---
_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
has_accepted_license: '1'
intvolume: ' 591'
isi: 1
issue: '24'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 3993 - 4008
pmid: 1
project:
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: FEBS letters
publication_identifier:
issn:
- 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: '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
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: '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'
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: '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'
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: '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: 2026-04-27T22:30:40Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
- _id: MaLo
doi: 10.3389/fncel.2017.00176
ec_funded: 1
external_id:
isi:
- '000404486700001'
file:
- access_level: open_access
checksum: dc1f5a475b918d09a0f9f587400b1626
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:40Z
date_updated: 2020-07-14T12:48:16Z
file_id: '4764'
file_name: IST-2017-830-v1+1_2017_Hansen_CellPolarity.pdf
file_size: 2153858
relation: main_file
file_date_updated: 2020-07-14T12:48:16Z
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25681D80-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '291734'
name: International IST Postdoc Fellowship Programme
- _id: 25985A36-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T00817-B21
name: The biochemical basis of PAR polarization
publication: Frontiers in Cellular Neuroscience
publication_identifier:
issn:
- 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'
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
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'
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: '2020'
abstract:
- lang: eng
text: The mammalian heart has long been considered a postmitotic organ, implying
that the total number of cardiomyocytes is set at birth. Analysis of cell division
in the mammalian heart is complicated by cardiomyocyte binucleation shortly after
birth, which makes it challenging to interpret traditional assays of cell turnover
[Laflamme MA, Murray CE (2011) Nature 473(7347):326–335; Bergmann O, et al. (2009)
Science 324(5923):98–102]. An elegant multi-isotope imaging-mass spectrometry
technique recently calculated the low, discrete rate of cardiomyocyte generation
in mice [Senyo SE, et al. (2013) Nature 493(7432):433–436], yet our cellular-level
understanding of postnatal cardiomyogenesis remains limited. Herein, we provide
a new line of evidence for the differentiated α-myosin heavy chain-expressing
cardiomyocyte as the cell of origin of postnatal cardiomyogenesis using the “mosaic
analysis with double markers” mouse model. We show limited, life-long, symmetric
division of cardiomyocytes as a rare event that is evident in utero but significantly
diminishes after the first month of life in mice; daughter cardiomyocytes divide
very seldom, which this study is the first to demonstrate, to our knowledge. Furthermore,
ligation of the left anterior descending coronary artery, which causes a myocardial
infarction in the mosaic analysis with double-marker mice, did not increase the
rate of cardiomyocyte division above the basal level for up to 4 wk after the
injury. The clonal analysis described here provides direct evidence of postnatal
mammalian cardiomyogenesis.
article_processing_charge: No
author:
- first_name: Shah
full_name: Ali, Shah
last_name: Ali
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Lily
full_name: Saadat, Lily
last_name: Saadat
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Irving
full_name: Weissman, Irving
last_name: Weissman
- first_name: Reza
full_name: Ardehali, Reza
last_name: Ardehali
citation:
ama: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. Existing cardiomyocytes
generate cardiomyocytes at a low rate after birth in mice. PNAS. 2014;111(24):8850-8855.
doi:10.1073/pnas.1408233111
apa: Ali, S., Hippenmeyer, S., Saadat, L., Luo, L., Weissman, I., & Ardehali,
R. (2014). Existing cardiomyocytes generate cardiomyocytes at a low rate after
birth in mice. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1408233111
chicago: Ali, Shah, Simon Hippenmeyer, Lily Saadat, Liqun Luo, Irving Weissman,
and Reza Ardehali. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low Rate
after Birth in Mice.” PNAS. National Academy of Sciences, 2014. https://doi.org/10.1073/pnas.1408233111.
ieee: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, and R. Ardehali, “Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice,” PNAS,
vol. 111, no. 24. National Academy of Sciences, pp. 8850–8855, 2014.
ista: Ali S, Hippenmeyer S, Saadat L, Luo L, Weissman I, Ardehali R. 2014. Existing
cardiomyocytes generate cardiomyocytes at a low rate after birth in mice. PNAS.
111(24), 8850–8855.
mla: Ali, Shah, et al. “Existing Cardiomyocytes Generate Cardiomyocytes at a Low
Rate after Birth in Mice.” PNAS, vol. 111, no. 24, National Academy of
Sciences, 2014, pp. 8850–55, doi:10.1073/pnas.1408233111.
short: S. Ali, S. Hippenmeyer, L. Saadat, L. Luo, I. Weissman, R. Ardehali, PNAS
111 (2014) 8850–8855.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-06-17T00:00:00Z
date_updated: 2025-09-29T11:59:35Z
day: '17'
department:
- _id: SiHi
doi: 10.1073/pnas.1408233111
external_id:
isi:
- '000337300100041'
intvolume: ' 111'
isi: 1
issue: '24'
language:
- iso: eng
month: '06'
oa_version: None
page: 8850 - 8855
publication: PNAS
publication_status: published
publisher: National Academy of Sciences
publist_id: '5052'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Existing cardiomyocytes generate cardiomyocytes at a low rate after birth in
mice
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 111
year: '2014'
...
