---
_id: '7399'
abstract:
- lang: eng
text: Long non-coding (lnc) RNAs are numerous and found throughout the mammalian
genome, and many are thought to be involved in the regulation of gene expression.
However, the majority remain relatively uncharacterised and of uncertain function
making the use of model systems to uncover their mode of action valuable. Imprinted
lncRNAs target and recruit epigenetic silencing factors to a cluster of imprinted
genes on the same chromosome, making them one of the best characterized lncRNAs
for silencing distant genes in cis. In this study we examined silencing of the
distant imprinted gene Slc22a3 by the lncRNA Airn in the Igf2r imprinted cluster
in mouse. Previously we proposed that imprinted lncRNAs may silence distant imprinted
genes by disrupting promoter-enhancer interactions by being transcribed through
the enhancer, which we called the enhancer interference hypothesis. Here we tested
this hypothesis by first using allele-specific chromosome conformation capture
(3C) to detect interactions between the Slc22a3 promoter and the locus of the
Airn lncRNA that silences it on the paternal chromosome. In agreement with the
model, we found interactions enriched on the maternal allele across the entire
Airn gene consistent with multiple enhancer-promoter interactions. Therefore,
to test the enhancer interference hypothesis we devised an approach to delete
the entire Airn gene. However, the deletion showed that there are no essential
enhancers for Slc22a2, Pde10a and Slc22a3 within the Airn gene, strongly indicating
that the Airn RNA rather than its transcription is responsible for silencing distant
imprinted genes. Furthermore, we found that silent imprinted genes were covered
with large blocks of H3K27me3 on the repressed paternal allele. Therefore we propose
an alternative hypothesis whereby the chromosome interactions may initially guide
the lncRNA to target imprinted promoters and recruit repressive chromatin, and
that these interactions are lost once silencing is established.
article_number: e1008268
article_processing_charge: No
article_type: original
author:
- first_name: Daniel
full_name: Andergassen, Daniel
last_name: Andergassen
- first_name: Markus
full_name: Muckenhuber, Markus
last_name: Muckenhuber
- first_name: Philipp C.
full_name: Bammer, Philipp C.
last_name: Bammer
- first_name: Tomasz M.
full_name: Kulinski, Tomasz M.
last_name: Kulinski
- first_name: Hans-Christian
full_name: Theussl, Hans-Christian
last_name: Theussl
- first_name: Takahiko
full_name: Shimizu, Takahiko
last_name: Shimizu
- first_name: Josef M.
full_name: Penninger, Josef M.
last_name: Penninger
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Quanah J.
full_name: Hudson, Quanah J.
last_name: Hudson
citation:
ama: Andergassen D, Muckenhuber M, Bammer PC, et al. The Airn lncRNA does not require
any DNA elements within its locus to silence distant imprinted genes. PLoS
Genetics. 2019;15(7). doi:10.1371/journal.pgen.1008268
apa: Andergassen, D., Muckenhuber, M., Bammer, P. C., Kulinski, T. M., Theussl,
H.-C., Shimizu, T., … Hudson, Q. J. (2019). The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
Public Library of Science. https://doi.org/10.1371/journal.pgen.1008268
chicago: Andergassen, Daniel, Markus Muckenhuber, Philipp C. Bammer, Tomasz M. Kulinski,
Hans-Christian Theussl, Takahiko Shimizu, Josef M. Penninger, Florian Pauler,
and Quanah J. Hudson. “The Airn LncRNA Does Not Require Any DNA Elements within
Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics. Public Library
of Science, 2019. https://doi.org/10.1371/journal.pgen.1008268.
ieee: D. Andergassen et al., “The Airn lncRNA does not require any DNA elements
within its locus to silence distant imprinted genes,” PLoS Genetics, vol.
15, no. 7. Public Library of Science, 2019.
ista: Andergassen D, Muckenhuber M, Bammer PC, Kulinski TM, Theussl H-C, Shimizu
T, Penninger JM, Pauler F, Hudson QJ. 2019. The Airn lncRNA does not require any
DNA elements within its locus to silence distant imprinted genes. PLoS Genetics.
15(7), e1008268.
mla: Andergassen, Daniel, et al. “The Airn LncRNA Does Not Require Any DNA Elements
within Its Locus to Silence Distant Imprinted Genes.” PLoS Genetics, vol.
15, no. 7, e1008268, Public Library of Science, 2019, doi:10.1371/journal.pgen.1008268.
short: D. Andergassen, M. Muckenhuber, P.C. Bammer, T.M. Kulinski, H.-C. Theussl,
