Neurosciences, vol. 27, no.
8. Elsevier, pp. 482–488, 2004.'
ista: 'Hippenmeyer S, Kramer I, Arber S. 2004. Control of neuronal phenotype: What
targets tell the cell bodies. Trends in Neurosciences. 27(8), 482–488.'
mla: 'Hippenmeyer, Simon, et al. “Control of Neuronal Phenotype: What Targets Tell
the Cell Bodies.” Trends in Neurosciences, vol. 27, no. 8, Elsevier, 2004,
pp. 482–88, doi:10.1016/j.tins.2004.05.012.'
short: S. Hippenmeyer, I. Kramer, S. Arber, Trends in Neurosciences 27 (2004) 482–488.
date_created: 2018-12-11T12:01:38Z
date_published: 2004-08-01T00:00:00Z
date_updated: 2019-04-26T07:22:25Z
day: '01'
doi: 10.1016/j.tins.2004.05.012
extern: 1
intvolume: ' 27'
issue: '8'
month: '08'
page: 482 - 488
publication: Trends in Neurosciences
publication_status: published
publisher: Elsevier
publist_id: '3555'
quality_controlled: 0
status: public
title: 'Control of neuronal phenotype: What targets tell the cell bodies'
type: review
volume: 27
year: '2004'
...
---
_id: '3139'
abstract:
- lang: eng
text: Significant advances have been made during the past few years in our understanding
of how the spinal monosynaptic reflex develops. Transcription factors in the Neurogenin,
Runt, ETS, and LIM families control sequential steps of the specification of various
subtypes of dorsal root ganglia sensory neurons. The initiation of muscle spindle
differentiation requires neuregulin 1, derived from Ia afferent sensory neurons,
and signaling through ErbB receptors in intrafusal muscle fibers. Several retrograde
signals from the periphery are important for the establishment of late connectivity
in the reflex circuit. Finally, neurotrophin 3 released from muscle spindles regulates
the strength of sensory-motor connections within the spinal cord postnatally.
author:
- first_name: Hsiao
full_name: Chen, Hsiao Huei
last_name: Chen
- first_name: Simon
full_name: Simon Hippenmeyer
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
- first_name: Eric
full_name: Frank, Eric
last_name: Frank
citation:
ama: Chen H, Hippenmeyer S, Arber S, Frank E. Development of the monosynaptic stretch
reflex circuit. Current Opinion in Neurobiology. 2003;13(1):96-102. doi:10.1016/S0959-4388(03)00006-0
apa: Chen, H., Hippenmeyer, S., Arber, S., & Frank, E. (2003). Development of
the monosynaptic stretch reflex circuit. Current Opinion in Neurobiology.
Elsevier. https://doi.org/10.1016/S0959-4388(03)00006-0
chicago: Chen, Hsiao, Simon Hippenmeyer, Silvia Arber, and Eric Frank. “Development
of the Monosynaptic Stretch Reflex Circuit.” Current Opinion in Neurobiology.
Elsevier, 2003. https://doi.org/10.1016/S0959-4388(03)00006-0.
ieee: H. Chen, S. Hippenmeyer, S. Arber, and E. Frank, “Development of the monosynaptic
stretch reflex circuit,” Current Opinion in Neurobiology, vol. 13, no.
1. Elsevier, pp. 96–102, 2003.
ista: Chen H, Hippenmeyer S, Arber S, Frank E. 2003. Development of the monosynaptic
stretch reflex circuit. Current Opinion in Neurobiology. 13(1), 96–102.
mla: Chen, Hsiao, et al. “Development of the Monosynaptic Stretch Reflex Circuit.”
Current Opinion in Neurobiology, vol. 13, no. 1, Elsevier, 2003, pp. 96–102,
doi:10.1016/S0959-4388(03)00006-0.
short: H. Chen, S. Hippenmeyer, S. Arber, E. Frank, Current Opinion in Neurobiology
13 (2003) 96–102.
date_created: 2018-12-11T12:01:37Z
date_published: 2003-02-01T00:00:00Z
date_updated: 2019-04-26T07:22:24Z
day: '01'
doi: 10.1016/S0959-4388(03)00006-0
extern: 1
intvolume: ' 13'
issue: '1'
month: '02'
page: 96 - 102
publication: Current Opinion in Neurobiology
publication_status: published
publisher: Elsevier
publist_id: '3557'
quality_controlled: 0
status: public
title: Development of the monosynaptic stretch reflex circuit
type: review
volume: 13
year: '2003'
...