---
_id: '2021'
abstract:
- lang: eng
text: Neurotrophins regulate diverse aspects of neuronal development and plasticity,
but their precise in vivo functions during neural circuit assembly in the central
brain remain unclear. We show that the neurotrophin receptor tropomyosin-related
kinase C (TrkC) is required for dendritic growth and branching of mouse cerebellar
Purkinje cells. Sparse TrkC knockout reduced dendrite complexity, but global Purkinje
cell knockout had no effect. Removal of the TrkC ligand neurotrophin-3 (NT-3)
from cerebellar granule cells, which provide major afferent input to developing
Purkinje cell dendrites, rescued the dendrite defects caused by sparse TrkC disruption
in Purkinje cells. Our data demonstrate that NT-3 from presynaptic neurons (granule
cells) is required for TrkC-dependent competitive dendrite morphogenesis in postsynaptic
neurons (Purkinje cells)—a previously unknown mechanism of neural circuit development.
article_processing_charge: No
author:
- first_name: Joo
full_name: William, Joo
last_name: William
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: William J, Hippenmeyer S, Luo L. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 2014;346(6209):626-629. doi:10.1126/science.1258996
apa: William, J., Hippenmeyer, S., & Luo, L. (2014). Dendrite morphogenesis
depends on relative levels of NT-3/TrkC signaling. Science. American Association
for the Advancement of Science. https://doi.org/10.1126/science.1258996
chicago: William, Joo, Simon Hippenmeyer, and Liqun Luo. “Dendrite Morphogenesis
Depends on Relative Levels of NT-3/TrkC Signaling.” Science. American Association
for the Advancement of Science, 2014. https://doi.org/10.1126/science.1258996.
ieee: J. William, S. Hippenmeyer, and L. Luo, “Dendrite morphogenesis depends on
relative levels of NT-3/TrkC signaling,” Science, vol. 346, no. 6209. American
Association for the Advancement of Science, pp. 626–629, 2014.
ista: William J, Hippenmeyer S, Luo L. 2014. Dendrite morphogenesis depends on relative
levels of NT-3/TrkC signaling. Science. 346(6209), 626–629.
mla: William, Joo, et al. “Dendrite Morphogenesis Depends on Relative Levels of
NT-3/TrkC Signaling.” Science, vol. 346, no. 6209, American Association
for the Advancement of Science, 2014, pp. 626–29, doi:10.1126/science.1258996.
short: J. William, S. Hippenmeyer, L. Luo, Science 346 (2014) 626–629.
date_created: 2018-12-11T11:55:15Z
date_published: 2014-10-31T00:00:00Z
date_updated: 2025-09-29T11:59:07Z
day: '31'
department:
- _id: SiHi
doi: 10.1126/science.1258996
external_id:
isi:
- '000343799700047'
intvolume: ' 346'
isi: 1
issue: '6209'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4631524/
month: '10'
oa: 1
oa_version: Submitted Version
page: 626 - 629
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
publist_id: '5051'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Dendrite morphogenesis depends on relative levels of NT-3/TrkC signaling
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 346
year: '2014'
...
---
_id: '2022'
abstract:
- lang: eng
text: Radial glial progenitors (RGPs) are responsible for producing nearly all neocortical
neurons. To gain insight into the patterns of RGP division and neuron production,
we quantitatively analyzed excitatory neuron genesis in the mouse neocortex using
Mosaic Analysis with Double Markers, which provides single-cell resolution of
progenitor division patterns and potential in vivo. We found that RGPs progress
through a coherent program in which their proliferative potential diminishes in
a predictable manner. Upon entry into the neurogenic phase, individual RGPs produce
∼8–9 neurons distributed in both deep and superficial layers, indicating a unitary
output in neuronal production. Removal of OTX1, a transcription factor transiently
expressed in RGPs, results in both deep- and superficial-layer neuron loss and
a reduction in neuronal unit size. Moreover, ∼1/6 of neurogenic RGPs proceed to
produce glia. These results suggest that progenitor behavior and histogenesis
in the mammalian neocortex conform to a remarkably orderly and deterministic program.
article_processing_charge: No
author:
- first_name: Peng
full_name: Gao, Peng
last_name: Gao
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Teresa
full_name: Krieger, Teresa
last_name: Krieger
- first_name: Luisirene
full_name: Hernandez, Luisirene
last_name: Hernandez
- first_name: Chao
full_name: Wang, Chao
last_name: Wang
- first_name: Zhi
full_name: Han, Zhi
last_name: Han
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Ekaterina
full_name: Papusheva, Ekaterina
id: 41DB591E-F248-11E8-B48F-1D18A9856A87
last_name: Papusheva
- first_name: Ryan
full_name: Insolera, Ryan
last_name: Insolera
- first_name: Kritika
full_name: Chugh, Kritika
last_name: Chugh
- first_name: Oren
full_name: Kodish, Oren
last_name: Kodish
- first_name: Kun
full_name: Huang, Kun
last_name: Huang
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Song
full_name: Shi, Song
last_name: Shi
citation:
ama: Gao P, Postiglione MP, Krieger T, et al. Deterministic progenitor behavior
and unitary production of neurons in the neocortex. Cell. 2014;159(4):775-788.
doi:10.1016/j.cell.2014.10.027
apa: Gao, P., Postiglione, M. P., Krieger, T., Hernandez, L., Wang, C., Han, Z.,
… Shi, S. (2014). Deterministic progenitor behavior and unitary production of
neurons in the neocortex. Cell. Cell Press. https://doi.org/10.1016/j.cell.2014.10.027
chicago: Gao, Peng, Maria P Postiglione, Teresa Krieger, Luisirene Hernandez, Chao
Wang, Zhi Han, Carmen Streicher, et al. “Deterministic Progenitor Behavior and
Unitary Production of Neurons in the Neocortex.” Cell. Cell Press, 2014.
https://doi.org/10.1016/j.cell.2014.10.027.
