---
_id: '6455'
abstract:
- lang: eng
  text: During corticogenesis, distinct subtypes of neurons are sequentially born
    from ventricular zone progenitors. How these cells are molecularly temporally
    patterned is poorly understood. We used single-cell RNA sequencing at high temporal
    resolution to trace the lineage of the molecular identities of successive generations
    of apical progenitors (APs) and their daughter neurons in mouse embryos. We identified
    a core set of evolutionarily conserved, temporally patterned genes that drive
    APs from internally driven to more exteroceptive states. We found that the Polycomb
    repressor complex 2 (PRC2) epigenetically regulates AP temporal progression. Embryonic
    age–dependent AP molecular states are transmitted to their progeny as successive
    ground states, onto which essentially conserved early postmitotic differentiation
    programs are applied, and are complemented by later-occurring environment-dependent
    signals. Thus, epigenetically regulated temporal molecular birthmarks present
    in progenitors act in their postmitotic progeny to seed adult neuronal diversity.
article_number: eaav2522
article_processing_charge: No
article_type: original
author:
- first_name: L
  full_name: Telley, L
  last_name: Telley
- first_name: G
  full_name: Agirman, G
  last_name: Agirman
- first_name: J
  full_name: Prados, J
  last_name: Prados
- first_name: Nicole
  full_name: Amberg, Nicole
  id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
  last_name: Amberg
  orcid: 0000-0002-3183-8207
- first_name: S
  full_name: Fièvre, S
  last_name: Fièvre
- first_name: P
  full_name: Oberst, P
  last_name: Oberst
- first_name: G
  full_name: Bartolini, G
  last_name: Bartolini
- first_name: I
  full_name: Vitali, I
  last_name: Vitali
- first_name: C
  full_name: Cadilhac, C
  last_name: Cadilhac
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: L
  full_name: Nguyen, L
  last_name: Nguyen
- first_name: A
  full_name: Dayer, A
  last_name: Dayer
- first_name: D
  full_name: Jabaudon, D
  last_name: Jabaudon
citation:
  ama: Telley L, Agirman G, Prados J, et al. Temporal patterning of apical progenitors
    and their daughter neurons in the developing neocortex. <i>Science</i>. 2019;364(6440).
    doi:<a href="https://doi.org/10.1126/science.aav2522">10.1126/science.aav2522</a>
  apa: Telley, L., Agirman, G., Prados, J., Amberg, N., Fièvre, S., Oberst, P., …
    Jabaudon, D. (2019). Temporal patterning of apical progenitors and their daughter
    neurons in the developing neocortex. <i>Science</i>. AAAS. <a href="https://doi.org/10.1126/science.aav2522">https://doi.org/10.1126/science.aav2522</a>
  chicago: Telley, L, G Agirman, J Prados, Nicole Amberg, S Fièvre, P Oberst, G Bartolini,
    et al. “Temporal Patterning of Apical Progenitors and Their Daughter Neurons in
    the Developing Neocortex.” <i>Science</i>. AAAS, 2019. <a href="https://doi.org/10.1126/science.aav2522">https://doi.org/10.1126/science.aav2522</a>.
  ieee: L. Telley <i>et al.</i>, “Temporal patterning of apical progenitors and their
    daughter neurons in the developing neocortex,” <i>Science</i>, vol. 364, no. 6440.
    AAAS, 2019.
  ista: Telley L, Agirman G, Prados J, Amberg N, Fièvre S, Oberst P, Bartolini G,
    Vitali I, Cadilhac C, Hippenmeyer S, Nguyen L, Dayer A, Jabaudon D. 2019. Temporal
    patterning of apical progenitors and their daughter neurons in the developing
    neocortex. Science. 364(6440), eaav2522.
  mla: Telley, L., et al. “Temporal Patterning of Apical Progenitors and Their Daughter
    Neurons in the Developing Neocortex.” <i>Science</i>, vol. 364, no. 6440, eaav2522,
    AAAS, 2019, doi:<a href="https://doi.org/10.1126/science.aav2522">10.1126/science.aav2522</a>.
  short: L. Telley, G. Agirman, J. Prados, N. Amberg, S. Fièvre, P. Oberst, G. Bartolini,
    I. Vitali, C. Cadilhac, S. Hippenmeyer, L. Nguyen, A. Dayer, D. Jabaudon, Science
    364 (2019).
date_created: 2019-05-14T13:07:47Z
date_published: 2019-05-10T00:00:00Z
date_updated: 2025-04-15T07:50:01Z
day: '10'
department:
- _id: SiHi
doi: 10.1126/science.aav2522
ec_funded: 1
external_id:
  isi:
  - '000467631800034'
  pmid:
  - '31073041'
intvolume: '       364'
isi: 1
issue: '6440'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://orbi.uliege.be/bitstream/2268/239604/1/Telley_Agirman_Science2019.pdf
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '725780'
  name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 268F8446-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: T01031
  name: Role of Eed in neural stem cell lineage progression
publication: Science
publication_identifier:
  eissn:
  - 1095-9203
  issn:
  - 0036-8075
publication_status: published
publisher: AAAS
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/how-to-generate-a-brain-of-correct-size-and-composition/
scopus_import: '1'
status: public
title: Temporal patterning of apical progenitors and their daughter neurons in the
  developing neocortex
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 364
year: '2019'
...
