---
OA_place: publisher
OA_type: green
_id: '6995'
abstract:
- lang: eng
text: Human brain organoids represent a powerful tool for the study of human neurological
diseases particularly those that impact brain growth and structure. However, many
neurological diseases lack obvious anatomical abnormalities, yet significantly
impact neural network functions, raising the question of whether organoids possess
sufficient neural network architecture and complexity to model these conditions.
Here, we explore the network level functions of brain organoids using calcium
sensor imaging and extracellular recording approaches that together reveal the
existence of complex oscillatory network behaviors reminiscent of intact brain
preparations. We further demonstrate strikingly abnormal epileptiform network
activity in organoids derived from a Rett Syndrome patient despite only modest
anatomical differences from isogenically matched controls, and rescue with an
unconventional neuromodulatory drug Pifithrin-α. Together, these findings provide
an essential foundation for the utilization of human brain organoids to study
intact and disordered human brain network formation and illustrate their utility
in therapeutic discovery.
acknowledgement: We thank S. Butler, T. Carmichael and members of the laboratory of
B.G.N. for helpful discussions and comments on the manuscript; N. Vishlaghi and
F. Turcios-Hernandez for technical assistance, and J. Lee, S.-K. Lee, H. Shinagawa
and K. Yoshikawa for valuable reagents. We also thank the UCLA Eli and Edythe Broad
Stem Cell Research Center (BSCRC) and Intellectual and Developmental Disabilities
Research Center microscopy cores for access to imaging facilities. This work was
supported by grants from the California Institute for Regenerative Medicine (CIRM)
(DISC1-08819 to B.G.N.), the National Institute of Health (R01NS089817, R01DA051897
and P50HD103557 to B.G.N.; K08NS119747 to R.A.S.; K99HD096105 to M.W.; R01MH123922,
R01MH121521 and P50HD103557 to M.J.G.; R01GM099134 to K.P.; R01NS103788 to W.E.L.;
R01NS088571 to J.M.P.; R01NS030549 and R01AG050474 to I.M.), and research awards
from the UCLA Jonsson Comprehensive Cancer Center and BSCRC Ablon Scholars Program
(to B.G.N.), the BSCRC Innovation Program (to B.G.N., K.P. and W.E.L.), the UCLA
BSCRC Steffy Brain Aging Research Fund (to B.G.N. and W.E.L.) and the UCLA Clinical
and Translational Science Institute (to B.G.N.), Paul Allen Family Foundation Frontiers
Group (to K.P. and W.E.L.), the March of Dimes Foundation (to W.E.L.) and the Simons
Foundation Autism Research Initiative Bridge to Independence Program (to R.A.S.
and M.J.G.). R.A.S. was also supported by the UCLA/NINDS Translational Neuroscience
Training Grant (R25NS065723), a Research and Training Fellowship from the American
Epilepsy Society, a Taking Flight Award from CURE Epilepsy and a Clinician Scientist
training award from the UCLA BSCRC. J.E.B. was supported by the UCLA BSCRC Rose
Hills Foundation Graduate Scholarship Training Program. M.W. was supported by postdoctoral
training awards provided by the UCLA BSCRC and the Uehara Memorial Foundation. O.A.M.
and A.K. were supported in part by the UCLA-California State University Northridge
CIRM-Bridges training program (EDUC2-08411). We also acknowledge the support of
the IDDRC Cells, Circuits and Systems Analysis, Microscopy and Genetics and Genomics
Cores of the Semel Institute of Neuroscience at UCLA, which are supported by the
NICHD (U54HD087101 and P50HD10355701). We lastly acknowledge support from a Quantitative
and Computational Biosciences Collaboratory Postdoctoral Fellowship to S.M. and
the Quantitative and Computational Biosciences Collaboratory community, directed
by M. Pellegrini.
article_processing_charge: No
article_type: review
author:
- first_name: Ranmal A.
full_name: Samarasinghe, Ranmal A.
last_name: Samarasinghe
- first_name: Osvaldo
full_name: Miranda, Osvaldo
id: 862A3C56-A8BF-11E9-B4FA-D9E3E5697425
last_name: Miranda
orcid: 0000-0001-6618-6889
- first_name: Jessie E.
full_name: Buth, Jessie E.
last_name: Buth
- first_name: Simon
full_name: Mitchell, Simon
last_name: Mitchell
- first_name: Isabella
full_name: Ferando, Isabella
last_name: Ferando
- first_name: Momoko
full_name: Watanabe, Momoko
last_name: Watanabe
- first_name: Arinnae
full_name: Kurdian, Arinnae
last_name: Kurdian
- first_name: Peyman
full_name: Golshani, Peyman
last_name: Golshani
- first_name: Kathrin
full_name: Plath, Kathrin
last_name: Plath
- first_name: William E.
full_name: Lowry, William E.
last_name: Lowry
- first_name: Jack M.
full_name: Parent, Jack M.
last_name: Parent
- first_name: Istvan
full_name: Mody, Istvan
last_name: Mody
- first_name: Bennett G.
full_name: Novitch, Bennett G.
last_name: Novitch
citation:
ama: Samarasinghe RA, Miranda O, Buth JE, et al. Identification of neural oscillations
and epileptiform changes in human brain organoids. Nature Neuroscience.
2021;24:32. doi:10.1038/s41593-021-00906-5
apa: Samarasinghe, R. A., Miranda, O., Buth, J. E., Mitchell, S., Ferando, I., Watanabe,
M., … Novitch, B. G. (2021). Identification of neural oscillations and epileptiform
changes in human brain organoids. Nature Neuroscience. Springer Nature.
https://doi.org/10.1038/s41593-021-00906-5
chicago: Samarasinghe, Ranmal A., Osvaldo Miranda, Jessie E. Buth, Simon Mitchell,
Isabella Ferando, Momoko Watanabe, Arinnae Kurdian, et al. “Identification of
Neural Oscillations and Epileptiform Changes in Human Brain Organoids.” Nature
Neuroscience. Springer Nature, 2021. https://doi.org/10.1038/s41593-021-00906-5.
ieee: R. A. Samarasinghe et al., “Identification of neural oscillations and
epileptiform changes in human brain organoids,” Nature Neuroscience, vol.
24. Springer Nature, p. 32, 2021.
ista: Samarasinghe RA, Miranda O, Buth JE, Mitchell S, Ferando I, Watanabe M, Kurdian
A, Golshani P, Plath K, Lowry WE, Parent JM, Mody I, Novitch BG. 2021. Identification
of neural oscillations and epileptiform changes in human brain organoids. Nature
Neuroscience. 24, 32.
mla: Samarasinghe, Ranmal A., et al. “Identification of Neural Oscillations and
Epileptiform Changes in Human Brain Organoids.” Nature Neuroscience, vol.
24, Springer Nature, 2021, p. 32, doi:10.1038/s41593-021-00906-5.
short: R.A. Samarasinghe, O. Miranda, J.E. Buth, S. Mitchell, I. Ferando, M. Watanabe,
A. Kurdian, P. Golshani, K. Plath, W.E. Lowry, J.M. Parent, I. Mody, B.G. Novitch,
Nature Neuroscience 24 (2021) 32.
date_created: 2019-11-10T11:23:58Z
date_published: 2021-08-23T00:00:00Z
date_updated: 2025-07-09T09:00:12Z
day: '23'
department:
- _id: GradSch
- _id: SiHi
doi: 10.1038/s41593-021-00906-5
external_id:
isi:
- '000687516300001'
pmid:
- '34426698 '
fulldoi: https://doi.org/10.1038/s41593-021-00906-5
intvolume: ' 24'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/820183
month: '08'
oa: 1
oa_version: Preprint
page: '32'
pmid: 1
publication: Nature Neuroscience
publication_identifier:
eissn:
- 1546-1726
issn:
- 1097-6256
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Identification of neural oscillations and epileptiform changes in human brain
organoids
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 24
year: '2021'
...
---
_id: '9906'
abstract:
- lang: eng
text: Endometriosis is a common gynecological disorder characterized by ectopic
growth of endometrium outside the uterus and is associated with chronic pain and
infertility. We investigated the role of the long intergenic noncoding RNA 01133
(LINC01133) in endometriosis, an lncRNA that has been implicated in several types
of cancer. We found that LINC01133 is upregulated in ectopic endometriotic lesions.
As expression appeared higher in the epithelial endometrial layer, we performed
a siRNA knockdown of LINC01133 in an endometriosis epithelial cell line. Phenotypic
assays indicated that LINC01133 may promote proliferation and suppress cellular
migration, and affect the cytoskeleton and morphology of the cells. Gene ontology
analysis of differentially expressed genes indicated that cell proliferation and
migration pathways were affected in line with the observed phenotype. We validated
upregulation of p21 and downregulation of Cyclin A at the protein level, which
together with the quantification of the DNA content using fluorescence-activated
cell sorting (FACS) analysis indicated that the observed effects on cellular proliferation
may be due to changes in cell cycle. Further, we found testis-specific protein
kinase 1 (TESK1) kinase upregulation corresponding with phosphorylation and inactivation
of actin severing protein Cofilin, which could explain changes in the cytoskeleton
and cellular migration. These results indicate that endometriosis is associated
with LINC01133 upregulation, which may affect pathogenesis via the cellular proliferation
and migration pathways.
acknowledgement: "Open access funding provided by Medical University of Vienna. The
authors would like to thank all the participants and health professionals involved
in the present study. We want to thank our technical assistants Barbara Widmar and
Matthias Witzmann-Stern for their diligent work and constant assistance. We would
like to thank Simon Hippenmeyer for access to\r\nbioinformatic infrastructure and
resources."
article_number: '8385'
article_processing_charge: Yes
article_type: original
author:
- first_name: Iveta
full_name: Yotova, Iveta
last_name: Yotova
- first_name: Quanah J.
full_name: Hudson, Quanah J.
last_name: Hudson
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Katharina
full_name: Proestling, Katharina
last_name: Proestling
- first_name: Isabella
full_name: Haslinger, Isabella
last_name: Haslinger
- first_name: Lorenz
full_name: Kuessel, Lorenz
last_name: Kuessel
- first_name: Alexandra
full_name: Perricos, Alexandra
last_name: Perricos
- first_name: Heinrich
full_name: Husslein, Heinrich
last_name: Husslein
- first_name: René
full_name: Wenzl, René
last_name: Wenzl
citation:
ama: Yotova I, Hudson QJ, Pauler F, et al. LINC01133 inhibits invasion and promotes
proliferation in an endometriosis epithelial cell line. International Journal
of Molecular Sciences. 2021;22(16). doi:10.3390/ijms22168385
apa: Yotova, I., Hudson, Q. J., Pauler, F., Proestling, K., Haslinger, I., Kuessel,
L., … Wenzl, R. (2021). LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line. International Journal of Molecular
Sciences. MDPI. https://doi.org/10.3390/ijms22168385
chicago: Yotova, Iveta, Quanah J. Hudson, Florian Pauler, Katharina Proestling,
Isabella Haslinger, Lorenz Kuessel, Alexandra Perricos, Heinrich Husslein, and
René Wenzl. “LINC01133 Inhibits Invasion and Promotes Proliferation in an Endometriosis
Epithelial Cell Line.” International Journal of Molecular Sciences. MDPI,
2021. https://doi.org/10.3390/ijms22168385.
ieee: I. Yotova et al., “LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line,” International Journal of Molecular
Sciences, vol. 22, no. 16. MDPI, 2021.
ista: Yotova I, Hudson QJ, Pauler F, Proestling K, Haslinger I, Kuessel L, Perricos
A, Husslein H, Wenzl R. 2021. LINC01133 inhibits invasion and promotes proliferation
in an endometriosis epithelial cell line. International Journal of Molecular Sciences.