ieee: P. Gao et al., “Deterministic progenitor behavior and unitary production
of neurons in the neocortex,” Cell, vol. 159, no. 4. Cell Press, pp. 775–788,
2014.
ista: Gao P, Postiglione MP, Krieger T, Hernandez L, Wang C, Han Z, Streicher C,
Papusheva E, Insolera R, Chugh K, Kodish O, Huang K, Simons B, Luo L, Hippenmeyer
S, Shi S. 2014. Deterministic progenitor behavior and unitary production of neurons
in the neocortex. Cell. 159(4), 775–788.
mla: Gao, Peng, et al. “Deterministic Progenitor Behavior and Unitary Production
of Neurons in the Neocortex.” Cell, vol. 159, no. 4, Cell Press, 2014,
pp. 775–88, doi:10.1016/j.cell.2014.10.027.
short: P. Gao, M.P. Postiglione, T. Krieger, L. Hernandez, C. Wang, Z. Han, C. Streicher,
E. Papusheva, R. Insolera, K. Chugh, O. Kodish, K. Huang, B. Simons, L. Luo, S.
Hippenmeyer, S. Shi, Cell 159 (2014) 775–788.
corr_author: '1'
date_created: 2018-12-11T11:55:16Z
date_published: 2014-11-06T00:00:00Z
date_updated: 2025-09-29T11:57:49Z
day: '06'
ddc:
- '570'
department:
- _id: SiHi
- _id: Bio
doi: 10.1016/j.cell.2014.10.027
ec_funded: 1
external_id:
isi:
- '000344522000011'
file:
- access_level: open_access
checksum: 6c5de8329bb2ffa71cba9fda750f14ce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:08:47Z
date_updated: 2020-07-14T12:45:25Z
file_id: '4709'
file_name: IST-2016-423-v1+1_1-s2.0-S0092867414013154-main.pdf
file_size: 4435787
relation: main_file
file_date_updated: 2020-07-14T12:45:25Z
has_accepted_license: '1'
intvolume: ' 159'
isi: 1
issue: '4'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
page: 775 - 788
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5050'
pubrep_id: '423'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Deterministic progenitor behavior and unitary production of neurons in the
neocortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 159
year: '2014'
...
---
_id: '1899'
abstract:
- lang: eng
text: Asymmetric cell divisions allow stem cells to balance proliferation and differentiation.
During embryogenesis, murine epidermis expands rapidly from a single layer of
unspecified basal layer progenitors to a stratified, differentiated epithelium.
Morphogenesis involves perpendicular (asymmetric) divisions and the spindle orientation
protein LGN, but little is known about how the apical localization of LGN is regulated.
Here, we combine conventional genetics and lentiviral-mediated in vivo RNAi to
explore the functions of the LGN-interacting proteins Par3, mInsc and Gα i3. Whereas
loss of each gene alone leads to randomized division angles, combined loss of
Gnai3 and mInsc causes a phenotype of mostly planar divisions, akin to loss of
LGN. These findings lend experimental support for the hitherto untested model
that Par3-mInsc and Gα i3 act cooperatively to polarize LGN and promote perpendicular
divisions. Finally, we uncover a developmental switch between delamination-driven
early stratification and spindle-orientation-dependent differentiation that occurs
around E15, revealing a two-step mechanism underlying epidermal maturation.
article_processing_charge: No
article_type: original
author:
- first_name: Scott
full_name: Williams, Scott
last_name: Williams
- first_name: Lyndsay
full_name: Ratliff, Lyndsay
last_name: Ratliff
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Juergen
full_name: Knoblich, Juergen
last_name: Knoblich
- first_name: Elaine
full_name: Fuchs, Elaine
last_name: Fuchs
citation:
ama: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. Par3-mInsc and
Gα i3 cooperate to promote oriented epidermal cell divisions through LGN. Nature
Cell Biology. 2014;16(8):758-769. doi:10.1038/ncb3001
apa: Williams, S., Ratliff, L., Postiglione, M. P., Knoblich, J., & Fuchs, E.
(2014). Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
through LGN. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3001
chicago: Williams, Scott, Lyndsay Ratliff, Maria P Postiglione, Juergen Knoblich,
and Elaine Fuchs. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented Epidermal
Cell Divisions through LGN.” Nature Cell Biology. Nature Publishing Group,
2014. https://doi.org/10.1038/ncb3001.
ieee: S. Williams, L. Ratliff, M. P. Postiglione, J. Knoblich, and E. Fuchs, “Par3-mInsc
and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN,”
Nature Cell Biology, vol. 16, no. 8. Nature Publishing Group, pp. 758–769,
2014.
ista: Williams S, Ratliff L, Postiglione MP, Knoblich J, Fuchs E. 2014. Par3-mInsc
and Gα i3 cooperate to promote oriented epidermal cell divisions through LGN.
Nature Cell Biology. 16(8), 758–769.
mla: Williams, Scott, et al. “Par3-MInsc and Gα I3 Cooperate to Promote Oriented
Epidermal Cell Divisions through LGN.” Nature Cell Biology, vol. 16, no.