---
_id: '6844'
abstract:
- lang: eng
  text: Studying the progression of the proliferative and differentiative patterns
    of neural stem cells at the individual cell level is crucial to the understanding
    of cortex development and how the disruption of such patterns can lead to malformations
    and neurodevelopmental diseases. However, our understanding of the precise lineage
    progression programme at single-cell resolution is still incomplete due to the
    technical variations in lineage- tracing approaches. One of the key challenges
    involves developing a robust theoretical framework in which we can integrate experimental
    observations and introduce correction factors to obtain a reliable and representative
    description of the temporal modulation of proliferation and differentiation. In
    order to obtain more conclusive insights, we carry out virtual clonal analysis
    using mathematical modelling and compare our results against experimental data.
    Using a dataset obtained with Mosaic Analysis with Double Markers, we illustrate
    how the theoretical description can be exploited to interpret and reconcile the
    disparity between virtual and experimental results.
article_processing_charge: No
article_type: original
author:
- first_name: Noemi
  full_name: Picco, Noemi
  last_name: Picco
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: Julio
  full_name: Rodarte, Julio
  id: 3C70A038-F248-11E8-B48F-1D18A9856A87
  last_name: Rodarte
- first_name: Carmen
  full_name: Streicher, Carmen
  id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
  last_name: Streicher
- first_name: Zoltán
  full_name: Molnár, Zoltán
  last_name: Molnár
- first_name: Philip K.
  full_name: Maini, Philip K.
  last_name: Maini
- first_name: Thomas E.
  full_name: Woolley, Thomas E.
  last_name: Woolley
citation:
  ama: Picco N, Hippenmeyer S, Rodarte J, et al. A mathematical insight into cell
    labelling experiments for clonal analysis. <i>Journal of Anatomy</i>. 2019;235(3):686-696.
    doi:<a href="https://doi.org/10.1111/joa.13001">10.1111/joa.13001</a>
  apa: Picco, N., Hippenmeyer, S., Rodarte, J., Streicher, C., Molnár, Z., Maini,
    P. K., &#38; Woolley, T. E. (2019). A mathematical insight into cell labelling
    experiments for clonal analysis. <i>Journal of Anatomy</i>. Wiley. <a href="https://doi.org/10.1111/joa.13001">https://doi.org/10.1111/joa.13001</a>
  chicago: Picco, Noemi, Simon Hippenmeyer, Julio Rodarte, Carmen Streicher, Zoltán
    Molnár, Philip K. Maini, and Thomas E. Woolley. “A Mathematical Insight into Cell
    Labelling Experiments for Clonal Analysis.” <i>Journal of Anatomy</i>. Wiley,
    2019. <a href="https://doi.org/10.1111/joa.13001">https://doi.org/10.1111/joa.13001</a>.
  ieee: N. Picco <i>et al.</i>, “A mathematical insight into cell labelling experiments
    for clonal analysis,” <i>Journal of Anatomy</i>, vol. 235, no. 3. Wiley, pp. 686–696,
    2019.
  ista: Picco N, Hippenmeyer S, Rodarte J, Streicher C, Molnár Z, Maini PK, Woolley
    TE. 2019. A mathematical insight into cell labelling experiments for clonal analysis.
    Journal of Anatomy. 235(3), 686–696.
  mla: Picco, Noemi, et al. “A Mathematical Insight into Cell Labelling Experiments
    for Clonal Analysis.” <i>Journal of Anatomy</i>, vol. 235, no. 3, Wiley, 2019,
    pp. 686–96, doi:<a href="https://doi.org/10.1111/joa.13001">10.1111/joa.13001</a>.
  short: N. Picco, S. Hippenmeyer, J. Rodarte, C. Streicher, Z. Molnár, P.K. Maini,
    T.E. Woolley, Journal of Anatomy 235 (2019) 686–696.
date_created: 2019-09-02T11:57:28Z
date_published: 2019-09-01T00:00:00Z
date_updated: 2025-04-14T07:43:05Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/joa.13001
ec_funded: 1
external_id:
  isi:
  - '000482426800017'
file:
- access_level: open_access
  checksum: 160f960844b204057f20896e0e1f8ee7
  content_type: application/pdf
  creator: dernst
  date_created: 2019-09-02T12:05:18Z
  date_updated: 2020-07-14T12:47:42Z
  file_id: '6845'
  file_name: 2019_JournalAnatomy_Picco.pdf
  file_size: 1192994
  relation: main_file
file_date_updated: 2020-07-14T12:47:42Z
has_accepted_license: '1'
intvolume: '       235'
isi: 1
issue: '3'
language:
- iso: eng
license: https://creativecommons.org/licenses/by-nc/4.0/
month: '09'
oa: 1
oa_version: Published Version
page: 686-696
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '725780'
  name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Anatomy
publication_identifier:
  eissn:
  - 1469-7580
  issn:
  - 0021-8782
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: A mathematical insight into cell labelling experiments for clonal analysis
tmp:
  image: /images/cc_by_nc.png
  legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)
  short: CC BY-NC (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 235
year: '2019'
...