22(16), 8385.
mla: Yotova, Iveta, et al. “LINC01133 Inhibits Invasion and Promotes Proliferation
in an Endometriosis Epithelial Cell Line.” International Journal of Molecular
Sciences, vol. 22, no. 16, 8385, MDPI, 2021, doi:10.3390/ijms22168385.
short: I. Yotova, Q.J. Hudson, F. Pauler, K. Proestling, I. Haslinger, L. Kuessel,
A. Perricos, H. Husslein, R. Wenzl, International Journal of Molecular Sciences
22 (2021).
date_created: 2021-08-15T22:01:27Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2025-06-12T06:29:07Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/ijms22168385
external_id:
isi:
- '000689147400001'
pmid:
- '34445100'
file:
- access_level: open_access
checksum: be7f0042607ca60549cb27513c19c6af
content_type: application/pdf
creator: asandaue
date_created: 2021-08-16T09:29:17Z
date_updated: 2021-08-16T09:29:17Z
file_id: '9922'
file_name: 2021_InternationalJournalOfMolecularSciences_Yotova.pdf
file_size: 2646018
relation: main_file
success: 1
file_date_updated: 2021-08-16T09:29:17Z
fulldoi: https://doi.org/10.3390/ijms22168385
has_accepted_license: '1'
intvolume: ' 22'
isi: 1
issue: '16'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
pmid: 1
publication: International Journal of Molecular Sciences
publication_identifier:
eissn:
- 1422-0067
issn:
- 1661-6596
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: LINC01133 inhibits invasion and promotes proliferation in an endometriosis
epithelial cell line
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: 22
year: '2021'
...
---
_id: '9082'
abstract:
- lang: eng
text: Acquired mutations are sufficiently frequent such that the genome of a single
cell offers a record of its history of cell divisions. Among more common somatic
genomic alterations are loss of heterozygosity (LOH). Large LOH events are potentially
detectable in single cell RNA sequencing (scRNA-seq) datasets as tracts of monoallelic
expression for constitutionally heterozygous single nucleotide variants (SNVs)
located among contiguous genes. We identified runs of monoallelic expression,
consistent with LOH, uniquely distributed throughout the genome in single cell
brain cortex transcriptomes of F1 hybrids involving different inbred mouse strains.
We then phylogenetically reconstructed single cell lineages and simultaneously
identified cell types by corresponding gene expression patterns. Our results are
consistent with progenitor cells giving rise to multiple cortical cell types through
stereotyped expansion and distinct waves of neurogenesis. Compared to engineered
recording systems, LOH events accumulate throughout the genome and across the
lifetime of an organism, affording tremendous capacity for encoding lineage information
and increasing resolution for later cell divisions. This approach can conceivably
be computationally incorporated into scRNA-seq analysis and may be useful for
organisms where genetic engineering is prohibitive, such as humans.
acknowledgement: "We thank Bill Bolosky, Microsoft Research, for earlier work showing
proof of concept in TCGA\r\nbulk RNA-seq data. Supported by the Paul G. Allen Frontiers
Group (University of Washington);\r\nNIH R00HG010152 (Dartmouth); and NÖ Forschung
und Bildung n[f+b] life science call grant\r\n(C13-002) to SH, and the European
Research Council (ERC) under the European Union’s\r\nHorizon 2020 research and innovation
program 725780 LinPro to SH."
article_processing_charge: No
author:
- first_name: Donovan J.
full_name: Anderson, Donovan J.
last_name: Anderson
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Aaron
full_name: McKenna, Aaron
last_name: McKenna
- first_name: Jay
full_name: Shendure, Jay
last_name: Shendure
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Marshall S.
full_name: Horwitz, Marshall S.
last_name: Horwitz
citation:
ama: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous
identification of brain cell type and lineage via single cell RNA sequencing.
bioRxiv. doi:10.1101/2020.12.31.425016
apa: Anderson, D. J., Pauler, F., McKenna, A., Shendure, J., Hippenmeyer, S., &
Horwitz, M. S. (n.d.). Simultaneous identification of brain cell type and lineage
via single cell RNA sequencing. bioRxiv. https://doi.org/10.1101/2020.12.31.425016
chicago: Anderson, Donovan J., Florian Pauler, Aaron McKenna, Jay Shendure, Simon
Hippenmeyer, and Marshall S. Horwitz. “Simultaneous Identification of Brain Cell
Type and Lineage via Single Cell RNA Sequencing.” BioRxiv, n.d. https://doi.org/10.1101/2020.12.31.425016.
ieee: D. J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, and M.
S. Horwitz, “Simultaneous identification of brain cell type and lineage via single
cell RNA sequencing,” bioRxiv. .
ista: Anderson DJ, Pauler F, McKenna A, Shendure J, Hippenmeyer S, Horwitz MS. Simultaneous
identification of brain cell type and lineage via single cell RNA sequencing.
bioRxiv, 10.1101/2020.12.31.425016.
mla: Anderson, Donovan J., et al. “Simultaneous Identification of Brain Cell Type
and Lineage via Single Cell RNA Sequencing.” BioRxiv, doi:10.1101/2020.12.31.425016.
short: D.J. Anderson, F. Pauler, A. McKenna, J. Shendure, S. Hippenmeyer, M.S. Horwitz,
BioRxiv (n.d.).
das_tickbox: '1'
date_created: 2021-02-04T07:23:23Z
date_published: 2021-01-01T00:00:00Z
date_updated: 2026-07-06T12:46:11Z
day: '01'
department:
- _id: SiHi
doi: 10.1101/2020.12.31.425016
ec_funded: 1
fulldoi: https://doi.org/10.1101/2020.12.31.425016
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.12.31.425016
month: '01'
oa: 1
oa_version: Preprint
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: bioRxiv
publication_status: submitted
status: public
title: Simultaneous identification of brain cell type and lineage via single cell
RNA sequencing
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2021'
...
---
OA_place: publisher
OA_type: free access
_id: '9793'
abstract:
- lang: eng
text: Astrocytes extensively infiltrate the neuropil to regulate critical aspects
of synaptic development and function. This process is regulated by transcellular
interactions between astrocytes and neurons via cell adhesion molecules. How astrocytes
coordinate developmental processes among one another to parse out the synaptic
neuropil and form non-overlapping territories is unknown. Here we identify a molecular
mechanism regulating astrocyte-astrocyte interactions during development to coordinate
astrocyte morphogenesis and gap junction coupling. We show that hepaCAM, a disease-linked,
astrocyte-enriched cell adhesion molecule, regulates astrocyte competition for
territory and morphological complexity in the developing mouse cortex. Furthermore,
conditional deletion of Hepacam from developing astrocytes significantly impairs
gap junction coupling between astrocytes and disrupts the balance between synaptic
excitation and inhibition. Mutations in HEPACAM cause megalencephalic leukoencephalopathy
with subcortical cysts in humans. Therefore, our findings suggest that disruption
of astrocyte self-organization mechanisms could be an underlying cause of neural
pathology.
acknowledgement: This work was supported by the National Institutes of Health (R01
DA047258 and R01 NS102237 to C.E., F32 NS100392 to K.T.B.) and the Holland-Trice
Brain Research Award (to C.E.). K.T.B. was supported by postdoctoral fellowships
from the Foerster-Bernstein Family and The Hartwell Foundation. The Hippenmeyer
lab was supported by the European Research Council (ERC) under the European Union’s
Horizon 2020 research and innovations program (725780 LinPro) to S.H. R.E. was supported
by Ministerio de Ciencia y Tecnología (RTI2018-093493-B-I00). We thank the Duke
Light Microscopy Core Facility, the Duke Transgenic Mouse Facility, Dr. U. Schulte
for assistance with proteomic experiments, and Dr. D. Silver for critical review
of the manuscript. Cartoon elements of figure panels were created using BioRender.com.
article_processing_charge: No
article_type: original
author:
- first_name: Katherine T.
full_name: Baldwin, Katherine T.
last_name: Baldwin
- first_name: Christabel X.
full_name: Tan, Christabel X.
last_name: Tan
- first_name: Samuel T.
full_name: Strader, Samuel T.
last_name: Strader
- first_name: Changyu
full_name: Jiang, Changyu
last_name: Jiang
- first_name: Justin T.
full_name: Savage, Justin T.
last_name: Savage
- first_name: Xabier
full_name: Elorza-Vidal, Xabier
last_name: Elorza-Vidal
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Thomas
full_name: Rülicke, Thomas
last_name: Rülicke
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Raúl
full_name: Estévez, Raúl
last_name: Estévez
- first_name: Ru-Rong
full_name: Ji, Ru-Rong
last_name: Ji
- first_name: Cagla
full_name: Eroglu, Cagla
last_name: Eroglu
citation:
ama: Baldwin KT, Tan CX, Strader ST, et al. HepaCAM controls astrocyte self-organization
and coupling. Neuron. 2021;109(15):2427-2442.e10. doi:10.1016/j.neuron.2021.05.025
apa: Baldwin, K. T., Tan, C. X., Strader, S. T., Jiang, C., Savage, J. T., Elorza-Vidal,
X., … Eroglu, C. (2021). HepaCAM controls astrocyte self-organization and coupling.
Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2021.05.025
chicago: Baldwin, Katherine T., Christabel X. Tan, Samuel T. Strader, Changyu Jiang,
Justin T. Savage, Xabier Elorza-Vidal, Ximena Contreras, et al. “HepaCAM Controls
Astrocyte Self-Organization and Coupling.” Neuron. Elsevier, 2021. https://doi.org/10.1016/j.neuron.2021.05.025.
ieee: K. T. Baldwin et al., “HepaCAM controls astrocyte self-organization
and coupling,” Neuron, vol. 109, no. 15. Elsevier, p. 2427–2442.e10, 2021.
ista: Baldwin KT, Tan CX, Strader ST, Jiang C, Savage JT, Elorza-Vidal X, Contreras
X, Rülicke T, Hippenmeyer S, Estévez R, Ji R-R, Eroglu C. 2021. HepaCAM controls
astrocyte self-organization and coupling. Neuron. 109(15), 2427–2442.e10.
mla: Baldwin, Katherine T., et al. “HepaCAM Controls Astrocyte Self-Organization
and Coupling.” Neuron, vol. 109, no. 15, Elsevier, 2021, p. 2427–2442.e10,
doi:10.1016/j.neuron.2021.05.025.
short: K.T. Baldwin, C.X. Tan, S.T. Strader, C. Jiang, J.T. Savage, X. Elorza-Vidal,
X. Contreras, T. Rülicke, S. Hippenmeyer, R. Estévez, R.-R. Ji, C. Eroglu, Neuron
109 (2021) 2427–2442.e10.
date_created: 2021-08-06T09:08:25Z
date_published: 2021-08-04T00:00:00Z
date_updated: 2026-07-28T12:30:05Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2021.05.025
ec_funded: 1
external_id:
isi:
- '000692851900010'
pmid:
- '34171291'
fulldoi: https://doi.org/10.1016/j.neuron.2021.05.025
intvolume: ' 109'
isi: 1
issue: '15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.neuron.2021.05.025
month: '08'
oa: 1
oa_version: Published Version
page: 2427-2442.e10
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
eissn:
- 1097-4199
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: HepaCAM controls astrocyte self-organization and coupling
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 109
year: '2021'
...
---
OA_place: publisher
_id: '9962'
abstract:
- lang: eng
text: The brain is one of the largest and most complex organs and it is composed
of billions of neurons that communicate together enabling e.g. consciousness.
The cerebral cortex is the largest site of neural integration in the central nervous
system. Concerted radial migration of newly born cortical projection neurons,
from their birthplace to their final position, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating radial neuronal
migration in vivo are however still unclear. Recent evidence suggests that distinct
signaling cues act cell-autonomously but differentially at certain steps during
the overall migration process. Moreover, functional analysis of genetic mosaics
(mutant neurons present in wild-type/heterozygote environment) using the MADM
(Mosaic Analysis with Double Markers) analyses in comparison to global knockout
also indicate a significant degree of non-cell-autonomous and/or community effects
in the control of cortical neuron migration. The interactions of cell-intrinsic
(cell-autonomous) and cell-extrinsic (non-cell-autonomous) components are largely
unknown. In part of this thesis work we established a MADM-based experimental
strategy for the quantitative analysis of cell-autonomous gene function versus
non-cell-autonomous and/or community effects. The direct comparison of mutant
neurons from the genetic mosaic (cell-autonomous) to mutant neurons in the conditional
and/or global knockout (cell-autonomous + non-cell-autonomous) allows to quantitatively
analyze non-cell-autonomous effects. Such analysis enable the high-resolution
analysis of projection neuron migration dynamics in distinct environments with
concomitant isolation of genomic and proteomic profiles. Using these experimental
paradigms and in combination with computational modeling we show and characterize
the nature of non-cell-autonomous effects to coordinate radial neuron migration.