8, Nature Publishing Group, 2014, pp. 758–69, doi:10.1038/ncb3001.
short: S. Williams, L. Ratliff, M.P. Postiglione, J. Knoblich, E. Fuchs, Nature
Cell Biology 16 (2014) 758–769.
date_created: 2018-12-11T11:54:36Z
date_published: 2014-07-13T00:00:00Z
date_updated: 2025-09-29T12:32:05Z
day: '13'
department:
- _id: SiHi
doi: 10.1038/ncb3001
external_id:
isi:
- '000339904900008'
pmid:
- '25016959'
intvolume: ' 16'
isi: 1
issue: '8'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4159251/
month: '07'
oa: 1
oa_version: Submitted Version
page: 758 - 769
pmid: 1
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5196'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Par3-mInsc and Gα i3 cooperate to promote oriented epidermal cell divisions
through LGN
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 16
year: '2014'
...
---
_id: '2175'
abstract:
- lang: eng
text: The cerebral cortex, the seat of our cognitive abilities, is composed of an
intricate network of billions of excitatory projection and inhibitory interneurons.
Postmitotic cortical neurons are generated by a diverse set of neural stem cell
progenitors within dedicated zones and defined periods of neurogenesis during
embryonic development. Disruptions in neurogenesis can lead to alterations in
the neuronal cytoarchitecture, which is thought to represent a major underlying
cause for several neurological disorders, including microcephaly, autism and epilepsy.
Although a number of signaling pathways regulating neurogenesis have been described,
the precise cellular and molecular mechanisms regulating the functional neural
stem cell properties in cortical neurogenesis remain unclear. Here, we discuss
the most up-to-date strategies to monitor the fundamental mechanistic parameters
of neuronal progenitor proliferation, and recent advances deciphering the logic
and dynamics of neurogenesis.
article_processing_charge: No
author:
- first_name: Maria P
full_name: Postiglione, Maria P
id: 2C67902A-F248-11E8-B48F-1D18A9856A87
last_name: Postiglione
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Postiglione MP, Hippenmeyer S. Monitoring neurogenesis in the cerebral cortex:
an update. Future Neurology. 2014;9(3):323-340. doi:10.2217/fnl.14.18'
apa: 'Postiglione, M. P., & Hippenmeyer, S. (2014). Monitoring neurogenesis
in the cerebral cortex: an update. Future Neurology. Future Science Group.
https://doi.org/10.2217/fnl.14.18'
chicago: 'Postiglione, Maria P, and Simon Hippenmeyer. “Monitoring Neurogenesis
in the Cerebral Cortex: An Update.” Future Neurology. Future Science Group,
2014. https://doi.org/10.2217/fnl.14.18.'
ieee: 'M. P. Postiglione and S. Hippenmeyer, “Monitoring neurogenesis in the cerebral
cortex: an update,” Future Neurology, vol. 9, no. 3. Future Science Group,
pp. 323–340, 2014.'
ista: 'Postiglione MP, Hippenmeyer S. 2014. Monitoring neurogenesis in the cerebral
cortex: an update. Future Neurology. 9(3), 323–340.'
mla: 'Postiglione, Maria P., and Simon Hippenmeyer. “Monitoring Neurogenesis in
the Cerebral Cortex: An Update.” Future Neurology, vol. 9, no. 3, Future
Science Group, 2014, pp. 323–40, doi:10.2217/fnl.14.18.'
short: M.P. Postiglione, S. Hippenmeyer, Future Neurology 9 (2014) 323–340.
corr_author: '1'
date_created: 2018-12-11T11:56:09Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2025-04-15T07:31:57Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.2217/fnl.14.18
ec_funded: 1
file:
- access_level: open_access
checksum: ba06659ecadabceec9a37dd8c4586dce
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:10:25Z
date_updated: 2020-07-14T12:45:31Z
file_id: '4812'
file_name: IST-2016-528-v1+1_fnl.14.18.pdf
file_size: 3848424
relation: main_file
file_date_updated: 2020-07-14T12:45:31Z
has_accepted_license: '1'
intvolume: ' 9'
issue: '3'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 323 - 340
project:
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Future Neurology
publication_identifier:
eissn:
- 1748-6971
issn:
- 1479-6708
publication_status: published
publisher: Future Science Group
publist_id: '4806'
pubrep_id: '528'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Monitoring neurogenesis in the cerebral cortex: an update'
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2014'
...
---
_id: '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).
date_created: 2018-12-11T11:56:38Z
date_published: 2014-03-05T00:00:00Z
date_updated: 2025-09-29T11:13:18Z
day: '05'
ddc:
- '571'
- '610'
department:
- _id: SiHi
doi: 10.1093/nar/gkt1290
external_id:
isi:
- '000333093600005'
file:
- access_level: open_access
checksum: e9268f5f96a820f04d7ebbf85927c3cb
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:09:15Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4738'
file_name: IST-2018-961-v1+1_2014_Hippenmeyer_DICE.pdf
file_size: 11044478
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 42'
isi: 1
issue: '5'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Preprint
publication: Nucleic Acids Research
publication_status: published
publisher: Oxford University Press
publist_id: '4684'
pubrep_id: '961'
quality_controlled: '1'
scopus_import: '1'
status: public
title: DICE, an efficient system for iterative genomic editing in human pluripotent
stem cells
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 42
year: '2014'
...