---
_id: '7005'
abstract:
- lang: eng
  text: Activity-dependent bulk endocytosis generates synaptic vesicles (SVs) during
    intense neuronal activity via a two-step process. First, bulk endosomes are formed
    direct from the plasma membrane from which SVs are then generated. SV generation
    from bulk endosomes requires the efflux of previously accumulated calcium and
    activation of the protein phosphatase calcineurin. However, it is still unknown
    how calcineurin mediates SV generation. We addressed this question using a series
    of acute interventions that decoupled the generation of SVs from bulk endosomes
    in rat primary neuronal culture. This was achieved by either disruption of protein–protein
    interactions via delivery of competitive peptides, or inhibition of enzyme activity
    by known inhibitors. SV generation was monitored using either a morphological
    horseradish peroxidase assay or an optical assay that monitors the replenishment
    of the reserve SV pool. We found that SV generation was inhibited by, (i) peptides
    that disrupt calcineurin interactions, (ii) an inhibitor of dynamin I GTPase activity
    and (iii) peptides that disrupt the phosphorylation-dependent dynamin I–syndapin
    I interaction. Peptides that disrupted syndapin I interactions with eps15 homology
    domain-containing proteins had no effect. This revealed that (i) calcineurin must
    be localized at bulk endosomes to mediate its effect, (ii) dynamin I GTPase activity
    is essential for SV fission and (iii) the calcineurin-dependent interaction between
    dynamin I and syndapin I is essential for SV generation. We therefore propose
    that a calcineurin-dependent dephosphorylation cascade that requires both dynamin
    I GTPase and syndapin I lipid-deforming activity is essential for SV generation
    from bulk endosomes.
article_processing_charge: No
article_type: original
author:
- first_name: Giselle T
  full_name: Cheung, Giselle T
  id: 471195F6-F248-11E8-B48F-1D18A9856A87
  last_name: Cheung
  orcid: 0000-0001-8457-2572
- first_name: Michael A.
  full_name: Cousin, Michael A.
  last_name: Cousin
citation:
  ama: Cheung GT, Cousin MA. Synaptic vesicle generation from activity‐dependent bulk
    endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction.
    <i>Journal of Neurochemistry</i>. 2019;151(5):570-583. doi:<a href="https://doi.org/10.1111/jnc.14862">10.1111/jnc.14862</a>
  apa: Cheung, G. T., &#38; Cousin, M. A. (2019). Synaptic vesicle generation from
    activity‐dependent bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin
    interaction. <i>Journal of Neurochemistry</i>. Wiley. <a href="https://doi.org/10.1111/jnc.14862">https://doi.org/10.1111/jnc.14862</a>
  chicago: Cheung, Giselle T, and Michael A. Cousin. “Synaptic Vesicle Generation
    from Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent
    Dynamin–Syndapin Interaction.” <i>Journal of Neurochemistry</i>. Wiley, 2019.
    <a href="https://doi.org/10.1111/jnc.14862">https://doi.org/10.1111/jnc.14862</a>.
  ieee: G. T. Cheung and M. A. Cousin, “Synaptic vesicle generation from activity‐dependent
    bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction,”
    <i>Journal of Neurochemistry</i>, vol. 151, no. 5. Wiley, pp. 570–583, 2019.
  ista: Cheung GT, Cousin MA. 2019. Synaptic vesicle generation from activity‐dependent
    bulk endosomes requires a dephosphorylation‐dependent dynamin–syndapin interaction.
    Journal of Neurochemistry. 151(5), 570–583.
  mla: Cheung, Giselle T., and Michael A. Cousin. “Synaptic Vesicle Generation from
    Activity‐dependent Bulk Endosomes Requires a Dephosphorylation‐dependent Dynamin–Syndapin
    Interaction.” <i>Journal of Neurochemistry</i>, vol. 151, no. 5, Wiley, 2019,
    pp. 570–83, doi:<a href="https://doi.org/10.1111/jnc.14862">10.1111/jnc.14862</a>.
  short: G.T. Cheung, M.A. Cousin, Journal of Neurochemistry 151 (2019) 570–583.
date_created: 2019-11-12T14:37:08Z
date_published: 2019-12-01T00:00:00Z
date_updated: 2023-08-30T07:21:50Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/jnc.14862
external_id:
  isi:
  - '000490703100001'
  pmid:
  - '31479508'
file:
- access_level: open_access
  checksum: ec1fb2aebb874009bc309adaada6e1d7
  content_type: application/pdf
  creator: dernst
  date_created: 2020-02-05T10:30:02Z
  date_updated: 2020-07-14T12:47:47Z
  file_id: '7452'
  file_name: 2019_JournNeurochemistry_Cheung.pdf
  file_size: 4334962
  relation: main_file
file_date_updated: 2020-07-14T12:47:47Z
has_accepted_license: '1'
intvolume: '       151'
isi: 1
issue: '5'
language:
- iso: eng
license: https://creativecommons.org/licenses/by/4.0/
month: '12'
oa: 1
oa_version: Published Version
page: 570-583
pmid: 1
publication: Journal of Neurochemistry
publication_identifier:
  eissn:
  - 1471-4159
  issn:
  - 0022-3042
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Synaptic vesicle generation from activity‐dependent bulk endosomes requires
  a dephosphorylation‐dependent dynamin–syndapin interaction
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 151
year: '2019'
...
---
_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. <i>PLoS
    Genetics</i>. 2019;15(7). doi:<a href="https://doi.org/10.1371/journal.pgen.1008268">10.1371/journal.pgen.1008268</a>
  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. <i>PLoS Genetics</i>.