Furthermore, this thesis discusses recent developments in neurodevelopment with
focus on neuronal polarization and non-cell-autonomous mechanisms in neuronal
migration.
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
citation:
ama: Hansen AH. Cell-autonomous gene function and non-cell-autonomous effects in
radial projection neuron migration. 2021. doi:10.15479/at:ista:9962
apa: Hansen, A. H. (2021). Cell-autonomous gene function and non-cell-autonomous
effects in radial projection neuron migration. Institute of Science and Technology
Austria. https://doi.org/10.15479/at:ista:9962
chicago: Hansen, Andi H. “Cell-Autonomous Gene Function and Non-Cell-Autonomous
Effects in Radial Projection Neuron Migration.” Institute of Science and Technology
Austria, 2021. https://doi.org/10.15479/at:ista:9962.
ieee: A. H. Hansen, “Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration,” Institute of Science and Technology Austria,
2021.
ista: Hansen AH. 2021. Cell-autonomous gene function and non-cell-autonomous effects
in radial projection neuron migration. Institute of Science and Technology Austria.
mla: Hansen, Andi H. Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration. Institute of Science and Technology
Austria, 2021, doi:10.15479/at:ista:9962.
short: A.H. Hansen, Cell-Autonomous Gene Function and Non-Cell-Autonomous Effects
in Radial Projection Neuron Migration, Institute of Science and Technology Austria,
2021.
corr_author: '1'
date_created: 2021-08-29T12:36:50Z
date_published: 2021-09-02T00:00:00Z
date_updated: 2026-04-08T07:19:09Z
day: '02'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: GradSch
- _id: SiHi
doi: 10.15479/at:ista:9962
file:
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checksum: 66b56f5b988b233dc66a4f4b4fb2cdfe
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date_created: 2021-08-30T09:17:39Z
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file_size: 10629190
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checksum: 204fa40321a1c6289b68c473634c4bf3
content_type: application/pdf
creator: ahansen
date_created: 2021-08-30T09:29:44Z
date_updated: 2022-09-03T22:30:04Z
embargo: 2022-09-02
file_id: '9972'
file_name: Thesis_Hansen_PDFA-1a.pdf
file_size: 13457469
relation: main_file
file_date_updated: 2022-09-03T22:30:04Z
fulldoi: https://doi.org/10.15479/at:ista:9962
has_accepted_license: '1'
keyword:
- Neuronal migration
- Non-cell-autonomous
- Cell-autonomous
- Neurodevelopmental disease
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: '182'
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '8569'
relation: part_of_dissertation
status: public
- id: '960'
relation: part_of_dissertation
status: public
status: public
supervisor:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
title: Cell-autonomous gene function and non-cell-autonomous effects in radial projection
neuron migration
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2021'
...
---
_id: '7593'
abstract:
- lang: eng
text: Heterozygous loss of human PAFAH1B1 (coding for LIS1) results in the disruption
of neurogenesis and neuronal migration via dysregulation of microtubule (MT) stability
and dynein motor function/localization that alters mitotic spindle orientation,
chromosomal segregation, and nuclear migration. Recently, human induced pluripotent
stem cell (iPSC) models revealed an important role for LIS1 in controlling the
length of terminal cell divisions of outer radial glial (oRG) progenitors, suggesting
cellular functions of LIS1 in regulating neural progenitor cell (NPC) daughter
cell separation. Here we examined the late mitotic stages NPCs in vivo and mouse
embryonic fibroblasts (MEFs) in vitro from Pafah1b1-deficient mutants. Pafah1b1-deficient
neocortical NPCs and MEFs similarly exhibited cleavage plane displacement with
mislocalization of furrow-associated markers, associated with actomyosin dysfunction
and cell membrane hyper-contractility. Thus, it suggests LIS1 acts as a key molecular
link connecting MTs/dynein and actomyosin, ensuring that cell membrane contractility
is tightly controlled to execute proper daughter cell separation.
article_number: '51512'
article_processing_charge: No
article_type: original
author:
- first_name: Hyang Mi
full_name: Moon, Hyang Mi
last_name: Moon
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Anthony
full_name: Wynshaw-Boris, Anthony
last_name: Wynshaw-Boris
citation:
ama: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. LIS1 determines cleavage plane
positioning by regulating actomyosin-mediated cell membrane contractility. eLife.
2020;9. doi:10.7554/elife.51512
apa: Moon, H. M., Hippenmeyer, S., Luo, L., & Wynshaw-Boris, A. (2020). LIS1
determines cleavage plane positioning by regulating actomyosin-mediated cell membrane
contractility. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.51512
chicago: Moon, Hyang Mi, Simon Hippenmeyer, Liqun Luo, and Anthony Wynshaw-Boris.
“LIS1 Determines Cleavage Plane Positioning by Regulating Actomyosin-Mediated
Cell Membrane Contractility.” ELife. eLife Sciences Publications, 2020.
https://doi.org/10.7554/elife.51512.
ieee: H. M. Moon, S. Hippenmeyer, L. Luo, and A. Wynshaw-Boris, “LIS1 determines
cleavage plane positioning by regulating actomyosin-mediated cell membrane contractility,”
eLife, vol. 9. eLife Sciences Publications, 2020.
ista: Moon HM, Hippenmeyer S, Luo L, Wynshaw-Boris A. 2020. LIS1 determines cleavage
plane positioning by regulating actomyosin-mediated cell membrane contractility.
eLife. 9, 51512.
mla: Moon, Hyang Mi, et al. “LIS1 Determines Cleavage Plane Positioning by Regulating
Actomyosin-Mediated Cell Membrane Contractility.” ELife, vol. 9, 51512,
eLife Sciences Publications, 2020, doi:10.7554/elife.51512.
short: H.M. Moon, S. Hippenmeyer, L. Luo, A. Wynshaw-Boris, ELife 9 (2020).
date_created: 2020-03-20T13:16:41Z
date_published: 2020-03-11T00:00:00Z
date_updated: 2023-08-18T07:06:31Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/elife.51512
external_id:
isi:
- '000522835800001'
pmid:
- '32159512'
file:
- access_level: open_access
checksum: 396ceb2dd10b102ef4e699666b9342c3
content_type: application/pdf
creator: dernst
date_created: 2020-09-24T07:03:20Z
date_updated: 2020-09-24T07:03:20Z
file_id: '8567'
file_name: 2020_elife_Moon.pdf
file_size: 15089438
relation: main_file
success: 1
file_date_updated: 2020-09-24T07:03:20Z
fulldoi: https://doi.org/10.7554/elife.51512
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/751958
month: '03'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_identifier:
issn:
- 2050-084X
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: LIS1 determines cleavage plane positioning by regulating actomyosin-mediated
cell membrane contractility
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2020'
...
---
_id: '7814'
abstract:
- lang: eng
text: 'Scientific research is to date largely restricted to wealthy laboratories
in developed nations due to the necessity of complex and expensive equipment.
This inequality limits the capacity of science to be used as a diplomatic channel.
Maker movements use open-source technologies including additive manufacturing
(3D printing) and laser cutting, together with low-cost computers for developing
novel products. This movement is setting the groundwork for a revolution, allowing
scientific equipment to be sourced at a fraction of the cost and has the potential
to increase the availability of equipment for scientists around the world. Science
education is increasingly recognized as another channel for science diplomacy.
In this perspective, we introduce the idea that the Maker movement and open-source
technologies have the potential to revolutionize science, technology, engineering
and mathematics (STEM) education worldwide. We present an open-source STEM didactic
tool called SCOPES (Sparking Curiosity through Open-source Platforms in Education
and Science). SCOPES is self-contained, independent of local resources, and cost-effective.
SCOPES can be adapted to communicate complex subjects from genetics to neurobiology,
perform real-world biological experiments and explore digitized scientific samples.
We envision such platforms will enhance science diplomacy by providing a means
for scientists to share their findings with classrooms and for educators to incorporate
didactic concepts into STEM lessons. By providing students the opportunity to
design, perform, and share scientific experiments, students also experience firsthand
the benefits of a multinational scientific community. We provide instructions
on how to build and use SCOPES on our webpage: http://scopeseducation.org.'
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
- _id: EM-Fac
article_number: '48'
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
citation:
ama: 'Beattie RJ, Hippenmeyer S, Pauler F. SCOPES: Sparking curiosity through Open-Source
platforms in education and science. Frontiers in Education. 2020;5. doi:10.3389/feduc.2020.00048'
apa: 'Beattie, R. J., Hippenmeyer, S., & Pauler, F. (2020). SCOPES: Sparking
curiosity through Open-Source platforms in education and science. Frontiers
in Education. Frontiers Media. https://doi.org/10.3389/feduc.2020.00048'
chicago: 'Beattie, Robert J, Simon Hippenmeyer, and Florian Pauler. “SCOPES: Sparking
Curiosity through Open-Source Platforms in Education and Science.” Frontiers
in Education. Frontiers Media, 2020. https://doi.org/10.3389/feduc.2020.00048.'
ieee: 'R. J. Beattie, S. Hippenmeyer, and F. Pauler, “SCOPES: Sparking curiosity
through Open-Source platforms in education and science,” Frontiers in Education,
vol. 5. Frontiers Media, 2020.'
ista: 'Beattie RJ, Hippenmeyer S, Pauler F. 2020. SCOPES: Sparking curiosity through
Open-Source platforms in education and science. Frontiers in Education. 5, 48.'
mla: 'Beattie, Robert J., et al. “SCOPES: Sparking Curiosity through Open-Source
Platforms in Education and Science.” Frontiers in Education, vol. 5, 48,
Frontiers Media, 2020, doi:10.3389/feduc.2020.00048.'
short: R.J. Beattie, S. Hippenmeyer, F. Pauler, Frontiers in Education 5 (2020).
corr_author: '1'
date_created: 2020-05-11T08:18:48Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2024-10-22T10:46:38Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/feduc.2020.00048
ec_funded: 1
file:
- access_level: open_access
checksum: a24ec24e38d843341ae620ec76c53688
content_type: application/pdf
creator: dernst
date_created: 2020-05-11T11:34:08Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7818'
file_name: 2020_FrontiersEduc_Beattie.pdf
file_size: 1402146
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
fulldoi: https://doi.org/10.3389/feduc.2020.00048
has_accepted_license: '1'
intvolume: ' 5'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Frontiers in Education
publication_identifier:
issn:
- 2504-284X
publication_status: published
publisher: Frontiers Media
quality_controlled: '1'
scopus_import: '1'
status: public
title: 'SCOPES: Sparking curiosity through Open-Source platforms in education and
science'
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2020'
...
---
_id: '8093'
abstract:
- lang: eng
text: "Background: The activation of the EGFR/Ras-signalling pathway in tumour cells
induces a distinct chemokine repertoire, which in turn modulates the tumour microenvironment.\r\nMethods:
The effects of EGFR/Ras on the expression and translation of CCL20 were analysed
in a large set of epithelial cancer cell lines and tumour tissues by RT-qPCR and
ELISA in vitro. CCL20 production was verified by immunohistochemistry in different
tumour tissues and correlated with clinical data. The effects of CCL20 on endothelial
cell migration and tumour-associated vascularisation were comprehensively analysed
with chemotaxis assays in vitro and in CCR6-deficient mice in vivo.\r\nResults:
Tumours facilitate progression by the EGFR/Ras-induced production of CCL20. Expression
of the chemokine CCL20 in tumours correlates with advanced tumour stage, increased
lymph node metastasis and decreased survival in patients. Microvascular endothelial
cells abundantly express the specific CCL20 receptor CCR6. CCR6 signalling in
endothelial cells induces angiogenesis. CCR6-deficient mice show significantly
decreased tumour growth and tumour-associated vascularisation. The observed phenotype
is dependent on CCR6 deficiency in stromal cells but not within the immune system.\r\nConclusion:
We propose that the chemokine axis CCL20–CCR6 represents a novel and promising
target to interfere with the tumour microenvironment, and opens an innovative
multimodal strategy for cancer therapy."
acknowledgement: "The authors would like to thank A. van Lierop for technical assistance.