---
_id: '2265'
abstract:
- lang: eng
text: Coordinated migration of newly-born neurons to their target territories is
essential for correct neuronal circuit assembly in the developing brain. Although
a cohort of signaling pathways has been implicated in the regulation of cortical
projection neuron migration, the precise molecular mechanisms and how a balanced
interplay of cell-autonomous and non-autonomous functions of candidate signaling
molecules controls the discrete steps in the migration process, are just being
revealed. In this chapter, I will focally review recent advances that improved
our understanding of the cell-autonomous and possible cell-nonautonomous functions
of the evolutionarily conserved LIS1/NDEL1-complex in regulating the sequential
steps of cortical projection neuron migration. I will then elaborate on the emerging
concept that the Reelin signaling pathway, acts exactly at precise stages in the
course of cortical projection neuron migration. Lastly, I will discuss how finely
tuned transcriptional programs and downstream effectors govern particular aspects
in driving radial migration at discrete stages and how they regulate the precise
positioning of cortical projection neurons in the developing cerebral cortex.
alternative_title:
- Advances in Experimental Medicine and Biology
article_processing_charge: No
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: 'Hippenmeyer S. Molecular pathways controlling the sequential steps of cortical
projection neuron migration. In: Nguyen L, ed. Cellular and Molecular Control
of Neuronal Migration. Vol 800. Springer; 2014:1-24. doi:10.1007/978-94-007-7687-6_1'
apa: Hippenmeyer, S. (2014). Molecular pathways controlling the sequential steps
of cortical projection neuron migration. In L. Nguyen (Ed.), Cellular and
Molecular Control of Neuronal Migration (Vol. 800, pp. 1–24). Springer. https://doi.org/10.1007/978-94-007-7687-6_1
chicago: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps
of Cortical Projection Neuron Migration.” In Cellular and Molecular Control
of Neuronal Migration, edited by Laurent Nguyen, 800:1–24. Springer, 2014.
https://doi.org/10.1007/978-94-007-7687-6_1.
ieee: S. Hippenmeyer, “Molecular pathways controlling the sequential steps of cortical
projection neuron migration,” in Cellular and Molecular Control of Neuronal
Migration, vol. 800, L. Nguyen, Ed. Springer, 2014, pp. 1–24.
ista: 'Hippenmeyer S. 2014.Molecular pathways controlling the sequential steps of
cortical projection neuron migration. In: Cellular and Molecular Control of Neuronal
Migration. Advances in Experimental Medicine and Biology, vol. 800, 1–24.'
mla: Hippenmeyer, Simon. “Molecular Pathways Controlling the Sequential Steps of
Cortical Projection Neuron Migration.” Cellular and Molecular Control of Neuronal
Migration, edited by Laurent Nguyen, vol. 800, Springer, 2014, pp. 1–24, doi:10.1007/978-94-007-7687-6_1.
short: S. Hippenmeyer, in:, L. Nguyen (Ed.), Cellular and Molecular Control of
Neuronal Migration, Springer, 2014, pp. 1–24.
corr_author: '1'
date_created: 2018-12-11T11:56:39Z
date_published: 2014-01-01T00:00:00Z
date_updated: 2025-09-29T11:12:48Z
day: '01'
department:
- _id: SiHi
doi: 10.1007/978-94-007-7687-6_1
editor:
- first_name: Laurent
full_name: Nguyen, Laurent
last_name: Nguyen
external_id:
isi:
- '000333646000002'
intvolume: ' 800'
isi: 1
language:
- iso: eng
month: '01'
oa_version: None
page: 1 - 24
publication: ' Cellular and Molecular Control of Neuronal Migration'
publication_status: published
publisher: Springer
publist_id: '4679'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular pathways controlling the sequential steps of cortical projection
neuron migration
type: book_chapter
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 800
year: '2014'
...
---
_id: '2838'
abstract:
- lang: eng
text: Individuals with Down syndrome (DS) present important motor deficits that
derive from altered motor development of infants and young children. DYRK1A, a
candidate gene for DS abnormalities has been implicated in motor function due
to its expression in motor nuclei in the adult brain, and its overexpression in
DS mouse models leads to hyperactivity and altered motor learning. However, its
precise role in the adult motor system, or its possible involvement in postnatal
locomotor development has not yet been clarified. During the postnatal period
we observed time-specific expression of Dyrk1A in discrete subsets of brainstem
nuclei and spinal cord motor neurons. Interestingly, we describe for the first
time the presence of Dyrk1A in the presynaptic terminal of the neuromuscular junctions
and its axonal transport from the facial nucleus, suggesting a function for Dyrk1A
in these structures. Relevant to DS, Dyrk1A overexpression in transgenic mice
(TgDyrk1A) produces motor developmental alterations possibly contributing to DS
motor phenotypes and modifies the numbers of motor cholinergic neurons, suggesting
that the kinase may have a role in the development of the brainstem and spinal
cord motor system.
article_number: e54285
article_processing_charge: No
author:
- first_name: Gloria
full_name: Arquè Fuste, Gloria
id: 3CF33908-F248-11E8-B48F-1D18A9856A87
last_name: Arquè Fuste
- first_name: Anna
full_name: Casanovas, Anna
last_name: Casanovas
- first_name: Mara
full_name: Dierssen, Mara
last_name: Dierssen
citation:
ama: 'Arquè Fuste G, Casanovas A, Dierssen M. Dyrk1A is dynamically expressed on
subsets of motor neurons and in the neuromuscular junction: Possible role in Down
syndrome. PLoS One. 2013;8(1). doi:10.1371/journal.pone.0054285'
apa: 'Arquè Fuste, G., Casanovas, A., & Dierssen, M. (2013). Dyrk1A is dynamically
expressed on subsets of motor neurons and in the neuromuscular junction: Possible
role in Down syndrome. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0054285'
chicago: 'Arquè Fuste, Gloria, Anna Casanovas, and Mara Dierssen. “Dyrk1A Is Dynamically
Expressed on Subsets of Motor Neurons and in the Neuromuscular Junction: Possible
Role in Down Syndrome.” PLoS One. Public Library of Science, 2013. https://doi.org/10.1371/journal.pone.0054285.'