    Public Library of Science. <a href="https://doi.org/10.1371/journal.pgen.1008268">https://doi.org/10.1371/journal.pgen.1008268</a>
  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.” <i>PLoS Genetics</i>. Public Library
    of Science, 2019. <a href="https://doi.org/10.1371/journal.pgen.1008268">https://doi.org/10.1371/journal.pgen.1008268</a>.
  ieee: D. Andergassen <i>et al.</i>, “The Airn lncRNA does not require any DNA elements
    within its locus to silence distant imprinted genes,” <i>PLoS Genetics</i>, 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.” <i>PLoS Genetics</i>, vol.
    15, no. 7, e1008268, Public Library of Science, 2019, doi:<a href="https://doi.org/10.1371/journal.pgen.1008268">10.1371/journal.pgen.1008268</a>.
  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
has_accepted_license: '1'
intvolume: '        15'
isi: 1
issue: '7'
language:
- iso: eng
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: '7202'
abstract:
- lang: eng
  text: The cerebral cortex contains multiple areas with distinctive cytoarchitectonical
    patterns, but the cellular mechanisms underlying the emergence of this diversity
    remain unclear. Here, we have investigated the neuronal output of individual progenitor
    cells in the developing mouse neocortex using a combination of methods that together
    circumvent the biases and limitations of individual approaches. Our experimental
    results indicate that progenitor cells generate pyramidal cell lineages with a
    wide range of sizes and laminar configurations. Mathematical modelling indicates
    that these outcomes are compatible with a stochastic model of cortical neurogenesis
    in which progenitor cells undergo a series of probabilistic decisions that lead
    to the specification of very heterogeneous progenies. Our findings support a mechanism
    for cortical neurogenesis whose flexibility would make it capable to generate
    the diverse cytoarchitectures that characterize distinct neocortical areas.
article_number: e51381
article_processing_charge: No
article_type: original
author:
- first_name: Alfredo
  full_name: Llorca, Alfredo
  last_name: Llorca
- first_name: Gabriele
  full_name: Ciceri, Gabriele
  last_name: Ciceri
- first_name: Robert J
  full_name: Beattie, Robert J
  id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
  last_name: Beattie
  orcid: 0000-0002-8483-8753
- first_name: Fong Kuan
  full_name: Wong, Fong Kuan
  last_name: Wong
- first_name: Giovanni
  full_name: Diana, Giovanni
  last_name: Diana
- first_name: Eleni
  full_name: Serafeimidou-Pouliou, Eleni
  last_name: Serafeimidou-Pouliou
- first_name: Marian
  full_name: Fernández-Otero, Marian
  last_name: Fernández-Otero
- first_name: Carmen
  full_name: Streicher, Carmen
  id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
  last_name: Streicher
- first_name: Sebastian J.
  full_name: Arnold, Sebastian J.
  last_name: Arnold
- first_name: Martin
  full_name: Meyer, Martin
  last_name: Meyer
- first_name: Simon
  full_name: Hippenmeyer, Simon
  id: 37B36620-F248-11E8-B48F-1D18A9856A87
  last_name: Hippenmeyer
  orcid: 0000-0003-2279-1061
- first_name: Miguel
  full_name: Maravall, Miguel
  last_name: Maravall
- first_name: Oscar
  full_name: Marín, Oscar
  last_name: Marín
citation:
  ama: Llorca A, Ciceri G, Beattie RJ, et al. A stochastic framework of neurogenesis
    underlies the assembly of neocortical cytoarchitecture. <i>eLife</i>. 2019;8.
    doi:<a href="https://doi.org/10.7554/eLife.51381">10.7554/eLife.51381</a>
  apa: Llorca, A., Ciceri, G., Beattie, R. J., Wong, F. K., Diana, G., Serafeimidou-Pouliou,
    E., … Marín, O. (2019). A stochastic framework of neurogenesis underlies the assembly
    of neocortical cytoarchitecture. <i>ELife</i>. eLife Sciences Publications. <a
    href="https://doi.org/10.7554/eLife.51381">https://doi.org/10.7554/eLife.51381</a>
  chicago: Llorca, Alfredo, Gabriele Ciceri, Robert J Beattie, Fong Kuan Wong, Giovanni
    Diana, Eleni Serafeimidou-Pouliou, Marian Fernández-Otero, et al. “A Stochastic
    Framework of Neurogenesis Underlies the Assembly of Neocortical Cytoarchitecture.”
    <i>ELife</i>. eLife Sciences Publications, 2019. <a href="https://doi.org/10.7554/eLife.51381">https://doi.org/10.7554/eLife.51381</a>.
  ieee: A. Llorca <i>et al.</i>, “A stochastic framework of neurogenesis underlies
    the assembly of neocortical cytoarchitecture,” <i>eLife</i>, vol. 8. eLife Sciences
    Publications, 2019.
  ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou-Pouliou E,
    Fernández-Otero M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M,
    Marín O. 2019. A stochastic framework of neurogenesis underlies the assembly of
    neocortical cytoarchitecture. eLife. 8, e51381.
  mla: Llorca, Alfredo, et al. “A Stochastic Framework of Neurogenesis Underlies the
    Assembly of Neocortical Cytoarchitecture.” <i>ELife</i>, vol. 8, e51381, eLife
    Sciences Publications, 2019, doi:<a href="https://doi.org/10.7554/eLife.51381">10.7554/eLife.51381</a>.
  short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou-Pouliou,
    M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
    O. Marín, ELife 8 (2019).
date_created: 2019-12-22T23:00:42Z
date_published: 2019-11-18T00:00:00Z
date_updated: 2026-04-03T09:46:33Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.51381
ec_funded: 1
external_id:
  isi:
  - '000508156800001'
  pmid:
  - '31736464'
file:
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  checksum: b460ecc33e1a68265e7adea775021f3a
  content_type: application/pdf
  creator: dernst
  date_created: 2020-02-18T15:19:26Z
  date_updated: 2020-07-14T12:47:53Z
  file_id: '7503'
  file_name: 2019_eLife_Llorca.pdf
  file_size: 2960543
  relation: main_file
file_date_updated: 2020-07-14T12:47:53Z
has_accepted_license: '1'
intvolume: '         8'
isi: 1
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '725780'
  name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: M02416
  name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
publication: eLife
publication_identifier:
  eissn:
  - 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: A stochastic framework of neurogenesis underlies the assembly of neocortical
  cytoarchitecture
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 8
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. <i>Neuron</i>.
    2019;103(5):750-752. doi:<a href="https://doi.org/10.1016/j.neuron.2019.08.021">10.1016/j.neuron.2019.08.021</a>
  apa: Contreras, X., &#38; Hippenmeyer, S. (2019). Memo1 tiles the radial glial cell
    grid. <i>Neuron</i>. Elsevier. <a href="https://doi.org/10.1016/j.neuron.2019.08.021">https://doi.org/10.1016/j.neuron.2019.08.021</a>
  chicago: Contreras, Ximena, and Simon Hippenmeyer. “Memo1 Tiles the Radial Glial
    Cell Grid.” <i>Neuron</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.neuron.2019.08.021">https://doi.org/10.1016/j.neuron.2019.08.021</a>.
  ieee: X. Contreras and S. Hippenmeyer, “Memo1 tiles the radial glial cell grid,”
    <i>Neuron</i>, 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.” <i>Neuron</i>, vol. 103, no. 5, Elsevier, 2019, pp. 750–52, doi:<a href="https://doi.org/10.1016/j.neuron.2019.08.021">10.1016/j.neuron.2019.08.021</a>.
  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: 2026-05-12T22:31:14Z
day: '04'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2019.08.021
external_id:
  isi:
  - '000484400200002'
  pmid:
  - '31487522'
intvolume: '       103'
isi: 1
issue: '5'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.neuron.2019.08.021
month: '09'
oa: 1
oa_version: Published Version
page: 750-752
pmid: 1
publication: Neuron
publication_identifier:
  eissn:
  - 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: ba8df636-2132-11f1-aed0-ed93e2281fdd
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.
    <i>BMC Genomics</i>. 2018;19(1). doi:<a href="https://doi.org/10.1186/s12864-018-5173-0">10.1186/s12864-018-5173-0</a>
  apa: Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
    Herzig, S., &#38; Scheideler, M. (2018). Norepinephrine triggers an immediate-early
    regulatory network response in primary human white adipocytes. <i>BMC Genomics</i>.
    BioMed Central. <a href="https://doi.org/10.1186/s12864-018-5173-0">https://doi.org/10.1186/s12864-018-5173-0</a>
  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.”
    <i>BMC Genomics</i>. BioMed Central, 2018. <a href="https://doi.org/10.1186/s12864-018-5173-0">https://doi.org/10.1186/s12864-018-5173-0</a>.
  ieee: J. Higareda Almaraz <i>et al.</i>, “Norepinephrine triggers an immediate-early
    regulatory network response in primary human white adipocytes,” <i>BMC Genomics</i>,
    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.” <i>BMC Genomics</i>,
    vol. 19, no. 1, BioMed Central, 2018, doi:<a href="https://doi.org/10.1186/s12864-018-5173-0">10.1186/s12864-018-5173-0</a>.
  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
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: '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. <i>bioRxiv</i>. doi:<a
    href="https://doi.org/10.1101/494088">10.1101/494088</a>
  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. <i>bioRxiv</i>. Cold Spring Harbor Laboratory.
    <a href="https://doi.org/10.1101/494088">https://doi.org/10.1101/494088</a>
  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.” <i>BioRxiv</i>.
    Cold Spring Harbor Laboratory, n.d. <a href="https://doi.org/10.1101/494088">https://doi.org/10.1101/494088</a>.
  ieee: A. Llorca <i>et al.</i>, “Heterogeneous progenitor cell behaviors underlie
    the assembly of neocortical cytoarchitecture,” <i>bioRxiv</i>. Cold Spring Harbor
    Laboratory.
  ista: Llorca A, Ciceri G, Beattie RJ, Wong FK, Diana G, Serafeimidou E, Fernández-Otero
    M, Streicher C, Arnold SJ, Meyer M, Hippenmeyer S, Maravall M, Marín O. Heterogeneous
    progenitor cell behaviors underlie the assembly of neocortical cytoarchitecture.
    bioRxiv, <a href="https://doi.org/10.1101/494088">10.1101/494088</a>.
  mla: Llorca, Alfredo, et al. “Heterogeneous Progenitor Cell Behaviors Underlie the
    Assembly of Neocortical Cytoarchitecture.” <i>BioRxiv</i>, Cold Spring Harbor
    Laboratory, doi:<a href="https://doi.org/10.1101/494088">10.1101/494088</a>.
  short: A. Llorca, G. Ciceri, R.J. Beattie, F.K. Wong, G. Diana, E. Serafeimidou,
    M. Fernández-Otero, C. Streicher, S.J. Arnold, M. Meyer, S. Hippenmeyer, M. Maravall,
    O. Marín, BioRxiv (n.d.).
date_created: 2020-09-21T12:01:50Z
date_published: 2018-12-13T00:00:00Z
date_updated: 2024-10-22T10:46:39Z
day: '13'
department:
- _id: SiHi
doi: 10.1101/494088
ec_funded: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1101/494088
month: '12'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '725780'
  name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: M02416
  name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
publication: bioRxiv
publication_status: submitted
publisher: Cold Spring Harbor Laboratory
status: public
title: Heterogeneous progenitor cell behaviors underlie the assembly of neocortical
  cytoarchitecture
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2018'
...