T. Shimizu, J.M. Penninger, F. Pauler, Q.J. Hudson, PLoS Genetics 15 (2019).
corr_author: '1'
date_created: 2020-01-29T16:14:07Z
date_published: 2019-07-22T00:00:00Z
date_updated: 2024-10-09T20:59:14Z
day: '22'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pgen.1008268
external_id:
isi:
- '000478689100025'
pmid:
- '31329595'
file:
- access_level: open_access
checksum: 2f51fc91e4a4199827adc51d432ad864
content_type: application/pdf
creator: dernst
date_created: 2020-02-04T10:11:55Z
date_updated: 2020-07-14T12:47:57Z
file_id: '7446'
file_name: 2019_PlosGenetics_Andergassen.pdf
file_size: 2302307
relation: main_file
file_date_updated: 2020-07-14T12:47:57Z
fulldoi: https://doi.org/10.1371/journal.pgen.1008268
has_accepted_license: '1'
intvolume: ' 15'
isi: 1
issue: '7'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '07'
oa: 1
oa_version: Published Version
pmid: 1
publication: PLoS Genetics
publication_identifier:
issn:
- 1553-7404
publication_status: published
publisher: Public Library of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: The Airn lncRNA does not require any DNA elements within its locus to silence
distant imprinted genes
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: 15
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: 2026-11-11T23:30:19Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.08.021
external_id:
isi:
- '000484400200002'
pmid:
- '31487522'
fulldoi: https://doi.org/10.1016/j.neuron.2019.08.021
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:
- 1097-4199
issn:
- 0896-6273
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 103
year: '2019'
...
---
_id: '20'
abstract:
- lang: eng
text: 'Background: Norepinephrine (NE) signaling has a key role in white adipose
tissue (WAT) functions, including lipolysis, free fatty acid liberation and, under
certain conditions, conversion of white into brite (brown-in-white) adipocytes.
However, acute effects of NE stimulation have not been described at the transcriptional
network level. Results: We used RNA-seq to uncover a broad transcriptional response.
The inference of protein-protein and protein-DNA interaction networks allowed
us to identify a set of immediate-early genes (IEGs) with high betweenness, validating
our approach and suggesting a hierarchical control of transcriptional regulation.
In addition, we identified a transcriptional regulatory network with IEGs as master
regulators, including HSF1 and NFIL3 as novel NE-induced IEG candidates. Moreover,
a functional enrichment analysis and gene clustering into functional modules suggest
a crosstalk between metabolic, signaling, and immune responses. Conclusions: Altogether,
our network biology approach explores for the first time the immediate-early systems
level response of human adipocytes to acute sympathetic activation, thereby providing
a first network basis of early cell fate programs and crosstalks between metabolic
and transcriptional networks required for proper WAT function.'
acknowledgement: This work was funded by the German Centre for Diabetes Research (DZD)
and the Austrian Science Fund (FWF, P25729-B19).
article_processing_charge: No
article_type: original
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: Higareda Almaraz J, Karbiener M, Giroud M, et al. Norepinephrine triggers an
immediate-early regulatory network response in primary human white adipocytes.
BMC Genomics. 2018;19(1). doi:10.1186/s12864-018-5173-0
apa: Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes. BMC Genomics.
BioMed Central. https://doi.org/10.1186/s12864-018-5173-0
chicago: Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.”
BMC Genomics. BioMed Central, 2018. https://doi.org/10.1186/s12864-018-5173-0.
ieee: J. Higareda Almaraz et al., “Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes,” BMC Genomics,
vol. 19, no. 1. BioMed Central, 2018.
ista: Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig S,
Scheideler M. 2018. Norepinephrine triggers an immediate-early regulatory network
response in primary human white adipocytes. BMC Genomics. 19(1).
mla: Higareda Almaraz, Juan, et al. “Norepinephrine Triggers an Immediate-Early
Regulatory Network Response in Primary Human White Adipocytes.” BMC Genomics,
vol. 19, no. 1, BioMed Central, 2018, doi:10.1186/s12864-018-5173-0.
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, BMC Genomics 19 (2018).
date_created: 2018-12-11T11:44:12Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1186/s12864-018-5173-0
external_id:
isi:
- '000450976700002'
file:
- access_level: open_access
checksum: a56516e734dab589dc7f3e1915973b4d
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T14:52:57Z
date_updated: 2020-07-14T12:45:23Z
file_id: '5712'
file_name: 2018_BMCGenomics_Higareda.pdf
file_size: 4629784
relation: main_file
file_date_updated: 2020-07-14T12:45:23Z
fulldoi: https://doi.org/10.1186/s12864-018-5173-0
has_accepted_license: '1'
intvolume: ' 19'
isi: 1
issue: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
publication: BMC Genomics
publication_identifier:
issn:
- 1471-2164
publication_status: published
publisher: BioMed Central
publist_id: '8035'
quality_controlled: '1'
related_material:
record:
- id: '9807'
relation: research_data
status: public
- id: '9808'
relation: research_data
status: public
scopus_import: '1'
status: public
title: Norepinephrine triggers an immediate-early regulatory network response in primary
human white adipocytes
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: 19
year: '2018'
...
---
_id: '9807'
abstract:
- lang: eng
text: Table S1. Genes with highest betweenness. Table S2. Local and Master regulators
up-regulated. Table S3. Local and Master regulators down-regulated (XLSX 23 kb).
article_processing_charge: No
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: 'Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. 2018. doi:10.6084/m9.figshare.7295339.v1'
apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295339.v1'
chicago: 'Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 1: Of
Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary
Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295339.v1.'
ieee: 'J. Higareda Almaraz et al., “Additional file 1: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes.” Springer Nature, 2018.'
ista: 'Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig
S, Scheideler M. 2018. Additional file 1: Of Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes, Springer Nature,
10.6084/m9.figshare.7295339.v1.'
mla: 'Higareda Almaraz, Juan, et al. Additional File 1: Of Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.
Springer Nature, 2018, doi:10.6084/m9.figshare.7295339.v1.'