ieee: 'G. Arquè Fuste, A. Casanovas, and M. Dierssen, “Dyrk1A is dynamically expressed
on subsets of motor neurons and in the neuromuscular junction: Possible role in
Down syndrome,” PLoS One, vol. 8, no. 1. Public Library of Science, 2013.'
ista: 'Arquè Fuste G, Casanovas A, Dierssen M. 2013. Dyrk1A is dynamically expressed
on subsets of motor neurons and in the neuromuscular junction: Possible role in
Down syndrome. PLoS One. 8(1), e54285.'
mla: 'Arquè Fuste, Gloria, et al. “Dyrk1A Is Dynamically Expressed on Subsets of
Motor Neurons and in the Neuromuscular Junction: Possible Role in Down Syndrome.”
PLoS One, vol. 8, no. 1, e54285, Public Library of Science, 2013, doi:10.1371/journal.pone.0054285.'
short: G. Arquè Fuste, A. Casanovas, M. Dierssen, PLoS One 8 (2013).
date_created: 2018-12-11T11:59:52Z
date_published: 2013-01-16T00:00:00Z
date_updated: 2025-09-29T13:46:22Z
day: '16'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1371/journal.pone.0054285
external_id:
isi:
- '000313682700103'
file:
- access_level: open_access
checksum: 512733b21419574a45f10cabef3d7f81
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:15:38Z
date_updated: 2020-07-14T12:45:50Z
file_id: '5160'
file_name: IST-2016-407-v1+1_journal.pone.0054285.pdf
file_size: 4795977
relation: main_file
file_date_updated: 2020-07-14T12:45:50Z
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: PLoS One
publication_status: published
publisher: Public Library of Science
publist_id: '3960'
pubrep_id: '407'
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'Dyrk1A is dynamically expressed on subsets of motor neurons and in the neuromuscular
junction: Possible role in Down syndrome'
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: 8
year: '2013'
...
---
_id: '2855'
abstract:
- lang: eng
text: Genomic imprinting leads to preferred expression of either the maternal or
paternal alleles of a subset of genes. Imprinting is essential for mammalian development,
and its deregulation causes many diseases. However, the functional relevance of
imprinting at the cellular level is poorly understood for most imprinted genes.
We used mosaic analysis with double markers (MADM) in mice to create uniparental
disomies (UPDs) and to visualize imprinting effects with single-cell resolution.
Although chromosome 12 UPD did not produce detectable phenotypes, chromosome 7
UPD caused highly significant paternal growth dominance in the liver and lung,
but not in the brain or heart. A single gene on chromosome 7, encoding the secreted
insulin-like growth factor 2 (IGF2), accounts for most of the paternal dominance
effect. Mosaic analyses implied additional imprinted loci on chromosome 7 acting
cell autonomously to transmit the IGF2 signal. Our study reveals chromosome- and
cell-type specificity of genomic imprinting effects.
article_processing_charge: No
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Randy
full_name: Johnson, Randy
last_name: Johnson
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
citation:
ama: Hippenmeyer S, Johnson R, Luo L. Mosaic analysis with double markers reveals
cell type specific paternal growth dominance. Cell Reports. 2013;3(3):960-967.
doi:10.1016/j.celrep.2013.02.002
apa: Hippenmeyer, S., Johnson, R., & Luo, L. (2013). Mosaic analysis with double
markers reveals cell type specific paternal growth dominance. Cell Reports.
Cell Press. https://doi.org/10.1016/j.celrep.2013.02.002
chicago: Hippenmeyer, Simon, Randy Johnson, and Liqun Luo. “Mosaic Analysis with
Double Markers Reveals Cell Type Specific Paternal Growth Dominance.” Cell
Reports. Cell Press, 2013. https://doi.org/10.1016/j.celrep.2013.02.002.
ieee: S. Hippenmeyer, R. Johnson, and L. Luo, “Mosaic analysis with double markers
reveals cell type specific paternal growth dominance,” Cell Reports, vol.
3, no. 3. Cell Press, pp. 960–967, 2013.
ista: Hippenmeyer S, Johnson R, Luo L. 2013. Mosaic analysis with double markers
reveals cell type specific paternal growth dominance. Cell Reports. 3(3), 960–967.
mla: Hippenmeyer, Simon, et al. “Mosaic Analysis with Double Markers Reveals Cell
Type Specific Paternal Growth Dominance.” Cell Reports, vol. 3, no. 3,
Cell Press, 2013, pp. 960–67, doi:10.1016/j.celrep.2013.02.002.
short: S. Hippenmeyer, R. Johnson, L. Luo, Cell Reports 3 (2013) 960–967.
corr_author: '1'
date_created: 2018-12-11T11:59:57Z
date_published: 2013-03-28T00:00:00Z
date_updated: 2025-09-29T13:40:05Z
day: '28'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.celrep.2013.02.002
external_id:
isi:
- '000321896000036'
file:
- access_level: open_access
checksum: 6e977b918e81384cd571ec5a9d812289
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:17:20Z
date_updated: 2020-07-14T12:45:51Z
file_id: '5274'
file_name: IST-2016-405-v1+1_1-s2.0-S2211124713000612-main.pdf
file_size: 1907211
relation: main_file
file_date_updated: 2020-07-14T12:45:51Z
has_accepted_license: '1'
intvolume: ' 3'
isi: 1
issue: '3'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 960 - 967
publication: Cell Reports
publication_status: published
publisher: Cell Press
publist_id: '3937'
pubrep_id: '405'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mosaic analysis with double markers reveals cell type specific paternal growth
dominance
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 3
year: '2013'
...