---
_id: '3140'
abstract:
- lang: eng
text: The maturation of synaptic structures depends on inductive interactions between
axons and their prospective targets. One example of such an interaction is the
influence of proprioceptive sensory axons on the differentiation of muscle spindles.
We have monitored the expression of three transcription factors, Egr3, Pea3, and
Erm, that delineate early muscle spindle development in an assay of muscle spindle-inducing
signals. We provide genetic evidence that Neuregulin1 (Nrg1) is required for proprioceptive
afferent-evoked induction of muscle spindle differentiation in the mouse. Ig-Nrg1
isoforms are preferentially expressed by proprioceptive sensory neurons and are
sufficient to induce muscle spindle differentiation in vivo, whereas CRD-Nrg1
isoforms are broadly expressed in sensory and motor neurons but are not required
for muscle spindle induction.
acknowledgement: We thank L. Role for generously providing the CRD-Nrg1 mutant allele
for these studies, L. Parada and D. Anderson for sharing the TrkC and Ngn1 mouse
strains, W. Tourtellotte for providing Egr3 mutant mice, E. Avetisova for expert
technical assistance, X. Yang for experimental help in the initial phase of these
studies, A. Garratt for advice with ErbB antibodies, and L. Role and G. Fischbach
for helpful discussions. The CRD-Nrg1 mutant allele was generated in the lab of
Dr. Lorna Role, with the support of NIH grant NS29071. S.A. and S.H. were supported
by a grant from the Swiss National Science Foundation and the Kanton of Basel-Stadt.
S.J.B. was supported by grants from the NINDS. N.A.S. was supported by a Howard
Hughes Medical Institute Postdoctoral Fellowship for Physicians and a Career Development
Award from the NINDS. T.M.J. was supported by grants from NINDS and is an Investigator
of the Howard Hughes Medical Institute.
article_processing_charge: No
article_type: original
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Neil
full_name: Shneider, Neil
last_name: Shneider
- first_name: Carmen
full_name: Birchmeier, Carmen
last_name: Birchmeier
- first_name: Steven
full_name: Burden, Steven
last_name: Burden
- first_name: Thomas
full_name: Jessell, Thomas
last_name: Jessell
- first_name: Silvia
full_name: Arber, Silvia
last_name: Arber
citation:
ama: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. A role
for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 2002;36(6):1035-1049.
doi:10.1016/S0896-6273(02)01101-7
apa: Hippenmeyer, S., Shneider, N., Birchmeier, C., Burden, S., Jessell, T., &
Arber, S. (2002). A role for Neuregulin1 signaling in muscle spindle differentiation.
Neuron. Elsevier. https://doi.org/10.1016/S0896-6273(02)01101-7
chicago: Hippenmeyer, Simon, Neil Shneider, Carmen Birchmeier, Steven Burden, Thomas
Jessell, and Silvia Arber. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron. Elsevier, 2002. https://doi.org/10.1016/S0896-6273(02)01101-7.
ieee: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, and S.
Arber, “A role for Neuregulin1 signaling in muscle spindle differentiation,” Neuron,
vol. 36, no. 6. Elsevier, pp. 1035–1049, 2002.
ista: Hippenmeyer S, Shneider N, Birchmeier C, Burden S, Jessell T, Arber S. 2002.
A role for Neuregulin1 signaling in muscle spindle differentiation. Neuron. 36(6),
1035–1049.
mla: Hippenmeyer, Simon, et al. “A Role for Neuregulin1 Signaling in Muscle Spindle
Differentiation.” Neuron, vol. 36, no. 6, Elsevier, 2002, pp. 1035–49,
doi:10.1016/S0896-6273(02)01101-7.
short: S. Hippenmeyer, N. Shneider, C. Birchmeier, S. Burden, T. Jessell, S. Arber,
Neuron 36 (2002) 1035–1049.
date_created: 2018-12-11T12:01:37Z
date_published: 2002-12-19T00:00:00Z
date_updated: 2023-07-17T11:46:43Z
day: '19'
doi: 10.1016/S0896-6273(02)01101-7
extern: '1'
external_id:
pmid:
- '12495620'
intvolume: ' 36'
issue: '6'
language:
- iso: eng
month: '12'
oa_version: None
page: 1035 - 1049
pmid: 1
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
publist_id: '3558'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A role for Neuregulin1 signaling in muscle spindle differentiation
type: journal_article
user_id: ea97e931-d5af-11eb-85d4-e6957dddbf17
volume: 36
year: '2002'
...