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, (2018).
date_created: 2021-08-06T12:26:53Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
department:
- _id: SiHi
doi: 10.6084/m9.figshare.7295339.v1
fulldoi: https://doi.org/10.6084/m9.figshare.7295339.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.7295339.v1
month: '11'
oa: 1
oa_version: Published Version
publisher: Springer Nature
related_material:
record:
- id: '20'
relation: used_in_publication
status: public
status: public
title: 'Additional file 1: Of Norepinephrine triggers an immediate-early regulatory
network response in primary human white adipocytes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2018'
...
---
_id: '9808'
abstract:
- lang: eng
text: Table S4. Counts per Gene per Million Reads Mapped. (XLSX 2751 kb).
article_processing_charge: No
author:
- first_name: Juan
full_name: Higareda Almaraz, Juan
last_name: Higareda Almaraz
- first_name: Michael
full_name: Karbiener, Michael
last_name: Karbiener
- first_name: Maude
full_name: Giroud, Maude
last_name: Giroud
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Teresa
full_name: Gerhalter, Teresa
last_name: Gerhalter
- first_name: Stephan
full_name: Herzig, Stephan
last_name: Herzig
- first_name: Marcel
full_name: Scheideler, Marcel
last_name: Scheideler
citation:
ama: 'Higareda Almaraz J, Karbiener M, Giroud M, et al. Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. 2018. doi:10.6084/m9.figshare.7295369.v1'
apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
Herzig, S., & Scheideler, M. (2018). Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes. Springer Nature. https://doi.org/10.6084/m9.figshare.7295369.v1'
chicago: 'Higareda Almaraz, Juan, Michael Karbiener, Maude Giroud, Florian Pauler,
Teresa Gerhalter, Stephan Herzig, and Marcel Scheideler. “Additional File 3: Of
Norepinephrine Triggers an Immediate-Early Regulatory Network Response in Primary
Human White Adipocytes.” Springer Nature, 2018. https://doi.org/10.6084/m9.figshare.7295369.v1.'
ieee: 'J. Higareda Almaraz et al., “Additional file 3: Of Norepinephrine
triggers an immediate-early regulatory network response in primary human white
adipocytes.” Springer Nature, 2018.'
ista: 'Higareda Almaraz J, Karbiener M, Giroud M, Pauler F, Gerhalter T, Herzig
S, Scheideler M. 2018. Additional file 3: Of Norepinephrine triggers an immediate-early
regulatory network response in primary human white adipocytes, Springer Nature,
10.6084/m9.figshare.7295369.v1.'
mla: 'Higareda Almaraz, Juan, et al. Additional File 3: Of Norepinephrine Triggers
an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes.
Springer Nature, 2018, doi:10.6084/m9.figshare.7295369.v1.'
short: J. Higareda Almaraz, M. Karbiener, M. Giroud, F. Pauler, T. Gerhalter, S.
Herzig, M. Scheideler, (2018).
date_created: 2021-08-06T12:31:57Z
date_published: 2018-11-03T00:00:00Z
date_updated: 2023-09-13T09:10:47Z
day: '03'
department:
- _id: SiHi
doi: 10.6084/m9.figshare.7295369.v1
fulldoi: https://doi.org/10.6084/m9.figshare.7295369.v1
main_file_link:
- open_access: '1'
url: https://doi.org/10.6084/m9.figshare.7295369.v1
month: '11'
oa: 1
oa_version: Published Version
publisher: Springer Nature
related_material:
record:
- id: '20'
relation: used_in_publication
status: public
status: public
title: 'Additional file 3: Of Norepinephrine triggers an immediate-early regulatory
network response in primary human white adipocytes'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2018'
...
---
_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. 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,
n.d. https://doi.org/10.1101/494088.
ieee: A. Llorca et al., “Heterogeneous progenitor cell behaviors underlie
the assembly of neocortical cytoarchitecture,” bioRxiv. .
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, 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.).
das_tickbox: '1'
date_created: 2020-09-21T12:01:50Z
date_published: 2018-12-13T00:00:00Z
date_updated: 2026-07-06T12:52:50Z
day: '13'
department:
- _id: SiHi
doi: 10.1101/494088
ec_funded: 1
fulldoi: https://doi.org/10.1101/494088
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 Neocortex
publication: bioRxiv
publication_status: submitted
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: 2026-11-11T23:30:19Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/brain/awy218
external_id:
isi:
- '000446548100012'
fulldoi: https://doi.org/10.1093/brain/awy218
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'
...
---
OA_place: publisher
_id: '10'
abstract:
- lang: eng
text: Genomic imprinting is an epigenetic process that leads to parent of origin-specific
gene expression in a subset of genes. Imprinted genes are essential for brain
development, and deregulation of imprinting is associated with neurodevelopmental
diseases and the pathogenesis of psychiatric disorders. However, the cell-type
specificity of imprinting at single cell resolution, and how imprinting and thus
gene dosage regulates neuronal circuit assembly is still largely unknown. Here,
MADM (Mosaic Analysis with Double Markers) technology was employed to assess genomic
imprinting at single cell level. By visualizing MADM-induced uniparental disomies
(UPDs) in distinct colors at single cell level in genetic mosaic animals, this
experimental paradigm provides a unique quantitative platform to systematically
assay the UPD-mediated imbalances in imprinted gene expression at unprecedented
resolution. An experimental pipeline based on FACS, RNA-seq and bioinformatics
analysis was established and applied to systematically map cell-type-specific
‘imprintomes’ in the mouse brain. The results revealed that parental-specific
expression of imprinted genes per se is rarely cell-type-specific even at the
individual cell level. Conversely, when we extended the comparison to downstream
responses resulting from imbalanced imprinted gene expression, we discovered an
unexpectedly high degree of cell-type specificity. Furthermore, we determined
a novel function of genomic imprinting in cortical astrocyte production and in
olfactory bulb (OB) granule cell generation. These results suggest important functional
implication of genomic imprinting for generating cell-type diversity in the brain.