---
_id: '2264'
abstract:
- lang: eng
text: Faithful progression through the cell cycle is crucial to the maintenance
and developmental potential of stem cells. Here, we demonstrate that neural stem
cells (NSCs) and intermediate neural progenitor cells (NPCs) employ a zinc-finger
transcription factor specificity protein 2 (Sp2) as a cell cycle regulator in
two temporally and spatially distinct progenitor domains. Differential conditional
deletion of Sp2 in early embryonic cerebral cortical progenitors, and perinatal
olfactory bulb progenitors disrupted transitions through G1, G2 and M phases,
whereas DNA synthesis appeared intact. Cell-autonomous function of Sp2 was identified
by deletion of Sp2 using mosaic analysis with double markers, which clearly established
that conditional Sp2-null NSCs and NPCs are M phase arrested in vivo. Importantly,
conditional deletion of Sp2 led to a decline in the generation of NPCs and neurons
in the developing and postnatal brains. Our findings implicate Sp2-dependent mechanisms
as novel regulators of cell cycle progression, the absence of which disrupts neurogenesis
in the embryonic and postnatal brain.
article_processing_charge: No
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Haifeng
full_name: Yin, Haifeng
last_name: Yin
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Jonathan
full_name: Horowitz, Jonathan
last_name: Horowitz
- first_name: Troy
full_name: Ghashghaei, Troy
last_name: Ghashghaei
citation:
ama: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. Neural development
is dependent on the function of specificity protein 2 in cell cycle progression.
Development. 2013;140(3):552-561. doi:10.1242/dev.085621
apa: Liang, H., Xiao, G., Yin, H., Hippenmeyer, S., Horowitz, J., & Ghashghaei,
T. (2013). Neural development is dependent on the function of specificity protein
2 in cell cycle progression. Development. Company of Biologists. https://doi.org/10.1242/dev.085621
chicago: Liang, Huixuan, Guanxi Xiao, Haifeng Yin, Simon Hippenmeyer, Jonathan Horowitz,
and Troy Ghashghaei. “Neural Development Is Dependent on the Function of Specificity
Protein 2 in Cell Cycle Progression.” Development. Company of Biologists,
2013. https://doi.org/10.1242/dev.085621.
ieee: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, and T. Ghashghaei,
“Neural development is dependent on the function of specificity protein 2 in cell
cycle progression,” Development, vol. 140, no. 3. Company of Biologists,
pp. 552–561, 2013.
ista: Liang H, Xiao G, Yin H, Hippenmeyer S, Horowitz J, Ghashghaei T. 2013. Neural
development is dependent on the function of specificity protein 2 in cell cycle
progression. Development. 140(3), 552–561.
mla: Liang, Huixuan, et al. “Neural Development Is Dependent on the Function of
Specificity Protein 2 in Cell Cycle Progression.” Development, vol. 140,
no. 3, Company of Biologists, 2013, pp. 552–61, doi:10.1242/dev.085621.
short: H. Liang, G. Xiao, H. Yin, S. Hippenmeyer, J. Horowitz, T. Ghashghaei, Development
140 (2013) 552–561.
date_created: 2018-12-11T11:56:39Z
date_published: 2013-02-01T00:00:00Z
date_updated: 2025-09-29T14:29:19Z
day: '01'
department:
- _id: SiHi
doi: 10.1242/dev.085621
external_id:
isi:
- '000313363500009'
pmid:
- '23293287'
intvolume: ' 140'
isi: 1
issue: '3'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3561788/
month: '02'
oa: 1
oa_version: Submitted Version
page: 552 - 561
pmid: 1
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '4681'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Neural development is dependent on the function of specificity protein 2 in
cell cycle progression
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 140
year: '2013'
...
---
_id: '2303'
abstract:
- lang: eng
text: MADM (Mosaic Analysis with Double Markers) technology offers a genetic approach
in mice to visualize and concomitantly manipulate genetically defined cells at
clonal level and single cell resolution. MADM employs Cre recombinase/loxP-dependent
interchromosomal mitotic recombination to reconstitute two split marker genes—green
GFP and red tdTomato—and can label sparse clones of homozygous mutant cells in
one color and wild-type cells in the other color in an otherwise unlabeled background.
At present, major MADM applications include lineage tracing, single cell labeling,
conditional knockouts in small populations of cells and induction of uniparental
chromosome disomy to assess effects of genomic imprinting. MADM can be applied
universally in the mouse with the sole limitation being the specificity of the
promoter controlling Cre recombinase expression. Here I review recent developments
and extensions of the MADM technique and give an overview of the major discoveries
and progresses enabled by the implementation of the novel genetic MADM tools.
acknowledgement: This work was supported by IST Austria institutional funds.
article_type: review
author:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hippenmeyer S. Dissection of gene function at clonal level using mosaic analysis
with double markers. Frontiers in Biology. 2013;8(6):557-568. doi:10.1007/s11515-013-1279-6
apa: Hippenmeyer, S. (2013). Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. Springer. https://doi.org/10.1007/s11515-013-1279-6
chicago: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using
Mosaic Analysis with Double Markers.” Frontiers in Biology. Springer, 2013.
https://doi.org/10.1007/s11515-013-1279-6.