In addition, we thank C. Dullin, J. Missbach-Güntner and S. Greco for advice and
assistance with fpVCT imaging. Furthermore, the authors would like to thank H. K.
Horst for advice on performing matrigel plug assays. This study has also been partially
presented in A. Schorr’s doctoral thesis and the funding report of the SPP 1190
‘The tumor-vessel interface’ of the ‘Deutsche Forschungsgemeinschaft’ (DFG).\r\nThis
project was funded by the SPP 1190 “The tumor-vessel interface” and HO 2092/8-1
of the ‘Deutsche Forschungsgemeinschaft’ (DFG) to B. Homey. In addition, it was
supported by grants from the Austrian Science Fund (FWF, W1212 to N. Amberg and
J. Klufa and I4300-B to T. Bauer), the WWTF project LS16-025 and the European Research
Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883) to M. Sibilia."
article_processing_charge: No
article_type: original
author:
- first_name: Andreas
full_name: Hippe, Andreas
last_name: Hippe
- first_name: Stephan Alexander
full_name: Braun, Stephan Alexander
last_name: Braun
- first_name: Péter
full_name: Oláh, Péter
last_name: Oláh
- first_name: Peter Arne
full_name: Gerber, Peter Arne
last_name: Gerber
- first_name: Anne
full_name: Schorr, Anne
last_name: Schorr
- first_name: Stephan
full_name: Seeliger, Stephan
last_name: Seeliger
- first_name: Stephanie
full_name: Holtz, Stephanie
last_name: Holtz
- first_name: Katharina
full_name: Jannasch, Katharina
last_name: Jannasch
- first_name: Andor
full_name: Pivarcsi, Andor
last_name: Pivarcsi
- first_name: Bettina
full_name: Buhren, Bettina
last_name: Buhren
- first_name: Holger
full_name: Schrumpf, Holger
last_name: Schrumpf
- first_name: Andreas
full_name: Kislat, Andreas
last_name: Kislat
- first_name: Erich
full_name: Bünemann, Erich
last_name: Bünemann
- first_name: Martin
full_name: Steinhoff, Martin
last_name: Steinhoff
- first_name: Jens
full_name: Fischer, Jens
last_name: Fischer
- first_name: Sérgio A.
full_name: Lira, Sérgio A.
last_name: Lira
- first_name: Petra
full_name: Boukamp, Petra
last_name: Boukamp
- first_name: Peter
full_name: Hevezi, Peter
last_name: Hevezi
- first_name: Nikolas Hendrik
full_name: Stoecklein, Nikolas Hendrik
last_name: Stoecklein
- first_name: Thomas
full_name: Hoffmann, Thomas
last_name: Hoffmann
- first_name: Frauke
full_name: Alves, Frauke
last_name: Alves
- first_name: Jonathan
full_name: Sleeman, Jonathan
last_name: Sleeman
- first_name: Thomas
full_name: Bauer, Thomas
last_name: Bauer
- first_name: Jörg
full_name: Klufa, Jörg
last_name: Klufa
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
- first_name: Albert
full_name: Zlotnik, Albert
last_name: Zlotnik
- first_name: Anja
full_name: Müller-Homey, Anja
last_name: Müller-Homey
- first_name: Bernhard
full_name: Homey, Bernhard
last_name: Homey
citation:
ama: Hippe A, Braun SA, Oláh P, et al. EGFR/Ras-induced CCL20 production modulates
the tumour microenvironment. British Journal of Cancer. 2020;123:942-954.
doi:10.1038/s41416-020-0943-2
apa: Hippe, A., Braun, S. A., Oláh, P., Gerber, P. A., Schorr, A., Seeliger, S.,
… Homey, B. (2020). EGFR/Ras-induced CCL20 production modulates the tumour microenvironment.
British Journal of Cancer. Springer Nature. https://doi.org/10.1038/s41416-020-0943-2
chicago: Hippe, Andreas, Stephan Alexander Braun, Péter Oláh, Peter Arne Gerber,
Anne Schorr, Stephan Seeliger, Stephanie Holtz, et al. “EGFR/Ras-Induced CCL20
Production Modulates the Tumour Microenvironment.” British Journal of Cancer.
Springer Nature, 2020. https://doi.org/10.1038/s41416-020-0943-2.
ieee: A. Hippe et al., “EGFR/Ras-induced CCL20 production modulates the tumour
microenvironment,” British Journal of Cancer, vol. 123. Springer Nature,
pp. 942–954, 2020.
ista: Hippe A, Braun SA, Oláh P, Gerber PA, Schorr A, Seeliger S, Holtz S, Jannasch
K, Pivarcsi A, Buhren B, Schrumpf H, Kislat A, Bünemann E, Steinhoff M, Fischer
J, Lira SA, Boukamp P, Hevezi P, Stoecklein NH, Hoffmann T, Alves F, Sleeman J,
Bauer T, Klufa J, Amberg N, Sibilia M, Zlotnik A, Müller-Homey A, Homey B. 2020.
EGFR/Ras-induced CCL20 production modulates the tumour microenvironment. British
Journal of Cancer. 123, 942–954.
mla: Hippe, Andreas, et al. “EGFR/Ras-Induced CCL20 Production Modulates the Tumour
Microenvironment.” British Journal of Cancer, vol. 123, Springer Nature,
2020, pp. 942–54, doi:10.1038/s41416-020-0943-2.
short: A. Hippe, S.A. Braun, P. Oláh, P.A. Gerber, A. Schorr, S. Seeliger, S. Holtz,
K. Jannasch, A. Pivarcsi, B. Buhren, H. Schrumpf, A. Kislat, E. Bünemann, M. Steinhoff,
J. Fischer, S.A. Lira, P. Boukamp, P. Hevezi, N.H. Stoecklein, T. Hoffmann, F.
Alves, J. Sleeman, T. Bauer, J. Klufa, N. Amberg, M. Sibilia, A. Zlotnik, A. Müller-Homey,
B. Homey, British Journal of Cancer 123 (2020) 942–954.
date_created: 2020-07-05T22:00:46Z
date_published: 2020-09-15T00:00:00Z
date_updated: 2023-08-22T07:51:12Z
day: '15'
ddc:
- '610'
department:
- _id: SiHi
doi: 10.1038/s41416-020-0943-2
external_id:
isi:
- '000544152500001'
pmid:
- '32601464'
file:
- access_level: open_access
checksum: 05a8e65d49c3f5b8e37ac4afe68287e2
content_type: application/pdf
creator: cchlebak
date_created: 2021-12-02T12:35:12Z
date_updated: 2021-12-02T12:35:12Z
file_id: '10398'
file_name: 2020_BrJournalCancer_Hippe.pdf
file_size: 3620691
relation: main_file
success: 1
file_date_updated: 2021-12-02T12:35:12Z
fulldoi: https://doi.org/10.1038/s41416-020-0943-2
has_accepted_license: '1'
intvolume: ' 123'
isi: 1
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 942-954
pmid: 1
publication: British Journal of Cancer
publication_identifier:
eissn:
- 1532-1827
issn:
- 0007-0920
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- relation: erratum
url: https://doi.org/10.1038/s41416-021-01563-y
record:
- id: '10170'
relation: later_version
status: deleted
scopus_import: '1'
status: public
title: EGFR/Ras-induced CCL20 production modulates the tumour microenvironment
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: 123
year: '2020'
...
---
_id: '8162'
abstract:
- lang: eng
text: In mammalian genomes, a subset of genes is regulated by genomic imprinting,
resulting in silencing of one parental allele. Imprinting is essential for cerebral
cortex development, but prevalence and functional impact in individual cells is
unclear. Here, we determined allelic expression in cortical cell types and established
a quantitative platform to interrogate imprinting in single cells. We created
cells with uniparental chromosome disomy (UPD) containing two copies of either
the maternal or the paternal chromosome; hence, imprinted genes will be 2-fold
overexpressed or not expressed. By genetic labeling of UPD, we determined cellular
phenotypes and transcriptional responses to deregulated imprinted gene expression
at unprecedented single-cell resolution. We discovered an unexpected degree of
cell-type specificity and a novel function of imprinting in the regulation of
cortical astrocyte survival. More generally, our results suggest functional relevance
of imprinted gene expression in glial astrocyte lineage and thus for generating
cortical cell-type diversity.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
acknowledgement: We thank A. Heger (IST Austria Preclinical Facility), A. Sommer and
C. Czepe (VBCF GmbH, NGS Unit), and A. Seitz and P. Moll (Lexogen GmbH) for technical
support; G. Arque, S. Resch, C. Igler, C. Dotter, C. Yahya, Q. Hudson, and D. Andergassen
for initial experiments and/or assistance; D. Barlow, O. Bell, and all members of
the Hippenmeyer lab for discussion; and N. Barton, B. Vicoso, M. Sixt, and L. Luo
for comments on earlier versions of the manuscript. This research was supported
by the Scientific Service Units (SSU) of IST Austria through resources provided
by the Bioimaging Facilities (BIF), Life Science Facilities (LSF), and Preclinical
Facilities (PCF). A.H.H. is a recipient of a DOC fellowship (24812) of the Austrian
Academy of Sciences. N.A. received support from the FWF Firnberg-Programm (T 1031).
R.B. received support from the FWF Meitner-Programm (M 2416). This work was also
supported by IST Austria institutional funds; a NÖ Forschung und Bildung n[f+b]
life science call grant (C13-002) to S.H.; a program grant from the Human Frontiers
Science Program (RGP0053/2014) to S.H.; the People Programme (Marie Curie Actions)
of the European Union’s Seventh Framework Programme (FP7/2007-2013) under REA grant
agreement 618444 to S.H.; and the European Research Council (ERC) under the European
Union’s Horizon 2020 research and innovation program (grant agreement 725780 LinPro)
to S.H.
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Thomas
full_name: Penz, Thomas
last_name: Penz
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
orcid: 0000-0001-6091-3088
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Pauler F, Beattie RJ, et al. Cell-type specificity of genomic imprinting
in cerebral cortex. Neuron. 2020;107(6):1160-1179.e9. doi:10.1016/j.neuron.2020.06.031
apa: Laukoter, S., Pauler, F., Beattie, R. J., Amberg, N., Hansen, A. H., Streicher,
C., … Hippenmeyer, S. (2020). Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2020.06.031
chicago: Laukoter, Susanne, Florian Pauler, Robert J Beattie, Nicole Amberg, Andi
H Hansen, Carmen Streicher, Thomas Penz, Christoph Bock, and Simon Hippenmeyer.
“Cell-Type Specificity of Genomic Imprinting in Cerebral Cortex.” Neuron.