In addition, MADM provides a powerful tool to study candidate genes by concomitant
genetic manipulation and fluorescent labelling of single cells. MADM-based candidate
gene approach was utilized to identify potential imprinted genes involved in the
generation of cortical astrocytes and OB granule cells. We investigated p57Kip2,
a maternally expressed gene and known cell cycle regulator. Although we found
that p57Kip2 does not play a role in these processes, we detected an unexpected
function of the paternal allele previously thought to be silent. Finally, we took
advantage of a key property of MADM which is to allow unambiguous investigation
of environmental impact on single cells. The experimental pipeline based on FACS
and RNA-seq analysis of MADM-labeled cells was established to probe the functional
differences of single cell loss of gene function compared to global loss of function
on a transcriptional level. With this method, both common and distinct responses
were isolated due to cell-autonomous and non-autonomous effects acting on genotypically
identical cells. As a result, transcriptional changes were identified which result
solely from the surrounding environment. Using the MADM technology to study genomic
imprinting at single cell resolution, we have identified cell-type-specific gene
expression, novel gene function and the impact of environment on single cell transcriptomes.
Together, these provide important insights to the understanding of mechanisms
regulating cell-type specificity and thus diversity in the brain.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
citation:
ama: Laukoter S. Role of genomic imprinting in cerebral cortex development. 2018:1-139.
doi:10.15479/AT:ISTA:th1057
apa: Laukoter, S. (2018). Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1057
chicago: Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.”
Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1057.
ieee: S. Laukoter, “Role of genomic imprinting in cerebral cortex development,”
Institute of Science and Technology Austria, 2018.
ista: Laukoter S. 2018. Role of genomic imprinting in cerebral cortex development.
Institute of Science and Technology Austria.
mla: Laukoter, Susanne. Role of Genomic Imprinting in Cerebral Cortex Development.
Institute of Science and Technology Austria, 2018, pp. 1–139, doi:10.15479/AT:ISTA:th1057.
short: S. Laukoter, Role of Genomic Imprinting in Cerebral Cortex Development, Institute
of Science and Technology Austria, 2018.
corr_author: '1'
date_created: 2018-12-11T11:44:08Z
date_published: 2018-11-21T00:00:00Z
date_updated: 2026-07-29T13:40:27Z
day: '21'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
- _id: GradSch
doi: 10.15479/AT:ISTA:th1057
doi_confirm: '1'
file:
- access_level: closed
checksum: 41fdbf5fdce312802935d88a8ad9932c
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2019-11-23T23:30:03Z
embargo_to: open_access
file_id: '6396'
file_name: Thesis_LaukoterSusanne_FINAL.docx
file_size: 17949175
relation: source_file
- access_level: open_access
checksum: 53001a9a0c9e570e598d861bb0af28aa
content_type: application/pdf
creator: dernst
date_created: 2019-05-10T07:47:04Z
date_updated: 2021-02-11T11:17:16Z
embargo: 2019-11-21
file_id: '6397'
file_name: Thesis_LaukoterSusanne_FINAL.pdf
file_size: 21187245
relation: main_file
file_date_updated: 2021-02-11T11:17:16Z
fulldoi: https://doi.org/10.15479/AT:ISTA:th1057
has_accepted_license: '1'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 1 - 139
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '8046'
pubrep_id: '1057'
status: public
supervisor:
- first_name: Beatriz
full_name: Vicoso, Beatriz
id: 49E1C5C6-F248-11E8-B48F-1D18A9856A87
last_name: Vicoso
orcid: 0000-0002-4579-8306
title: Role of genomic imprinting in cerebral cortex development
type: dissertation
user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9
year: '2018'
...
---
_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.
corr_author: '1'
date_created: 2018-12-11T11:47:32Z
date_published: 2017-12-01T00:00:00Z
date_updated: 2025-09-11T07:31:36Z
day: '01'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1002/1873-3468.12906
ec_funded: 1
external_id:
isi:
- '000418825700004'
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
fulldoi: https://doi.org/10.1002/1873-3468.12906
has_accepted_license: '1'
intvolume: ' 591'
isi: 1
issue: '24'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
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:
- 0014-5793
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 591
year: '2017'
...