---
_id: '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:<a href="https://doi.org/10.6084/m9.figshare.7295339.v1">10.6084/m9.figshare.7295339.v1</a>'
  apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
    Herzig, S., &#38; Scheideler, M. (2018). Additional file 1: Of Norepinephrine
    triggers an immediate-early regulatory network response in primary human white
    adipocytes. Springer Nature. <a href="https://doi.org/10.6084/m9.figshare.7295339.v1">https://doi.org/10.6084/m9.figshare.7295339.v1</a>'
  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. <a href="https://doi.org/10.6084/m9.figshare.7295339.v1">https://doi.org/10.6084/m9.figshare.7295339.v1</a>.'
  ieee: 'J. Higareda Almaraz <i>et al.</i>, “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,
    <a href="https://doi.org/10.6084/m9.figshare.7295339.v1">10.6084/m9.figshare.7295339.v1</a>.'
  mla: 'Higareda Almaraz, Juan, et al. <i>Additional File 1: Of Norepinephrine Triggers
    an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes</i>.
    Springer Nature, 2018, doi:<a href="https://doi.org/10.6084/m9.figshare.7295339.v1">10.6084/m9.figshare.7295339.v1</a>.'
  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
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:<a href="https://doi.org/10.6084/m9.figshare.7295369.v1">10.6084/m9.figshare.7295369.v1</a>'
  apa: 'Higareda Almaraz, J., Karbiener, M., Giroud, M., Pauler, F., Gerhalter, T.,
    Herzig, S., &#38; Scheideler, M. (2018). Additional file 3: Of Norepinephrine
    triggers an immediate-early regulatory network response in primary human white
    adipocytes. Springer Nature. <a href="https://doi.org/10.6084/m9.figshare.7295369.v1">https://doi.org/10.6084/m9.figshare.7295369.v1</a>'
  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. <a href="https://doi.org/10.6084/m9.figshare.7295369.v1">https://doi.org/10.6084/m9.figshare.7295369.v1</a>.'
  ieee: 'J. Higareda Almaraz <i>et al.</i>, “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,
    <a href="https://doi.org/10.6084/m9.figshare.7295369.v1">10.6084/m9.figshare.7295369.v1</a>.'
  mla: 'Higareda Almaraz, Juan, et al. <i>Additional File 3: Of Norepinephrine Triggers
    an Immediate-Early Regulatory Network Response in Primary Human White Adipocytes</i>.
    Springer Nature, 2018, doi:<a href="https://doi.org/10.6084/m9.figshare.7295369.v1">10.6084/m9.figshare.7295369.v1</a>.'
  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
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'
...
---
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:<a href="https://doi.org/10.15479/AT:ISTA:th1057">10.15479/AT:ISTA:th1057</a>
  apa: Laukoter, S. (2018). <i>Role of genomic imprinting in cerebral cortex development</i>.
    Institute of Science and Technology Austria. <a href="https://doi.org/10.15479/AT:ISTA:th1057">https://doi.org/10.15479/AT:ISTA:th1057</a>
  chicago: Laukoter, Susanne. “Role of Genomic Imprinting in Cerebral Cortex Development.”
    Institute of Science and Technology Austria, 2018. <a href="https://doi.org/10.15479/AT:ISTA:th1057">https://doi.org/10.15479/AT:ISTA:th1057</a>.
  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. <i>Role of Genomic Imprinting in Cerebral Cortex Development</i>.
    Institute of Science and Technology Austria, 2018, pp. 1–139, doi:<a href="https://doi.org/10.15479/AT:ISTA:th1057">10.15479/AT:ISTA:th1057</a>.
  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: 2026-04-08T14:12:45Z
day: '21'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
doi: 10.15479/AT:ISTA:th1057
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
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: ba8df636-2132-11f1-aed0-ed93e2281fdd
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. <i>Brain
    a journal of neurology</i>. 2018;141(9):2542-2544. doi:<a href="https://doi.org/10.1093/brain/awy218">10.1093/brain/awy218</a>
  apa: Contreras, X., &#38; Hippenmeyer, S. (2018). Incorrect trafficking route leads
    to autism. <i>Brain a Journal of Neurology</i>. Oxford University Press. <a href="https://doi.org/10.1093/brain/awy218">https://doi.org/10.1093/brain/awy218</a>
  chicago: Contreras, Ximena, and Simon Hippenmeyer. “Incorrect Trafficking Route
    Leads to Autism.” <i>Brain a Journal of Neurology</i>. Oxford University Press,
    2018. <a href="https://doi.org/10.1093/brain/awy218">https://doi.org/10.1093/brain/awy218</a>.
  ieee: X. Contreras and S. Hippenmeyer, “Incorrect trafficking route leads to autism,”
    <i>Brain a journal of neurology</i>, 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.” <i>Brain a Journal of Neurology</i>, vol. 141, no. 9, Oxford University
    Press, 2018, pp. 2542–44, doi:<a href="https://doi.org/10.1093/brain/awy218">10.1093/brain/awy218</a>.