Elsevier, 2020. https://doi.org/10.1016/j.neuron.2020.06.031.
ieee: S. Laukoter et al., “Cell-type specificity of genomic imprinting in
cerebral cortex,” Neuron, vol. 107, no. 6. Elsevier, p. 1160–1179.e9, 2020.
ista: Laukoter S, Pauler F, Beattie RJ, Amberg N, Hansen AH, Streicher C, Penz T,
Bock C, Hippenmeyer S. 2020. Cell-type specificity of genomic imprinting in cerebral
cortex. Neuron. 107(6), 1160–1179.e9.
mla: Laukoter, Susanne, et al. “Cell-Type Specificity of Genomic Imprinting in Cerebral
Cortex.” Neuron, vol. 107, no. 6, Elsevier, 2020, p. 1160–1179.e9, doi:10.1016/j.neuron.2020.06.031.
short: S. Laukoter, F. Pauler, R.J. Beattie, N. Amberg, A.H. Hansen, C. Streicher,
T. Penz, C. Bock, S. Hippenmeyer, Neuron 107 (2020) 1160–1179.e9.
corr_author: '1'
date_created: 2020-07-23T16:03:12Z
date_published: 2020-09-23T00:00:00Z
date_updated: 2025-06-12T07:19:46Z
day: '23'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.neuron.2020.06.031
ec_funded: 1
external_id:
isi:
- '000579698700006'
pmid:
- '32707083'
file:
- access_level: open_access
checksum: 7becdc16a6317304304631087ae7dd7f
content_type: application/pdf
creator: dernst
date_created: 2020-12-02T09:26:46Z
date_updated: 2020-12-02T09:26:46Z
file_id: '8828'
file_name: 2020_Neuron_Laukoter.pdf
file_size: 8911830
relation: main_file
success: 1
file_date_updated: 2020-12-02T09:26:46Z
fulldoi: https://doi.org/10.1016/j.neuron.2020.06.031
has_accepted_license: '1'
intvolume: ' 107'
isi: 1
issue: '6'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 1160-1179.e9
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T01031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Neuron
publication_identifier:
issn:
- 0896-6273
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Website
relation: press_release
url: https://ist.ac.at/en/news/cells-react-differently-to-genomic-imprinting/
scopus_import: '1'
status: public
title: Cell-type specificity of genomic imprinting in cerebral cortex
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 107
year: '2020'
...
---
_id: '8592'
abstract:
- lang: eng
text: Glioblastoma is the most malignant cancer in the brain and currently incurable.
It is urgent to identify effective targets for this lethal disease. Inhibition
of such targets should suppress the growth of cancer cells and, ideally also precancerous
cells for early prevention, but minimally affect their normal counterparts. Using
genetic mouse models with neural stem cells (NSCs) or oligodendrocyte precursor
cells (OPCs) as the cells‐of‐origin/mutation, it is shown that the susceptibility
of cells within the development hierarchy of glioma to the knockout of insulin‐like
growth factor I receptor (IGF1R) is determined not only by their oncogenic states,
but also by their cell identities/states. Knockout of IGF1R selectively disrupts
the growth of mutant and transformed, but not normal OPCs, or NSCs. The desirable
outcome of IGF1R knockout on cell growth requires the mutant cells to commit to
the OPC identity regardless of its development hierarchical status. At the molecular
level, oncogenic mutations reprogram the cellular network of OPCs and force them
to depend more on IGF1R for their growth. A new‐generation brain‐penetrable, orally
available IGF1R inhibitor harnessing tumor OPCs in the brain is also developed.
The findings reveal the cellular window of IGF1R targeting and establish IGF1R
as an effective target for the prevention and treatment of glioblastoma.
acknowledgement: The authors thank Drs. J. Eisen, QR. Lu, S. Duan, Z‐H. Li, W. Mo,
and Q. Wu for their critical comments on the manuscript. They also thank Dr. H.
Zong for providing the CKO_NG2‐CreER model. This work is supported by the National
Key Research and Development Program of China, Stem Cell and Translational Research
(2016YFA0101201 to C.L., 2016YFA0100303 to Y.J.W.), the National Natural Science
Foundation of China (81673035 and 81972915 to C.L., 81472722 to Y.J.W.), the Science
Foundation for Distinguished Young Scientists of Zhejiang Province (LR17H160001
to C.L.), Fundamental Research Funds for the Central Universities (2016QNA7023 and
2017QNA7028 to C.L.) and the Thousand Talent Program for Young Outstanding Scientists,
China (to C.L.), IST Austria institutional funds (to S.H.), European Research Council
(ERC) under the European Union's Horizon 2020 research and innovation programme
(725780 LinPro to S.H.). C.L. is a scholar of K. C. Wong Education Foundation.
article_number: '2001724'
article_processing_charge: No
article_type: original
author:
- first_name: Anhao
full_name: Tian, Anhao
last_name: Tian
- first_name: Bo
full_name: Kang, Bo
last_name: Kang
- first_name: Baizhou
full_name: Li, Baizhou
last_name: Li
- first_name: Biying
full_name: Qiu, Biying
last_name: Qiu
- first_name: Wenhong
full_name: Jiang, Wenhong
last_name: Jiang
- first_name: Fangjie
full_name: Shao, Fangjie
last_name: Shao
- first_name: Qingqing
full_name: Gao, Qingqing
last_name: Gao
- first_name: Rui
full_name: Liu, Rui
last_name: Liu
- first_name: Chengwei
full_name: Cai, Chengwei
last_name: Cai
- first_name: Rui
full_name: Jing, Rui
last_name: Jing
- first_name: Wei
full_name: Wang, Wei
last_name: Wang
- first_name: Pengxiang
full_name: Chen, Pengxiang
last_name: Chen
- first_name: Qinghui
full_name: Liang, Qinghui
last_name: Liang
- first_name: Lili
full_name: Bao, Lili
last_name: Bao
- first_name: Jianghong
full_name: Man, Jianghong
last_name: Man
- first_name: Yan
full_name: Wang, Yan
last_name: Wang
- first_name: Yu
full_name: Shi, Yu
last_name: Shi
- first_name: Jin
full_name: Li, Jin
last_name: Li
- first_name: Minmin
full_name: Yang, Minmin
last_name: Yang
- first_name: Lisha
full_name: Wang, Lisha
last_name: Wang
- first_name: Jianmin
full_name: Zhang, Jianmin
last_name: Zhang
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Junming
full_name: Zhu, Junming
last_name: Zhu
- first_name: Xiuwu
full_name: Bian, Xiuwu
last_name: Bian
- first_name: Ying‐Jie
full_name: Wang, Ying‐Jie
last_name: Wang
- first_name: Chong
full_name: Liu, Chong
last_name: Liu
citation:
ama: Tian A, Kang B, Li B, et al. Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting. Advanced Science. 2020;7(21). doi:10.1002/advs.202001724
apa: Tian, A., Kang, B., Li, B., Qiu, B., Jiang, W., Shao, F., … Liu, C. (2020).
Oncogenic state and cell identity combinatorially dictate the susceptibility of
cells within glioma development hierarchy to IGF1R targeting. Advanced Science.
Wiley. https://doi.org/10.1002/advs.202001724
chicago: Tian, Anhao, Bo Kang, Baizhou Li, Biying Qiu, Wenhong Jiang, Fangjie Shao,
Qingqing Gao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science. Wiley, 2020. https://doi.org/10.1002/advs.202001724.
ieee: A. Tian et al., “Oncogenic state and cell identity combinatorially
dictate the susceptibility of cells within glioma development hierarchy to IGF1R
targeting,” Advanced Science, vol. 7, no. 21. Wiley, 2020.
ista: Tian A, Kang B, Li B, Qiu B, Jiang W, Shao F, Gao Q, Liu R, Cai C, Jing R,
Wang W, Chen P, Liang Q, Bao L, Man J, Wang Y, Shi Y, Li J, Yang M, Wang L, Zhang
J, Hippenmeyer S, Zhu J, Bian X, Wang Y, Liu C. 2020. Oncogenic state and cell
identity combinatorially dictate the susceptibility of cells within glioma development
hierarchy to IGF1R targeting. Advanced Science. 7(21), 2001724.
mla: Tian, Anhao, et al. “Oncogenic State and Cell Identity Combinatorially Dictate
the Susceptibility of Cells within Glioma Development Hierarchy to IGF1R Targeting.”
Advanced Science, vol. 7, no. 21, 2001724, Wiley, 2020, doi:10.1002/advs.202001724.
short: A. Tian, B. Kang, B. Li, B. Qiu, W. Jiang, F. Shao, Q. Gao, R. Liu, C. Cai,
R. Jing, W. Wang, P. Chen, Q. Liang, L. Bao, J. Man, Y. Wang, Y. Shi, J. Li, M.
Yang, L. Wang, J. Zhang, S. Hippenmeyer, J. Zhu, X. Bian, Y. Wang, C. Liu, Advanced
Science 7 (2020).
date_created: 2020-10-01T09:44:13Z
date_published: 2020-11-04T00:00:00Z
date_updated: 2025-06-12T06:59:38Z
day: '04'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1002/advs.202001724
ec_funded: 1
external_id:
isi:
- '000573860700001'
pmid:
- '33173731'
file:
- access_level: open_access
checksum: 92818c23ecc70e35acfa671f3cfb9909
content_type: application/pdf
creator: dernst
date_created: 2020-12-10T14:07:24Z
date_updated: 2020-12-10T14:07:24Z
file_id: '8938'
file_name: 2020_AdvScience_Tian.pdf
file_size: 7835833
relation: main_file
success: 1
file_date_updated: 2020-12-10T14:07:24Z
fulldoi: https://doi.org/10.1002/advs.202001724
has_accepted_license: '1'
intvolume: ' 7'
isi: 1
issue: '21'
keyword:
- General Engineering
- General Physics and Astronomy
- General Materials Science
- Medicine (miscellaneous)
- General Chemical Engineering
- Biochemistry
- Genetics and Molecular Biology (miscellaneous)
language:
- iso: eng
month: '11'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Advanced Science
publication_identifier:
issn:
- 2198-3844
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Oncogenic state and cell identity combinatorially dictate the susceptibility
of cells within glioma development hierarchy to IGF1R targeting
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 7
year: '2020'
...
---
_id: '8949'
abstract:
- lang: eng
text: Development of the nervous system undergoes important transitions,
including one from neurogenesis to gliogenesis which occurs late during embryonic
gestation. Here we report on clonal analysis of gliogenesis in mice using Mosaic
Analysis with Double Markers (MADM) with quantitative and computational methods.
Results reveal that developmental gliogenesis in the cerebral cortex occurs in
a fraction of earlier neurogenic clones, accelerating around E16.5, and giving
rise to both astrocytes and oligodendrocytes. Moreover, MADM-based genetic deletion
of the epidermal growth factor receptor (Egfr) in gliogenic clones revealed that
Egfr is cell autonomously required for gliogenesis in the mouse dorsolateral cortices.
A broad range in the proliferation capacity, symmetry of clones, and competitive
advantage of MADM cells was evident in clones that contained one cellular lineage
with double dosage of Egfr relative to their environment, while their sibling
Egfr-null cells failed to generate glia. Remarkably, the total numbers of glia
in MADM clones balance out regardless of significant alterations in clonal symmetries.