---
_id: '1016'
abstract:
- lang: eng
text: The integrity and dynamic properties of the microtubule cytoskeleton are indispensable
for the development of the mammalian brain. Consequently, mutations in the genes
that encode the structural component (the α/β-tubulin heterodimer) can give rise
to severe, sporadic neurodevelopmental disorders. These are commonly referred
to as the tubulinopathies. Here we report the addition of recessive quadrupedalism,
also known as Uner Tan syndrome (UTS), to the growing list of diseases caused
by tubulin variants. Analysis of a consanguineous UTS family identified a biallelic
TUBB2B mutation, resulting in a p.R390Q amino acid substitution. In addition to
the identifying quadrupedal locomotion, all three patients showed severe cerebellar
hypoplasia. None, however, displayed the basal ganglia malformations typically
associated with TUBB2B mutations. Functional analysis of the R390Q substitution
revealed that it did not affect the ability of β-tubulin to fold or become assembled
into the α/β-heterodimer, nor did it influence the incorporation of mutant-containing
heterodimers into microtubule polymers. The 390Q mutation in S. cerevisiae TUB2
did not affect growth under basal conditions, but did result in increased sensitivity
to microtubule-depolymerizing drugs, indicative of a mild impact of this mutation
on microtubule function. The TUBB2B mutation described here represents an unusual
recessive mode of inheritance for missense-mediated tubulinopathies and reinforces
the sensitivity of the developing cerebellum to microtubule defects.
article_processing_charge: No
author:
- first_name: Martin
full_name: Breuss, Martin
last_name: Breuss
- first_name: Thai
full_name: Nguyen, Thai
last_name: Nguyen
- first_name: Anjana
full_name: Srivatsan, Anjana
last_name: Srivatsan
- first_name: Ines
full_name: Leca, Ines
last_name: Leca
- first_name: Guoling
full_name: Tian, Guoling
last_name: Tian
- first_name: Tanja
full_name: Fritz, Tanja
last_name: Fritz
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Damir
full_name: Musaev, Damir
last_name: Musaev
- first_name: Jennifer
full_name: Mcevoy Venneri, Jennifer
last_name: Mcevoy Venneri
- first_name: James
full_name: Kiely, James
last_name: Kiely
- first_name: Rasim
full_name: Rosti, Rasim
last_name: Rosti
- first_name: Eric
full_name: Scott, Eric
last_name: Scott
- first_name: Uner
full_name: Tan, Uner
last_name: Tan
- first_name: Richard
full_name: Kolodner, Richard
last_name: Kolodner
- first_name: Nicholas
full_name: Cowan, Nicholas
last_name: Cowan
- first_name: David
full_name: Keays, David
last_name: Keays
- first_name: Joseph
full_name: Gleeson, Joseph
last_name: Gleeson
citation:
ama: Breuss M, Nguyen T, Srivatsan A, et al. Uner Tan syndrome caused by a homozygous
TUBB2B mutation affecting microtubule stability. Human Molecular Genetics.
2017;26(2):258-269. doi:10.1093/hmg/ddw383
apa: Breuss, M., Nguyen, T., Srivatsan, A., Leca, I., Tian, G., Fritz, T., … Gleeson,
J. (2017). Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting
microtubule stability. Human Molecular Genetics. Oxford University Press.
https://doi.org/10.1093/hmg/ddw383
chicago: Breuss, Martin, Thai Nguyen, Anjana Srivatsan, Ines Leca, Guoling Tian,
Tanja Fritz, Andi H Hansen, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B
Mutation Affecting Microtubule Stability.” Human Molecular Genetics. Oxford
University Press, 2017. https://doi.org/10.1093/hmg/ddw383.
ieee: M. Breuss et al., “Uner Tan syndrome caused by a homozygous TUBB2B
mutation affecting microtubule stability,” Human Molecular Genetics, vol.
26, no. 2. Oxford University Press, pp. 258–269, 2017.
ista: Breuss M, Nguyen T, Srivatsan A, Leca I, Tian G, Fritz T, Hansen AH, Musaev
D, Mcevoy Venneri J, Kiely J, Rosti R, Scott E, Tan U, Kolodner R, Cowan N, Keays
D, Gleeson J. 2017. Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting
microtubule stability. Human Molecular Genetics. 26(2), 258–269.
mla: Breuss, Martin, et al. “Uner Tan Syndrome Caused by a Homozygous TUBB2B Mutation
Affecting Microtubule Stability.” Human Molecular Genetics, vol. 26, no.
2, Oxford University Press, 2017, pp. 258–69, doi:10.1093/hmg/ddw383.
short: M. Breuss, T. Nguyen, A. Srivatsan, I. Leca, G. Tian, T. Fritz, A.H. Hansen,
D. Musaev, J. Mcevoy Venneri, J. Kiely, R. Rosti, E. Scott, U. Tan, R. Kolodner,
N. Cowan, D. Keays, J. Gleeson, Human Molecular Genetics 26 (2017) 258–269.
date_created: 2018-12-11T11:49:42Z
date_published: 2017-01-01T00:00:00Z
date_updated: 2026-04-16T09:56:51Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/hmg/ddw383
external_id:
isi:
- '000397066400002'
fulldoi: https://doi.org/10.1093/hmg/ddw383
intvolume: ' 26'
isi: 1
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 258 - 269
publication: Human Molecular Genetics
publication_identifier:
issn:
- 0964-6906
publication_status: published
publisher: Oxford University Press
publist_id: '6379'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Uner Tan syndrome caused by a homozygous TUBB2B mutation affecting microtubule
stability
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 26
year: '2017'
...