ieee: S. Hippenmeyer, “Dissection of gene function at clonal level using mosaic
analysis with double markers,” Frontiers in Biology, vol. 8, no. 6. Springer,
pp. 557–568, 2013.
ista: Hippenmeyer S. 2013. Dissection of gene function at clonal level using mosaic
analysis with double markers. Frontiers in Biology. 8(6), 557–568.
mla: Hippenmeyer, Simon. “Dissection of Gene Function at Clonal Level Using Mosaic
Analysis with Double Markers.” Frontiers in Biology, vol. 8, no. 6, Springer,
2013, pp. 557–68, doi:10.1007/s11515-013-1279-6.
short: S. Hippenmeyer, Frontiers in Biology 8 (2013) 557–568.
corr_author: '1'
date_created: 2018-12-11T11:56:52Z
date_published: 2013-09-03T00:00:00Z
date_updated: 2024-10-09T20:55:16Z
day: '03'
department:
- _id: SiHi
doi: 10.1007/s11515-013-1279-6
intvolume: ' 8'
issue: '6'
language:
- iso: eng
month: '09'
oa_version: None
page: 557 - 568
publication: Frontiers in Biology
publication_status: published
publisher: Springer
publist_id: '4624'
quality_controlled: '1'
scopus_import: 1
status: public
title: Dissection of gene function at clonal level using mosaic analysis with double
markers
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 8
year: '2013'
...
---
_id: '2263'
abstract:
- lang: eng
text: Nestin-cre transgenic mice have been widely used to direct recombination to
neural stem cells (NSCs) and intermediate neural progenitor cells (NPCs). Here
we report that a readily utilized, and the only commercially available, Nestin-cre
line is insufficient for directing recombination in early embryonic NSCs and NPCs.
Analysis of recombination efficiency in multiple cre-dependent reporters and a
genetic mosaic line revealed consistent temporal and spatial patterns of recombination
in NSCs and NPCs. For comparison we utilized a knock-in Emx1cre line and found
robust recombination in NSCs and NPCs in ventricular and subventricular zones
of the cerebral cortices as early as embryonic day 12.5. In addition we found
that the rate of Nestin-cre driven recombination only reaches sufficiently high
levels in NSCs and NPCs during late embryonic and early postnatal periods. These
findings are important when commercially available cre lines are considered for
directing recombination to embryonic NSCs and NPCs.
article_processing_charge: No
author:
- first_name: Huixuan
full_name: Liang, Huixuan
last_name: Liang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H.
full_name: Ghashghaei, H.
last_name: Ghashghaei
citation:
ama: Liang H, Hippenmeyer S, Ghashghaei H. A Nestin-cre transgenic mouse is insufficient
for recombination in early embryonic neural progenitors. Biology open.
2012;1(12):1200-1203. doi:10.1242/bio.20122287
apa: Liang, H., Hippenmeyer, S., & Ghashghaei, H. (2012). A Nestin-cre transgenic
mouse is insufficient for recombination in early embryonic neural progenitors.
Biology Open. The Company of Biologists. https://doi.org/10.1242/bio.20122287
chicago: Liang, Huixuan, Simon Hippenmeyer, and H. Ghashghaei. “A Nestin-Cre Transgenic
Mouse Is Insufficient for Recombination in Early Embryonic Neural Progenitors.”
Biology Open. The Company of Biologists, 2012. https://doi.org/10.1242/bio.20122287.
ieee: H. Liang, S. Hippenmeyer, and H. Ghashghaei, “A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors,” Biology
open, vol. 1, no. 12. The Company of Biologists, pp. 1200–1203, 2012.
ista: Liang H, Hippenmeyer S, Ghashghaei H. 2012. A Nestin-cre transgenic mouse
is insufficient for recombination in early embryonic neural progenitors. Biology
open. 1(12), 1200–1203.
mla: Liang, Huixuan, et al. “A Nestin-Cre Transgenic Mouse Is Insufficient for Recombination
in Early Embryonic Neural Progenitors.” Biology Open, vol. 1, no. 12, The
Company of Biologists, 2012, pp. 1200–03, doi:10.1242/bio.20122287.
short: H. Liang, S. Hippenmeyer, H. Ghashghaei, Biology Open 1 (2012) 1200–1203.
date_created: 2018-12-11T11:56:38Z
date_published: 2012-12-15T00:00:00Z
date_updated: 2025-09-30T08:22:45Z
day: '15'
ddc:
- '576'
department:
- _id: SiHi
doi: 10.1242/bio.20122287
external_id:
isi:
- '000209205700005'
file:
- access_level: open_access
checksum: 605a1800b81227848c361fd6ba7d22ba
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:13:09Z
date_updated: 2020-07-14T12:45:35Z
file_id: '4990'
file_name: IST-2015-387-v1+1_1200.full.pdf
file_size: 726695
relation: main_file
file_date_updated: 2020-07-14T12:45:35Z
has_accepted_license: '1'
intvolume: ' 1'
isi: 1
issue: '12'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc-sa/4.0/
month: '12'
oa: 1
oa_version: Published Version
page: 1200 - 1203
publication: Biology open
publication_status: published
publisher: The Company of Biologists
publist_id: '4682'
pubrep_id: '387'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A Nestin-cre transgenic mouse is insufficient for recombination in early embryonic
neural progenitors
tmp:
image: /images/cc_by_nc_sa.png
legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC
BY-NC-SA 4.0)
short: CC BY-NC-SA (4.0)
type: journal_article
user_id: 317138e5-6ab7-11ef-aa6d-ffef3953e345
volume: 1
year: '2012'
...