The variability in glial clones shows stochastic patterns that we define mathematically,
which are different from the deterministic patterns in neuronal clones. This study
sets a foundation for studying the biological significance of stochastic and deterministic
clonal principles underlying tissue development, and identifying mechanisms that
differentiate between neurogenesis and gliogenesis.
acknowledgement: This research was funded by grants from the National Institutes of
Health to H.T.G. (R01NS098370 and R01NS089795). C.V.M. was supported by a National
Science Foundation Graduate Research Fellowship (DGE-1746939). R.B. was supported
by the FWF Lise-Meitner program (M 2416), and S.H. was supported by the European
Research Council (ERC) under the European Union’s Horizon 2020 research and innovation
programme (grant agreement No 725780 LinPro).The authors thank members of the Ghashghaei
lab for discussions, technical support, and help with preparation of the manuscript.
article_number: '2662'
article_processing_charge: No
article_type: original
author:
- first_name: Xuying
full_name: Zhang, Xuying
last_name: Zhang
- first_name: Christine V.
full_name: Mennicke, Christine V.
last_name: Mennicke
- first_name: Guanxi
full_name: Xiao, Guanxi
last_name: Xiao
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Mansoor
full_name: Haider, Mansoor
last_name: Haider
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: H. Troy
full_name: Ghashghaei, H. Troy
last_name: Ghashghaei
citation:
ama: Zhang X, Mennicke CV, Xiao G, et al. Clonal analysis of gliogenesis in the
cerebral cortex reveals stochastic expansion of glia and cell autonomous responses
to Egfr dosage. Cells. 2020;9(12). doi:10.3390/cells9122662
apa: Zhang, X., Mennicke, C. V., Xiao, G., Beattie, R. J., Haider, M., Hippenmeyer,
S., & Ghashghaei, H. T. (2020). Clonal analysis of gliogenesis in the cerebral
cortex reveals stochastic expansion of glia and cell autonomous responses to Egfr
dosage. Cells. MDPI. https://doi.org/10.3390/cells9122662
chicago: Zhang, Xuying, Christine V. Mennicke, Guanxi Xiao, Robert J Beattie, Mansoor
Haider, Simon Hippenmeyer, and H. Troy Ghashghaei. “Clonal Analysis of Gliogenesis
in the Cerebral Cortex Reveals Stochastic Expansion of Glia and Cell Autonomous
Responses to Egfr Dosage.” Cells. MDPI, 2020. https://doi.org/10.3390/cells9122662.
ieee: X. Zhang et al., “Clonal analysis of gliogenesis in the cerebral cortex
reveals stochastic expansion of glia and cell autonomous responses to Egfr dosage,”
Cells, vol. 9, no. 12. MDPI, 2020.
ista: Zhang X, Mennicke CV, Xiao G, Beattie RJ, Haider M, Hippenmeyer S, Ghashghaei
HT. 2020. Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic
expansion of glia and cell autonomous responses to Egfr dosage. Cells. 9(12),
2662.
mla: Zhang, Xuying, et al. “Clonal Analysis of Gliogenesis in the Cerebral Cortex
Reveals Stochastic Expansion of Glia and Cell Autonomous Responses to Egfr Dosage.”
Cells, vol. 9, no. 12, 2662, MDPI, 2020, doi:10.3390/cells9122662.
short: X. Zhang, C.V. Mennicke, G. Xiao, R.J. Beattie, M. Haider, S. Hippenmeyer,
H.T. Ghashghaei, Cells 9 (2020).
date_created: 2020-12-14T08:04:03Z
date_published: 2020-12-11T00:00:00Z
date_updated: 2025-06-12T07:02:43Z
day: '11'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3390/cells9122662
ec_funded: 1
external_id:
isi:
- '000601787300001'
pmid:
- '33322301'
file:
- access_level: open_access
checksum: 5095cbdc728c9a510c5761cf60a8861c
content_type: application/pdf
creator: dernst
date_created: 2020-12-14T08:09:43Z
date_updated: 2020-12-14T08:09:43Z
file_id: '8950'
file_name: 2020_Cells_Zhang.pdf
file_size: 3504525
relation: main_file
success: 1
file_date_updated: 2020-12-14T08:09:43Z
fulldoi: https://doi.org/10.3390/cells9122662
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Cells
publication_identifier:
issn:
- 2073-4409
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: Clonal analysis of gliogenesis in the cerebral cortex reveals stochastic expansion
of glia and cell autonomous responses to Egfr dosage
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 9
year: '2020'
...
---
_id: '8978'
abstract:
- lang: eng
text: "Mosaic analysis with double markers (MADM) technology enables concomitant
fluorescent cell labeling and induction of uniparental chromosome disomy (UPD)
with single-cell resolution. In UPD, imprinted genes are either overexpressed
2-fold or are not expressed. Here, the MADM platform is utilized to probe imprinting
phenotypes at the transcriptional level. This protocol highlights major steps
for the generation and isolation of projection neurons and astrocytes with MADM-induced
UPD from mouse cerebral cortex for downstream single-cell and low-input sample
RNA-sequencing experiments.\r\n\r\nFor complete details on the use and execution
of this protocol, please refer to Laukoter et al. (2020b)."
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: This research was supported by the Scientific Service Units (SSU)
at IST Austria through resources provided by the Bioimaging (BIF) and Preclinical
Facilities (PCF). N.A received support from the FWF Firnberg-Programm (T 1031).
This work was also supported by IST Austria institutional funds; FWF SFB F78 to
S.H.; NÖ Forschung und Bildung n[f+b] life science call grant (C13-002) to S.H.;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement no. 618444 to S.H.; and the
European Research Council (ERC) under the European Union’s Horizon 2020 research
and innovation programme (grant agreement no. 725780 LinPro) to S.H.
article_number: '100215'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. Generation and isolation of
single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 2020;1(3). doi:10.1016/j.xpro.2020.100215
apa: Laukoter, S., Amberg, N., Pauler, F., & Hippenmeyer, S. (2020). Generation
and isolation of single cells from mouse brain with mosaic analysis with double
markers-induced uniparental chromosome disomy. STAR Protocols. Elsevier.
https://doi.org/10.1016/j.xpro.2020.100215
chicago: Laukoter, Susanne, Nicole Amberg, Florian Pauler, and Simon Hippenmeyer.
“Generation and Isolation of Single Cells from Mouse Brain with Mosaic Analysis
with Double Markers-Induced Uniparental Chromosome Disomy.” STAR Protocols.
Elsevier, 2020. https://doi.org/10.1016/j.xpro.2020.100215.
ieee: S. Laukoter, N. Amberg, F. Pauler, and S. Hippenmeyer, “Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy,” STAR Protocols, vol. 1, no. 3. Elsevier,
2020.
ista: Laukoter S, Amberg N, Pauler F, Hippenmeyer S. 2020. Generation and isolation
of single cells from mouse brain with mosaic analysis with double markers-induced
uniparental chromosome disomy. STAR Protocols. 1(3), 100215.
mla: Laukoter, Susanne, et al. “Generation and Isolation of Single Cells from Mouse
Brain with Mosaic Analysis with Double Markers-Induced Uniparental Chromosome
Disomy.” STAR Protocols, vol. 1, no. 3, 100215, Elsevier, 2020, doi:10.1016/j.xpro.2020.100215.
short: S. Laukoter, N. Amberg, F. Pauler, S. Hippenmeyer, STAR Protocols 1 (2020).
corr_author: '1'
date_created: 2020-12-30T10:17:07Z
date_published: 2020-12-18T00:00:00Z
date_updated: 2025-04-15T08:23:06Z
day: '18'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1016/j.xpro.2020.100215
ec_funded: 1
external_id:
pmid:
- '33377108'
file:
- access_level: open_access
checksum: f1e9a433e9cb0f41f7b6df6b76db1f6e
content_type: application/pdf
creator: dernst
date_created: 2021-01-07T15:57:27Z
date_updated: 2021-01-07T15:57:27Z
file_id: '8996'
file_name: 2020_STARProtocols_Laukoter.pdf
file_size: 4031449
relation: main_file
success: 1
file_date_updated: 2021-01-07T15:57:27Z
fulldoi: https://doi.org/10.1016/j.xpro.2020.100215
has_accepted_license: '1'
intvolume: ' 1'
issue: '3'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T01031
name: Role of Eed in neural stem cell lineage progression
- _id: 059F6AB4-7A3F-11EA-A408-12923DDC885E
grant_number: F7805
name: Stem Cell Modulation in Neural Development and Regeneration/ P05-Molecular
Mechanisms of Neural Stem Cell Lineage Progression
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: STAR Protocols
publication_identifier:
issn:
- 2666-1667
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Generation and isolation of single cells from mouse brain with mosaic analysis
with double markers-induced uniparental chromosome disomy
tmp:
image: /images/cc_by_nc_nd.png
legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
(CC BY-NC-ND 4.0)
short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 1
year: '2020'
...
---
_id: '7253'
abstract:
- lang: eng
text: The cyclin-dependent kinase inhibitor p57KIP2 is encoded by the imprinted
Cdkn1c locus, exhibits maternal expression, and is essential for cerebral cortex
development. How Cdkn1c regulates corticogenesis is however not clear. To this
end we employ Mosaic Analysis with Double Markers (MADM) technology to genetically
dissect Cdkn1c gene function in corticogenesis at single cell resolution. We find
that the previously described growth-inhibitory Cdkn1c function is a non-cell-autonomous
one, acting on the whole organism. In contrast we reveal a growth-promoting cell-autonomous
Cdkn1c function which at the mechanistic level mediates radial glial progenitor
cell and nascent projection neuron survival. Strikingly, the growth-promoting
function of Cdkn1c is highly dosage sensitive but not subject to genomic imprinting.
Collectively, our results suggest that the Cdkn1c locus regulates cortical development
through distinct cell-autonomous and non-cell-autonomous mechanisms. More generally,
our study highlights the importance to probe the relative contributions of cell
intrinsic gene function and tissue-wide mechanisms to the overall phenotype.
acknowledged_ssus:
- _id: PreCl
article_number: '195'
article_processing_charge: No
article_type: original
author:
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Keiichi I.
full_name: Nakayama, Keiichi I.
last_name: Nakayama
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. Imprinted
Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral cortex
development. Nature Communications. 2020;11. doi:10.1038/s41467-019-14077-2
apa: Laukoter, S., Beattie, R. J., Pauler, F., Amberg, N., Nakayama, K. I., &
Hippenmeyer, S. (2020). Imprinted Cdkn1c genomic locus cell-autonomously promotes
cell survival in cerebral cortex development. Nature Communications. Springer
Nature. https://doi.org/10.1038/s41467-019-14077-2
chicago: Laukoter, Susanne, Robert J Beattie, Florian Pauler, Nicole Amberg, Keiichi
I. Nakayama, and Simon Hippenmeyer. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications.
Springer Nature, 2020. https://doi.org/10.1038/s41467-019-14077-2.
ieee: S. Laukoter, R. J. Beattie, F. Pauler, N. Amberg, K. I. Nakayama, and S. Hippenmeyer,
“Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development,” Nature Communications, vol. 11. Springer Nature, 2020.
ista: Laukoter S, Beattie RJ, Pauler F, Amberg N, Nakayama KI, Hippenmeyer S. 2020.
Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in cerebral
cortex development. Nature Communications. 11, 195.
mla: Laukoter, Susanne, et al. “Imprinted Cdkn1c Genomic Locus Cell-Autonomously
Promotes Cell Survival in Cerebral Cortex Development.” Nature Communications,
vol. 11, 195, Springer Nature, 2020, doi:10.1038/s41467-019-14077-2.
short: S. Laukoter, R.J. Beattie, F. Pauler, N. Amberg, K.I. Nakayama, S. Hippenmeyer,
Nature Communications 11 (2020).
corr_author: '1'
date_created: 2020-01-11T10:42:48Z
date_published: 2020-01-10T00:00:00Z
date_updated: 2025-06-12T07:30:49Z
day: '10'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1038/s41467-019-14077-2
ec_funded: 1
external_id:
isi:
- '000551459000005'
pmid:
- '31924768'
file:
- access_level: open_access
checksum: ebf1ed522f4e0be8d94c939c1806a709
content_type: application/pdf
creator: dernst
date_created: 2020-01-13T07:42:31Z
date_updated: 2020-07-14T12:47:54Z
file_id: '7261'
file_name: 2020_NatureComm_Laukoter.pdf
file_size: 8063333
relation: main_file
file_date_updated: 2020-07-14T12:47:54Z
fulldoi: https://doi.org/10.1038/s41467-019-14077-2
has_accepted_license: '1'
intvolume: ' 11'
isi: 1
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T01031
name: Role of Eed in neural stem cell lineage progression
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
publication: Nature Communications
publication_identifier:
issn:
- 2041-1723
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/new-function-for-potential-tumour-suppressor-in-brain-development/
scopus_import: '1'
status: public
title: Imprinted Cdkn1c genomic locus cell-autonomously promotes cell survival in
cerebral cortex development
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 11
year: '2020'
...