---
_id: '1017'
abstract:
- lang: eng
text: The development of the vertebrate central nervous system is reliant on a complex
cascade of biological processes that include mitotic division, relocation of migrating
neurons, and the extension of dendritic and axonal processes. Each of these cellular
events requires the diverse functional repertoire of the microtubule cytoskeleton
for the generation of forces, assembly of macromolecular complexes and transport
of molecules and organelles. The tubulins are a multi-gene family that encode
for the constituents of microtubules, and have been implicated in a spectrum of
neurological disorders. Evidence is building that different tubulins tune the
functional properties of the microtubule cytoskeleton dependent on the cell type,
developmental profile and subcellular localisation. Here we review of the origins
of the functional specification of the tubulin gene family in the developing brain
at a transcriptional, translational, and post-transcriptional level. We remind
the reader that tubulins are not just loading controls for your average Western
blot.
article_processing_charge: No
author:
- first_name: Martin
full_name: Breuss, Martin
last_name: Breuss
- first_name: Ines
full_name: Leca, Ines
last_name: Leca
- first_name: Thomas
full_name: Gstrein, Thomas
last_name: Gstrein
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: David
full_name: Keays, David
last_name: Keays
citation:
ama: 'Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. Tubulins and brain development:
The origins of functional specification. Molecular and Cellular Neuroscience.
2017;84:58-67. doi:10.1016/j.mcn.2017.03.002'
apa: 'Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., & Keays, D. (2017).
Tubulins and brain development: The origins of functional specification. Molecular
and Cellular Neuroscience. Academic Press. https://doi.org/10.1016/j.mcn.2017.03.002'
chicago: 'Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays.
“Tubulins and Brain Development: The Origins of Functional Specification.” Molecular
and Cellular Neuroscience. Academic Press, 2017. https://doi.org/10.1016/j.mcn.2017.03.002.'
ieee: 'M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and
brain development: The origins of functional specification,” Molecular and
Cellular Neuroscience, vol. 84. Academic Press, pp. 58–67, 2017.'
ista: 'Breuss M, Leca I, Gstrein T, Hansen AH, Keays D. 2017. Tubulins and brain
development: The origins of functional specification. Molecular and Cellular Neuroscience.
84, 58–67.'
mla: 'Breuss, Martin, et al. “Tubulins and Brain Development: The Origins of Functional
Specification.” Molecular and Cellular Neuroscience, vol. 84, Academic
Press, 2017, pp. 58–67, doi:10.1016/j.mcn.2017.03.002.'
short: M. Breuss, I. Leca, T. Gstrein, A.H. Hansen, D. Keays, Molecular and Cellular
Neuroscience 84 (2017) 58–67.
date_created: 2018-12-11T11:49:42Z
date_published: 2017-10-01T00:00:00Z
date_updated: 2025-07-10T11:49:44Z
day: '01'
ddc:
- '571'
department:
- _id: SiHi
doi: 10.1016/j.mcn.2017.03.002
external_id:
isi:
- '000415140700007'
file:
- access_level: open_access
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:19Z
date_updated: 2018-12-12T10:09:19Z
file_id: '4742'
file_name: IST-2017-806-v1+2_1-s2.0-S1044743116302500-main_1_.pdf
file_size: 1436377
relation: main_file
file_date_updated: 2018-12-12T10:09:19Z
fulldoi: https://doi.org/10.1016/j.mcn.2017.03.002
has_accepted_license: '1'
intvolume: ' 84'
isi: 1
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-nd/4.0/
month: '10'
oa: 1
oa_version: Published Version
page: 58 - 67
publication: Molecular and Cellular Neuroscience
publication_identifier:
issn:
- 1044-7431
publication_status: published
publisher: Academic Press
publist_id: '6377'
pubrep_id: '806'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Tubulins and brain development: The origins of functional specification'
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: 84
year: '2017'
...
---
_id: '805'
abstract:
- lang: eng
text: During corticogenesis, distinct classes of neurons are born from progenitor
cells located in the ventricular and subventricular zones, from where they migrate
towards the pial surface to assemble into highly organized layer-specific circuits.
However, the precise and coordinated transcriptional network activity defining
neuronal identity is still not understood. Here, we show that genetic depletion
of the basic helix-loop-helix (bHLH) transcription factor E2A splice variant E47
increased the number of Tbr1-positive deep layer and Satb2-positive upper layer
neurons at E14.5, while depletion of the alternatively spliced E12 variant did
not affect layer-specific neurogenesis. While ChIP-Seq identified a big overlap
for E12- and E47-specific binding sites in embryonic NSCs, including sites at
the cyclin-dependent kinase inhibitor (CDKI) Cdkn1c gene locus, RNA-Seq revealed
a unique transcriptional regulation by each splice variant. E47 activated the
expression of the CDKI Cdkn1c through binding to a distal enhancer. Finally, overexpression
of E47 in embryonic NSCs in vitro impaired neurite outgrowth and E47 overexpression
in vivo by in utero electroporation disturbed proper layer-specific neurogenesis
and upregulated p57(KIP2) expression. Overall, this study identified E2A target
genes in embryonic NSCs and demonstrates that E47 regulates neuronal differentiation
via p57(KIP2).