  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: 2026-05-12T22:31:14Z
day: '01'
department:
- _id: SiHi
doi: 10.1093/brain/awy218
external_id:
  isi:
  - '000446548100012'
intvolume: '       141'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa_version: None
page: 2542 - 2544
publication: Brain a journal of neurology
publication_status: published
publisher: Oxford University Press
quality_controlled: '1'
related_material:
  record:
  - id: '7902'
    relation: part_of_dissertation
    status: public
scopus_import: '1'
status: public
title: Incorrect trafficking route leads to autism
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 141
year: '2018'
...
---
_id: '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. <i>Molecular and Cellular Neuroscience</i>.
    2017;84:58-67. doi:<a href="https://doi.org/10.1016/j.mcn.2017.03.002">10.1016/j.mcn.2017.03.002</a>'
  apa: 'Breuss, M., Leca, I., Gstrein, T., Hansen, A. H., &#38; Keays, D. (2017).
    Tubulins and brain development: The origins of functional specification. <i>Molecular
    and Cellular Neuroscience</i>. Academic Press. <a href="https://doi.org/10.1016/j.mcn.2017.03.002">https://doi.org/10.1016/j.mcn.2017.03.002</a>'
  chicago: 'Breuss, Martin, Ines Leca, Thomas Gstrein, Andi H Hansen, and David Keays.
    “Tubulins and Brain Development: The Origins of Functional Specification.” <i>Molecular
    and Cellular Neuroscience</i>. Academic Press, 2017. <a href="https://doi.org/10.1016/j.mcn.2017.03.002">https://doi.org/10.1016/j.mcn.2017.03.002</a>.'
  ieee: 'M. Breuss, I. Leca, T. Gstrein, A. H. Hansen, and D. Keays, “Tubulins and
    brain development: The origins of functional specification,” <i>Molecular and
    Cellular Neuroscience</i>, 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.” <i>Molecular and Cellular Neuroscience</i>, vol. 84, Academic
    Press, 2017, pp. 58–67, doi:<a href="https://doi.org/10.1016/j.mcn.2017.03.002">10.1016/j.mcn.2017.03.002</a>.'
  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
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. <i>Development</i>.
    2017;144:3917-3931. doi:<a href="https://doi.org/10.1242/dev.145698">10.1242/dev.145698</a>
  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. <i>Development</i>.
    Company of Biologists. <a href="https://doi.org/10.1242/dev.145698">https://doi.org/10.1242/dev.145698</a>
  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.”
    <i>Development</i>. Company of Biologists, 2017. <a href="https://doi.org/10.1242/dev.145698">https://doi.org/10.1242/dev.145698</a>.
  ieee: S. Pfurr <i>et al.</i>, “The E2A splice variant E47 regulates the differentiation
    of projection neurons via p57(KIP2) during cortical development,” <i>Development</i>,
    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.” <i>Development</i>,
    vol. 144, Company of Biologists, 2017, pp. 3917–31, doi:<a href="https://doi.org/10.1242/dev.145698">10.1242/dev.145698</a>.
  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'
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: '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:<a href="https://doi.org/10.5061/dryad.pk16b">10.5061/dryad.pk16b</a>'
  apa: 'Riccio, P., Cebrián, C., Zong, H., Hippenmeyer, S., &#38; Costantini, F. (2017).
    Data from: Ret and Etv4 promote directed movements of progenitor cells during
    renal branching morphogenesis. Dryad. <a href="https://doi.org/10.5061/dryad.pk16b">https://doi.org/10.5061/dryad.pk16b</a>'
  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. <a href="https://doi.org/10.5061/dryad.pk16b">https://doi.org/10.5061/dryad.pk16b</a>.'
  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, <a href="https://doi.org/10.5061/dryad.pk16b">10.5061/dryad.pk16b</a>.'
  mla: 'Riccio, Paul, et al. <i>Data from: Ret and Etv4 Promote Directed Movements
    of Progenitor Cells during Renal Branching Morphogenesis</i>. Dryad, 2017, doi:<a
    href="https://doi.org/10.5061/dryad.pk16b">10.5061/dryad.pk16b</a>.'
  short: P. Riccio, C. Cebrián, H. Zong, S. Hippenmeyer, F. Costantini, (2017).
date_created: 2021-07-23T09:39:34Z
date_published: 2017-01-14T00:00:00Z
date_updated: 2022-08-25T13:34:55Z
day: '14'
department:
- _id: SiHi
doi: 10.5061/dryad.pk16b
main_file_link:
- open_access: '1'
  url: https://doi.org/10.5061/dryad.pk16b
month: '01'
oa: 1
oa_version: Published Version
publisher: Dryad
related_material:
  record:
  - id: '9702'
    relation: used_in_publication
    status: deleted
status: public
title: 'Data from: Ret and Etv4 promote directed movements of progenitor cells during
  renal branching morphogenesis'
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2017'
...