---
_id: '8813'
abstract:
- lang: eng
text: 'In mammals, chromatin marks at imprinted genes are asymmetrically inherited
to control parentally-biased gene expression. This control is thought predominantly
to involve parent-specific differentially methylated regions (DMR) in genomic
DNA. However, neither parent-of-origin-specific transcription nor DMRs have been
comprehensively mapped. We here address this by integrating transcriptomic and
epigenomic approaches in mouse preimplantation embryos (blastocysts). Transcriptome-analysis
identified 71 genes expressed with previously unknown parent-of-origin-specific
expression in blastocysts (nBiX: novel blastocyst-imprinted expression). Uniparental
expression of nBiX genes disappeared soon after implantation. Micro-whole-genome
bisulfite sequencing (μWGBS) of individual uniparental blastocysts detected 859
DMRs. Only 18% of nBiXs were associated with a DMR, whereas 60% were associated
with parentally-biased H3K27me3. This suggests a major role for Polycomb-mediated
imprinting in blastocysts. Five nBiX-clusters contained at least one known imprinted
gene, and five novel clusters contained exclusively nBiX-genes. These data suggest
a complex program of stage-specific imprinting involving different tiers of regulation.'
article_processing_charge: No
author:
- first_name: Laura
full_name: Santini, Laura
last_name: Santini
- first_name: Florian
full_name: Halbritter, Florian
last_name: Halbritter
- first_name: Fabian
full_name: Titz-Teixeira, Fabian
last_name: Titz-Teixeira
- first_name: Toru
full_name: Suzuki, Toru
last_name: Suzuki
- first_name: Maki
full_name: Asami, Maki
last_name: Asami
- first_name: Julia
full_name: Ramesmayer, Julia
last_name: Ramesmayer
- first_name: Xiaoyan
full_name: Ma, Xiaoyan
last_name: Ma
- first_name: Andreas
full_name: Lackner, Andreas
last_name: Lackner
- first_name: Nick
full_name: Warr, Nick
last_name: Warr
- first_name: Florian
full_name: Pauler, Florian
id: 48EA0138-F248-11E8-B48F-1D18A9856A87
last_name: Pauler
orcid: 0000-0002-7462-0048
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Ernest
full_name: Laue, Ernest
last_name: Laue
- first_name: Matthias
full_name: Farlik, Matthias
last_name: Farlik
- first_name: Christoph
full_name: Bock, Christoph
last_name: Bock
- first_name: Andreas
full_name: Beyer, Andreas
last_name: Beyer
- first_name: Anthony C. F.
full_name: Perry, Anthony C. F.
last_name: Perry
- first_name: Martin
full_name: Leeb, Martin
last_name: Leeb
citation:
ama: Santini L, Halbritter F, Titz-Teixeira F, et al. Novel imprints in mouse blastocysts
are predominantly DNA methylation independent. bioRxiv. doi:10.1101/2020.11.03.366948
apa: Santini, L., Halbritter, F., Titz-Teixeira, F., Suzuki, T., Asami, M., Ramesmayer,
J., … Leeb, M. (n.d.). Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv. https://doi.org/10.1101/2020.11.03.366948
chicago: Santini, Laura, Florian Halbritter, Fabian Titz-Teixeira, Toru Suzuki,
Maki Asami, Julia Ramesmayer, Xiaoyan Ma, et al. “Novel Imprints in Mouse Blastocysts
Are Predominantly DNA Methylation Independent.” BioRxiv, n.d. https://doi.org/10.1101/2020.11.03.366948.
ieee: L. Santini et al., “Novel imprints in mouse blastocysts are predominantly
DNA methylation independent,” bioRxiv. .
ista: Santini L, Halbritter F, Titz-Teixeira F, Suzuki T, Asami M, Ramesmayer J,
Ma X, Lackner A, Warr N, Pauler F, Hippenmeyer S, Laue E, Farlik M, Bock C, Beyer
A, Perry ACF, Leeb M. Novel imprints in mouse blastocysts are predominantly DNA
methylation independent. bioRxiv, 10.1101/2020.11.03.366948.
mla: Santini, Laura, et al. “Novel Imprints in Mouse Blastocysts Are Predominantly
DNA Methylation Independent.” BioRxiv, doi:10.1101/2020.11.03.366948.
short: L. Santini, F. Halbritter, F. Titz-Teixeira, T. Suzuki, M. Asami, J. Ramesmayer,
X. Ma, A. Lackner, N. Warr, F. Pauler, S. Hippenmeyer, E. Laue, M. Farlik, C.
Bock, A. Beyer, A.C.F. Perry, M. Leeb, BioRxiv (n.d.).
das_tickbox: '1'
date_created: 2020-11-26T07:17:19Z
date_published: 2020-11-05T00:00:00Z
date_updated: 2026-07-06T12:45:07Z
day: '05'
department:
- _id: SiHi
doi: 10.1101/2020.11.03.366948
external_id:
pmid:
- 'PPR234457 '
fulldoi: https://doi.org/10.1101/2020.11.03.366948
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1101/2020.11.03.366948
month: '11'
oa: 1
oa_version: Preprint
pmid: 1
publication: bioRxiv
publication_status: submitted
status: public
title: Novel imprints in mouse blastocysts are predominantly DNA methylation independent
type: preprint
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
_id: '7815'
abstract:
- lang: eng
text: Beginning from a limited pool of progenitors, the mammalian cerebral cortex
forms highly organized functional neural circuits. However, the underlying cellular
and molecular mechanisms regulating lineage transitions of neural stem cells (NSCs)
and eventual production of neurons and glia in the developing neuroepithelium
remains unclear. Methods to trace NSC division patterns and map the lineage of
clonally related cells have advanced dramatically. However, many contemporary
lineage tracing techniques suffer from the lack of cellular resolution of progeny
cell fate, which is essential for deciphering progenitor cell division patterns.
Presented is a protocol using mosaic analysis with double markers (MADM) to perform
in vivo clonal analysis. MADM concomitantly manipulates individual progenitor
cells and visualizes precise division patterns and lineage progression at unprecedented
single cell resolution. MADM-based interchromosomal recombination events during
the G2-X phase of mitosis, together with temporally inducible CreERT2, provide
exact information on the birth dates of clones and their division patterns. Thus,
MADM lineage tracing provides unprecedented qualitative and quantitative optical
readouts of the proliferation mode of stem cell progenitors at the single cell
level. MADM also allows for examination of the mechanisms and functional requirements
of candidate genes in NSC lineage progression. This method is unique in that comparative
analysis of control and mutant subclones can be performed in the same tissue environment
in vivo. Here, the protocol is described in detail, and experimental paradigms
to employ MADM for clonal analysis and lineage tracing in the developing cerebral
cortex are demonstrated. Importantly, this protocol can be adapted to perform
MADM clonal analysis in any murine stem cell niche, as long as the CreERT2 driver
is present.
acknowledged_ssus:
- _id: Bio
- _id: LifeSc
- _id: PreCl
article_number: e61147
article_processing_charge: No
article_type: original
author:
- first_name: Robert J
full_name: Beattie, Robert J
id: 2E26DF60-F248-11E8-B48F-1D18A9856A87
last_name: Beattie
orcid: 0000-0002-8483-8753
- first_name: Carmen
full_name: Streicher, Carmen
id: 36BCB99C-F248-11E8-B48F-1D18A9856A87
last_name: Streicher
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Giselle T
full_name: Cheung, Giselle T
id: 471195F6-F248-11E8-B48F-1D18A9856A87
last_name: Cheung
orcid: 0000-0001-8457-2572
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Beattie RJ, Streicher C, Amberg N, et al. Lineage tracing and clonal analysis
in developing cerebral cortex using mosaic analysis with double markers (MADM).
Journal of Visual Experiments. 2020;(159). doi:10.3791/61147
apa: Beattie, R. J., Streicher, C., Amberg, N., Cheung, G. T., Contreras, X., Hansen,
A. H., & Hippenmeyer, S. (2020). Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM). Journal of
Visual Experiments. MyJove Corporation. https://doi.org/10.3791/61147
chicago: Beattie, Robert J, Carmen Streicher, Nicole Amberg, Giselle T Cheung, Ximena
Contreras, Andi H Hansen, and Simon Hippenmeyer. “Lineage Tracing and Clonal Analysis
in Developing Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).”
Journal of Visual Experiments. MyJove Corporation, 2020. https://doi.org/10.3791/61147.
ieee: R. J. Beattie et al., “Lineage tracing and clonal analysis in developing
cerebral cortex using mosaic analysis with double markers (MADM),” Journal
of Visual Experiments, no. 159. MyJove Corporation, 2020.
ista: Beattie RJ, Streicher C, Amberg N, Cheung GT, Contreras X, Hansen AH, Hippenmeyer
S. 2020. Lineage tracing and clonal analysis in developing cerebral cortex using
mosaic analysis with double markers (MADM). Journal of Visual Experiments. (159),
e61147.
mla: Beattie, Robert J., et al. “Lineage Tracing and Clonal Analysis in Developing
Cerebral Cortex Using Mosaic Analysis with Double Markers (MADM).” Journal
of Visual Experiments, no. 159, e61147, MyJove Corporation, 2020, doi:10.3791/61147.
short: R.J. Beattie, C. Streicher, N. Amberg, G.T. Cheung, X. Contreras, A.H. Hansen,
S. Hippenmeyer, Journal of Visual Experiments (2020).
corr_author: '1'
date_created: 2020-05-11T08:31:20Z
date_published: 2020-05-08T00:00:00Z
date_updated: 2026-10-11T22:30:24Z
day: '08'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3791/61147
ec_funded: 1
external_id:
isi:
- '000546406600043'
pmid:
- '32449730'
file:
- access_level: open_access
checksum: 3154ea7f90b9fb45e084cd1c2770597d
content_type: application/pdf
creator: rbeattie
date_created: 2020-05-11T08:28:38Z
date_updated: 2020-07-14T12:48:03Z
file_id: '7816'
file_name: jove-protocol-61147-lineage-tracing-clonal-analysis-developing-cerebral-cortex-using.pdf
file_size: 1352186
relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
fulldoi: https://doi.org/10.3791/61147
has_accepted_license: '1'
isi: 1
issue: '159'
language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 264E56E2-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: M02416
name: Molecular Mechanisms Regulating Gliogenesis in the Neocortex
- _id: 268F8446-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: T01031
name: Role of Eed in neural stem cell lineage progression
- _id: 260C2330-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '754411'
name: ISTplus - Postdoctoral Fellowships
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Visual Experiments
publication_identifier:
issn:
- 1940-087X
publication_status: published
publisher: MyJove Corporation
quality_controlled: '1'
related_material:
record:
- id: '7902'
relation: part_of_dissertation
status: public
scopus_import: '1'
status: public
title: Lineage tracing and clonal analysis in developing cerebral cortex using mosaic
analysis with double markers (MADM)
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2020'
...