article_processing_charge: No
author:
- first_name: Sabrina
full_name: Pfurr, Sabrina
last_name: Pfurr
- first_name: Yu
full_name: Chu, Yu
last_name: Chu
- first_name: Christian
full_name: Bohrer, Christian
last_name: Bohrer
- first_name: Franziska
full_name: Greulich, Franziska
last_name: Greulich
- 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: Könül
full_name: Mammadzada, Könül
last_name: Mammadzada
- first_name: Miriam
full_name: Hils, Miriam
last_name: Hils
- first_name: Sebastian
full_name: Arnold, Sebastian
last_name: Arnold
- first_name: Verdon
full_name: Taylor, Verdon
last_name: Taylor
- first_name: Kristina
full_name: Schachtrup, Kristina
last_name: Schachtrup
- first_name: N Henriette
full_name: Uhlenhaut, N Henriette
last_name: Uhlenhaut
- first_name: Christian
full_name: Schachtrup, Christian
last_name: Schachtrup
citation:
ama: Pfurr S, Chu Y, Bohrer C, et al. The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development. Development.
2017;144:3917-3931. doi:10.1242/dev.145698
apa: Pfurr, S., Chu, Y., Bohrer, C., Greulich, F., Beattie, R. J., Mammadzada, K.,
… Schachtrup, C. (2017). The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development. Development.
Company of Biologists. https://doi.org/10.1242/dev.145698
chicago: Pfurr, Sabrina, Yu Chu, Christian Bohrer, Franziska Greulich, Robert J
Beattie, Könül Mammadzada, Miriam Hils, et al. “The E2A Splice Variant E47 Regulates
the Differentiation of Projection Neurons via P57(KIP2) during Cortical Development.”
Development. Company of Biologists, 2017. https://doi.org/10.1242/dev.145698.
ieee: S. Pfurr et al., “The E2A splice variant E47 regulates the differentiation
of projection neurons via p57(KIP2) during cortical development,” Development,
vol. 144. Company of Biologists, pp. 3917–3931, 2017.
ista: Pfurr S, Chu Y, Bohrer C, Greulich F, Beattie RJ, Mammadzada K, Hils M, Arnold
S, Taylor V, Schachtrup K, Uhlenhaut NH, Schachtrup C. 2017. The E2A splice variant
E47 regulates the differentiation of projection neurons via p57(KIP2) during cortical
development. Development. 144, 3917–3931.
mla: Pfurr, Sabrina, et al. “The E2A Splice Variant E47 Regulates the Differentiation
of Projection Neurons via P57(KIP2) during Cortical Development.” Development,
vol. 144, Company of Biologists, 2017, pp. 3917–31, doi:10.1242/dev.145698.
short: S. Pfurr, Y. Chu, C. Bohrer, F. Greulich, R.J. Beattie, K. Mammadzada, M.
Hils, S. Arnold, V. Taylor, K. Schachtrup, N.H. Uhlenhaut, C. Schachtrup, Development
144 (2017) 3917–3931.
date_created: 2018-12-11T11:48:36Z
date_published: 2017-10-31T00:00:00Z
date_updated: 2023-09-26T16:20:09Z
day: '31'
department:
- _id: SiHi
doi: 10.1242/dev.145698
external_id:
isi:
- '000414025600007'
fulldoi: https://doi.org/10.1242/dev.145698
intvolume: ' 144'
isi: 1
language:
- iso: eng
month: '10'
oa_version: None
page: 3917 - 3931
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '6846'
quality_controlled: '1'
scopus_import: '1'
status: public
title: The E2A splice variant E47 regulates the differentiation of projection neurons
via p57(KIP2) during cortical development
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 144
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.
corr_author: '1'
date_created: 2018-12-11T11:49:20Z
date_published: 2017-05-03T00:00:00Z
date_updated: 2026-04-16T09:57:27Z
day: '03'
department:
- _id: SiHi
- _id: MaJö
doi: 10.1016/j.neuron.2017.04.012
ec_funded: 1
external_id:
isi:
- '000400466700011'
fulldoi: https://doi.org/10.1016/j.neuron.2017.04.012
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:
- 0896-6273
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 94
year: '2017'
...
---
_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
fulldoi: https://doi.org/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: '713'
abstract:
- lang: eng
text: To determine the dynamics of allelic-specific expression during mouse development,
we analyzed RNA-seq data from 23 F1 tissues from different developmental stages,
including 19 female tissues allowing X chromosome inactivation (XCI) escapers
to also be detected. We demonstrate that allelic expression arising from genetic
or epigenetic differences is highly tissue-specific. We find that tissue-specific
strain-biased gene expression may be regulated by tissue-specific enhancers or
by post-transcriptional differences in stability between the alleles. We also
find that escape from X-inactivation is tissue-specific, with leg muscle showing
an unexpectedly high rate of XCI escapers. By surveying a range of tissues during
development, and performing extensive validation, we are able to provide a high
confidence list of mouse imprinted genes including 18 novel genes. This shows
that cluster size varies dynamically during development and can be substantially
larger than previously thought, with the Igf2r cluster extending over 10 Mb in
placenta.