---
_id: '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. <i>FEBS letters</i>. 2017;591(24):3993-4008. doi:<a href="https://doi.org/10.1002/1873-3468.12906">10.1002/1873-3468.12906</a>
  apa: Beattie, R. J., &#38; Hippenmeyer, S. (2017). Mechanisms of radial glia progenitor
    cell lineage progression. <i>FEBS Letters</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/1873-3468.12906">https://doi.org/10.1002/1873-3468.12906</a>
  chicago: Beattie, Robert J, and Simon Hippenmeyer. “Mechanisms of Radial Glia Progenitor
    Cell Lineage Progression.” <i>FEBS Letters</i>. Wiley-Blackwell, 2017. <a href="https://doi.org/10.1002/1873-3468.12906">https://doi.org/10.1002/1873-3468.12906</a>.
  ieee: R. J. Beattie and S. Hippenmeyer, “Mechanisms of radial glia progenitor cell
    lineage progression,” <i>FEBS letters</i>, 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.” <i>FEBS Letters</i>, vol. 591, no. 24, Wiley-Blackwell,
    2017, pp. 3993–4008, doi:<a href="https://doi.org/10.1002/1873-3468.12906">10.1002/1873-3468.12906</a>.
  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. <i>eLife</i>. 2017;6. doi:<a
    href="https://doi.org/10.7554/eLife.25125">10.7554/eLife.25125</a>
  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. <i>ELife</i>. eLife Sciences Publications. <a href="https://doi.org/10.7554/eLife.25125">https://doi.org/10.7554/eLife.25125</a>
  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.” <i>ELife</i>. eLife
    Sciences Publications, 2017. <a href="https://doi.org/10.7554/eLife.25125">https://doi.org/10.7554/eLife.25125</a>.
  ieee: D. Andergassen <i>et al.</i>, “Mapping the mouse Allelome reveals tissue specific
    regulation of allelic expression,” <i>eLife</i>, 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.” <i>ELife</i>, vol. 6, e25125, eLife Sciences
    Publications, 2017, doi:<a href="https://doi.org/10.7554/eLife.25125">10.7554/eLife.25125</a>.
  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. <i>Neuron</i>.
    2017;94(3):517-533.e3. doi:<a href="https://doi.org/10.1016/j.neuron.2017.04.012">10.1016/j.neuron.2017.04.012</a>
  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. <i>Neuron</i>. Cell
    Press. <a href="https://doi.org/10.1016/j.neuron.2017.04.012">https://doi.org/10.1016/j.neuron.2017.04.012</a>
  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.” <i>Neuron</i>.
    Cell Press, 2017. <a href="https://doi.org/10.1016/j.neuron.2017.04.012">https://doi.org/10.1016/j.neuron.2017.04.012</a>.
  ieee: R. J. Beattie <i>et al.</i>, “Mosaic analysis with double markers reveals
    distinct sequential functions of Lgl1 in neural stem cells,” <i>Neuron</i>, 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.” <i>Neuron</i>, vol. 94, no.
    3, Cell Press, 2017, p. 517–533.e3, doi:<a href="https://doi.org/10.1016/j.neuron.2017.04.012">10.1016/j.neuron.2017.04.012</a>.
  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. <i>Human Molecular Genetics</i>.
    2017;26(2):258-269. doi:<a href="https://doi.org/10.1093/hmg/ddw383">10.1093/hmg/ddw383</a>
  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. <i>Human Molecular Genetics</i>. Oxford University Press.
    <a href="https://doi.org/10.1093/hmg/ddw383">https://doi.org/10.1093/hmg/ddw383</a>
  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.” <i>Human Molecular Genetics</i>. Oxford
    University Press, 2017. <a href="https://doi.org/10.1093/hmg/ddw383">https://doi.org/10.1093/hmg/ddw383</a>.
  ieee: M. Breuss <i>et al.</i>, “Uner Tan syndrome caused by a homozygous TUBB2B
    mutation affecting microtubule stability,” <i>Human Molecular Genetics</i>, 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.” <i>Human Molecular Genetics</i>, vol. 26, no.
    2, Oxford University Press, 2017, pp. 258–69, doi:<a href="https://doi.org/10.1093/hmg/ddw383">10.1093/hmg/ddw383</a>.
  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. <i>Frontiers
    in Cellular Neuroscience</i>. 2017;11. doi:<a href="https://doi.org/10.3389/fncel.2017.00176">10.3389/fncel.2017.00176</a>
  apa: Hansen, A. H., Düllberg, C. F., Mieck, C., Loose, M., &#38; Hippenmeyer, S.
    (2017). Cell polarity in cerebral cortex development - cellular architecture shaped
    by biochemical networks. <i>Frontiers in Cellular Neuroscience</i>. Frontiers
    Research Foundation. <a href="https://doi.org/10.3389/fncel.2017.00176">https://doi.org/10.3389/fncel.2017.00176</a>
  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.” <i>Frontiers in Cellular Neuroscience</i>. Frontiers
    Research Foundation, 2017. <a href="https://doi.org/10.3389/fncel.2017.00176">https://doi.org/10.3389/fncel.2017.00176</a>.
  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,” <i>Frontiers in Cellular Neuroscience</i>, 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.” <i>Frontiers in Cellular Neuroscience</i>,
    vol. 11, 176, Frontiers Research Foundation, 2017, doi:<a href="https://doi.org/10.3389/fncel.2017.00176">10.3389/fncel.2017.00176</a>.
  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: 2026-05-12T22:30:52Z
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'
...