article_number: e25125
article_processing_charge: No
author:
- first_name: Daniel
full_name: Andergassen, Daniel
last_name: Andergassen
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Dyniel
full_name: Wenzel, Dyniel
last_name: Wenzel
- first_name: Verena
full_name: Sigl, Verena
last_name: Sigl
- first_name: Philipp
full_name: Bammer, Philipp
last_name: Bammer
- first_name: Markus
full_name: Muckenhuber, Markus
last_name: Muckenhuber
- first_name: Daniela
full_name: Mayer, Daniela
last_name: Mayer
- first_name: Tomasz
full_name: Kulinski, Tomasz
last_name: Kulinski
- first_name: Hans
full_name: Theussl, Hans
last_name: Theussl
- first_name: Josef
full_name: Penninger, Josef
last_name: Penninger
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Denise
full_name: Barlow, Denise
last_name: Barlow
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Quanah
full_name: Hudson, Quanah
last_name: Hudson
citation:
ama: Andergassen D, Dotter C, Wenzel D, et al. Mapping the mouse Allelome reveals
tissue specific regulation of allelic expression. eLife. 2017;6. doi:10.7554/eLife.25125
apa: Andergassen, D., Dotter, C., Wenzel, D., Sigl, V., Bammer, P., Muckenhuber,
M., … Hudson, Q. (2017). Mapping the mouse Allelome reveals tissue specific regulation
of allelic expression. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.25125
chicago: Andergassen, Daniel, Christoph Dotter, Dyniel Wenzel, Verena Sigl, Philipp
Bammer, Markus Muckenhuber, Daniela Mayer, et al. “Mapping the Mouse Allelome
Reveals Tissue Specific Regulation of Allelic Expression.” ELife. eLife
Sciences Publications, 2017. https://doi.org/10.7554/eLife.25125.
ieee: D. Andergassen et al., “Mapping the mouse Allelome reveals tissue specific
regulation of allelic expression,” eLife, vol. 6. eLife Sciences Publications,
2017.
ista: Andergassen D, Dotter C, Wenzel D, Sigl V, Bammer P, Muckenhuber M, Mayer
D, Kulinski T, Theussl H, Penninger J, Bock C, Barlow D, Pauler F, Hudson Q. 2017.
Mapping the mouse Allelome reveals tissue specific regulation of allelic expression.
eLife. 6, e25125.
mla: Andergassen, Daniel, et al. “Mapping the Mouse Allelome Reveals Tissue Specific
Regulation of Allelic Expression.” ELife, vol. 6, e25125, eLife Sciences
Publications, 2017, doi:10.7554/eLife.25125.
short: D. Andergassen, C. Dotter, D. Wenzel, V. Sigl, P. Bammer, M. Muckenhuber,
D. Mayer, T. Kulinski, H. Theussl, J. Penninger, C. Bock, D. Barlow, F. Pauler,
Q. Hudson, ELife 6 (2017).
corr_author: '1'
date_created: 2018-12-11T11:48:05Z
date_published: 2017-08-14T00:00:00Z
date_updated: 2025-09-10T11:02:33Z
day: '14'
ddc:
- '576'
department:
- _id: GaNo
- _id: SiHi
doi: 10.7554/eLife.25125
external_id:
isi:
- '000407617200001'
file:
- access_level: open_access
checksum: 1ace3462e64a971b9ead896091829549
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:36Z
date_updated: 2020-07-14T12:47:50Z
file_id: '5020'
file_name: IST-2017-885-v1+1_elife-25125-figures-v2.pdf
file_size: 6399510
relation: main_file
- access_level: open_access
checksum: 6241dc31eeb87b03facadec3a53a6827
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:36Z
date_updated: 2020-07-14T12:47:50Z
file_id: '5021'
file_name: IST-2017-885-v1+2_elife-25125-v2.pdf
file_size: 4264398
relation: main_file
file_date_updated: 2020-07-14T12:47:50Z
fulldoi: https://doi.org/10.7554/eLife.25125
has_accepted_license: '1'
intvolume: ' 6'
isi: 1
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
project:
- _id: 25E9AF9E-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P27201-B22
name: Revealing the mechanisms underlying drug interactions
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
publist_id: '6971'
pubrep_id: '885'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mapping the mouse Allelome reveals tissue specific regulation of allelic expression
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 6
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: 2026-11-11T23:30:56Z
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
fulldoi: https://doi.org/10.3389/fncel.2017.00176
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:
- 1662-5102
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: 2DF688A6-F248-11E8-B48F-1D18A9856A87
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.
article_processing_charge: No
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: 2025-09-22T09:48:17Z
day: '09'
department:
- _id: SiHi
doi: 10.1523/JNEUROSCI.2359-16.2016
external_id:
isi:
- '000391054300003'
fulldoi: https://doi.org/10.1523/JNEUROSCI.2359-16.2016
intvolume: ' 36'
isi: 1
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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
article_processing_charge: No
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: 2025-09-18T11:28:32Z
day: '19'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pbio.1002382
external_id:
isi:
- '000371883600013'
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
fulldoi: https://doi.org/10.1371/journal.pbio.1002382
has_accepted_license: '1'
intvolume: ' 14'
isi: 1
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
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"
article_processing_charge: No
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: 2025-09-23T08:16:35Z
day: '02'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2015.07.011
external_id:
isi:
- '000361146300009'
pmid:
- '26299473'
fulldoi: https://doi.org/10.1016/j.neuron.2015.07.011
intvolume: ' 87'
isi: 1
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: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 87
year: '2015'
...
---
_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
article_processing_charge: No
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).
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