---
OA_place: publisher
_id: '7902'
abstract:
- lang: eng
text: "Mosaic genetic analysis has been widely used in different model organisms
such as the fruit fly to study gene-function in a cell-autonomous or tissue-specific
fashion. More recently, and less easily conducted, mosaic genetic analysis in
mice has also been enabled with the ambition to shed light on human gene function
and disease. These genetic tools are of particular interest, but not restricted
to, the study of the brain. Notably, the MADM technology offers a genetic approach
in mice to visualize and concomitantly manipulate small subsets of genetically
defined cells at a clonal level and single cell resolution. MADM-based analysis
has already advanced the study of genetic mechanisms regulating brain development
and is expected that further MADM-based analysis of genetic alterations will continue
to reveal important insights on the fundamental principles of development and
disease to potentially assist in the development of new therapies or treatments.\r\nIn
summary, this work completed and characterized the necessary genome-wide genetic
tools to perform MADM-based analysis at single cell level of the vast majority
of mouse genes in virtually any cell type and provided a protocol to perform lineage
tracing using the novel MADM resource. Importantly, this work also explored and
revealed novel aspects of biologically relevant events in an in vivo context,
such as the chromosome-specific bias of chromatid sister segregation pattern,
the generation of cell-type diversity in the cerebral cortex and in the cerebellum
and finally, the relevance of the interplay between the cell-autonomous gene function
and cell-non-autonomous (community) effects in radial glial progenitor lineage
progression.\r\nThis work provides a foundation and opens the door to further
elucidating the molecular mechanisms underlying neuronal diversity and astrocyte
generation."
acknowledged_ssus:
- _id: PreCl
- _id: Bio
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
citation:
ama: Contreras X. Genetic dissection of neural development in health and disease
at single cell resolution. 2020. doi:10.15479/AT:ISTA:7902
apa: Contreras, X. (2020). Genetic dissection of neural development in health
and disease at single cell resolution. Institute of Science and Technology
Austria. https://doi.org/10.15479/AT:ISTA:7902
chicago: Contreras, Ximena. “Genetic Dissection of Neural Development in Health
and Disease at Single Cell Resolution.” Institute of Science and Technology Austria,
2020. https://doi.org/10.15479/AT:ISTA:7902.
ieee: X. Contreras, “Genetic dissection of neural development in health and disease
at single cell resolution,” Institute of Science and Technology Austria, 2020.
ista: Contreras X. 2020. Genetic dissection of neural development in health and
disease at single cell resolution. Institute of Science and Technology Austria.
mla: Contreras, Ximena. Genetic Dissection of Neural Development in Health and
Disease at Single Cell Resolution. Institute of Science and Technology Austria,
2020, doi:10.15479/AT:ISTA:7902.
short: X. Contreras, Genetic Dissection of Neural Development in Health and Disease
at Single Cell Resolution, Institute of Science and Technology Austria, 2020.
corr_author: '1'
date_created: 2020-05-29T08:27:32Z
date_published: 2020-06-05T00:00:00Z
date_updated: 2026-06-18T19:12:39Z
day: '05'
ddc:
- '570'
degree_awarded: PhD
department:
- _id: SiHi
doi: 10.15479/AT:ISTA:7902
ec_funded: 1
file:
- access_level: closed
checksum: 43c172bf006c95b65992d473c7240d13
content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document
creator: xcontreras
date_created: 2020-06-05T08:18:08Z
date_updated: 2021-06-07T22:30:03Z
embargo_to: open_access
file_id: '7927'
file_name: PhDThesis_Contreras.docx
file_size: 53134142
relation: source_file
- access_level: open_access
checksum: addfed9128271be05cae3608e03a6ec0
content_type: application/pdf
creator: xcontreras
date_created: 2020-06-05T08:18:07Z
date_updated: 2021-06-07T22:30:03Z
embargo: 2021-06-06
file_id: '7928'
file_name: PhDThesis_Contreras.pdf
file_size: 35117191
relation: main_file
file_date_updated: 2021-06-07T22:30:03Z
fulldoi: https://doi.org/10.15479/AT:ISTA:7902
has_accepted_license: '1'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
page: '214'
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_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
related_material:
record:
- id: '28'
relation: dissertation_contains
status: public
- id: '7815'
relation: dissertation_contains
status: public
- id: '6830'
relation: dissertation_contains
status: public
status: public
supervisor:
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
title: Genetic dissection of neural development in health and disease at single cell
resolution
type: dissertation
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
year: '2020'
...
---
_id: '8569'
abstract:
- lang: eng
text: Concerted radial migration of newly born cortical projection neurons, from
their birthplace to their final target lamina, is a key step in the assembly of
the cerebral cortex. The cellular and molecular mechanisms regulating the specific
sequential steps of radial neuronal migration in vivo are however still unclear,
let alone the effects and interactions with the extracellular environment. In
any in vivo context, cells will always be exposed to a complex extracellular environment
consisting of (1) secreted factors acting as potential signaling cues, (2) the
extracellular matrix, and (3) other cells providing cell–cell interaction through
receptors and/or direct physical stimuli. Most studies so far have described and
focused mainly on intrinsic cell-autonomous gene functions in neuronal migration
but there is accumulating evidence that non-cell-autonomous-, local-, systemic-,
and/or whole tissue-wide effects substantially contribute to the regulation of
radial neuronal migration. These non-cell-autonomous effects may differentially
affect cortical neuron migration in distinct cellular environments. However, the
cellular and molecular natures of such non-cell-autonomous mechanisms are mostly
unknown. Furthermore, physical forces due to collective migration and/or community
effects (i.e., interactions with surrounding cells) may play important roles in
neocortical projection neuron migration. In this concise review, we first outline
distinct models of non-cell-autonomous interactions of cortical projection neurons
along their radial migration trajectory during development. We then summarize
experimental assays and platforms that can be utilized to visualize and potentially
probe non-cell-autonomous mechanisms. Lastly, we define key questions to address
in the future.
acknowledgement: AH was a recipient of a DOC Fellowship (24812) of the Austrian Academy
of Sciences. This work also received support from IST Austria institutional funds;
the People Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007–2013) under REA Grant Agreement No. 618444 to SH.
article_number: '574382'
article_processing_charge: Yes (via OA deal)
article_type: original
author:
- first_name: Andi H
full_name: Hansen, Andi H
id: 38853E16-F248-11E8-B48F-1D18A9856A87
last_name: Hansen
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Hansen AH, Hippenmeyer S. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 2020;8(9). doi:10.3389/fcell.2020.574382
apa: Hansen, A. H., & Hippenmeyer, S. (2020). Non-cell-autonomous mechanisms
in radial projection neuron migration in the developing cerebral cortex. Frontiers
in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2020.574382
chicago: Hansen, Andi H, and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms
in Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology. Frontiers, 2020. https://doi.org/10.3389/fcell.2020.574382.
ieee: A. H. Hansen and S. Hippenmeyer, “Non-cell-autonomous mechanisms in radial
projection neuron migration in the developing cerebral cortex,” Frontiers in
Cell and Developmental Biology, vol. 8, no. 9. Frontiers, 2020.
ista: Hansen AH, Hippenmeyer S. 2020. Non-cell-autonomous mechanisms in radial projection
neuron migration in the developing cerebral cortex. Frontiers in Cell and Developmental
Biology. 8(9), 574382.
mla: Hansen, Andi H., and Simon Hippenmeyer. “Non-Cell-Autonomous Mechanisms in
Radial Projection Neuron Migration in the Developing Cerebral Cortex.” Frontiers
in Cell and Developmental Biology, vol. 8, no. 9, 574382, Frontiers, 2020,
doi:10.3389/fcell.2020.574382.
short: A.H. Hansen, S. Hippenmeyer, Frontiers in Cell and Developmental Biology
8 (2020).
corr_author: '1'
date_created: 2020-09-26T06:11:07Z
date_published: 2020-09-25T00:00:00Z
date_updated: 2026-10-11T22:31:05Z
day: '25'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.3389/fcell.2020.574382
ec_funded: 1
external_id:
isi:
- '000577915900001'
pmid:
- '33102480'
file:
- access_level: open_access
checksum: 01f731824194c94c81a5da360d997073
content_type: application/pdf
creator: dernst
date_created: 2020-09-28T13:11:17Z
date_updated: 2020-09-28T13:11:17Z
file_id: '8584'
file_name: 2020_Frontiers_Hansen.pdf
file_size: 5527139
relation: main_file
success: 1
file_date_updated: 2020-09-28T13:11:17Z
fulldoi: https://doi.org/10.3389/fcell.2020.574382
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
issue: '9'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
pmid: 1
project:
- _id: 2625A13E-B435-11E9-9278-68D0E5697425
grant_number: '24812'
name: Molecular mechanisms of radial neuronal migration
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
publication: Frontiers in Cell and Developmental Biology
publication_identifier:
issn:
- 2296-634X
publication_status: published
publisher: Frontiers
quality_controlled: '1'
related_material:
record:
- id: '9962'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Non-cell-autonomous mechanisms in radial projection neuron migration in the
developing cerebral cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2020'
...
---
_id: '27'
abstract:
- lang: eng
text: The cerebral cortex is composed of a large variety of distinct cell-types
including projection neurons, interneurons and glial cells which emerge from distinct
neural stem cell (NSC) lineages. The vast majority of cortical projection neurons
and certain classes of glial cells are generated by radial glial progenitor cells
(RGPs) in a highly orchestrated manner. Recent studies employing single cell analysis
and clonal lineage tracing suggest that NSC and RGP lineage progression are regulated
in a profound deterministic manner. In this review we focus on recent advances
based mainly on correlative phenotypic data emerging from functional genetic studies
in mice. We establish hypotheses to test in future research and outline a conceptual
framework how epigenetic cues modulate the generation of cell-type diversity during
cortical development. This article is protected by copyright. All rights reserved.
acknowledgement: " This work was supported by IST Austria institutional funds; NÖ
Forschung und Bildung \r\nn[f+b] (C13-002) to SH; a program grant from
\ the Human Frontiers Science Program (RGP0053/2014) to SH; the People
\ Programme (Marie Curie Actions) of the European Union’s Seventh Framework
Programme (FP7/2007-2013) under REA grant agreement No 618444 to SH, and the European
\ Research Council (ERC) under the European Union’s Horizon 2020 research
\ and innovation programme (grant agreement No 725780 LinPro)to SH.\r\n"
article_processing_charge: Yes (via OA deal)
article_type: review
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Susanne
full_name: Laukoter, Susanne
id: 2D6B7A9A-F248-11E8-B48F-1D18A9856A87
last_name: Laukoter
orcid: 0000-0002-7903-3010
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
citation:
ama: Amberg N, Laukoter S, Hippenmeyer S. Epigenetic cues modulating the generation
of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
2019;149(1):12-26. doi:10.1111/jnc.14601
apa: Amberg, N., Laukoter, S., & Hippenmeyer, S. (2019). Epigenetic cues modulating
the generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
Wiley. https://doi.org/10.1111/jnc.14601
chicago: Amberg, Nicole, Susanne Laukoter, and Simon Hippenmeyer. “Epigenetic Cues
Modulating the Generation of Cell Type Diversity in the Cerebral Cortex.” Journal
of Neurochemistry. Wiley, 2019. https://doi.org/10.1111/jnc.14601.
ieee: N. Amberg, S. Laukoter, and S. Hippenmeyer, “Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex,” Journal of Neurochemistry,
vol. 149, no. 1. Wiley, pp. 12–26, 2019.
ista: Amberg N, Laukoter S, Hippenmeyer S. 2019. Epigenetic cues modulating the
generation of cell type diversity in the cerebral cortex. Journal of Neurochemistry.
149(1), 12–26.
mla: Amberg, Nicole, et al. “Epigenetic Cues Modulating the Generation of Cell Type
Diversity in the Cerebral Cortex.” Journal of Neurochemistry, vol. 149,
no. 1, Wiley, 2019, pp. 12–26, doi:10.1111/jnc.14601.
short: N. Amberg, S. Laukoter, S. Hippenmeyer, Journal of Neurochemistry 149 (2019)
12–26.
corr_author: '1'
date_created: 2018-12-11T11:44:14Z
date_published: 2019-04-01T00:00:00Z
date_updated: 2025-04-14T07:43:05Z
day: '01'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.1111/jnc.14601
ec_funded: 1
external_id:
isi:
- '000462680200002'
file:
- access_level: open_access
checksum: db027721a95d36f5de36aadcd0bdf7e6
content_type: application/pdf
creator: kschuh
date_created: 2020-01-07T13:35:52Z
date_updated: 2020-07-14T12:45:45Z
file_id: '7239'
file_name: 2019_Wiley_Amberg.pdf
file_size: 889709
relation: main_file
file_date_updated: 2020-07-14T12:45:45Z
fulldoi: https://doi.org/10.1111/jnc.14601
has_accepted_license: '1'
intvolume: ' 149'
isi: 1
issue: '1'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 12-26
project:
- _id: 25D92700-B435-11E9-9278-68D0E5697425
grant_number: LS13-002
name: Mapping Cell-Type Specificity of the Genomic Imprintome in the Brain
- _id: 25D7962E-B435-11E9-9278-68D0E5697425
grant_number: RGP0053/2014
name: Quantitative Structure-Function Analysis of Cerebral Cortex Assembly at Clonal
Level
- _id: 25D61E48-B435-11E9-9278-68D0E5697425
call_identifier: FP7
grant_number: '618444'
name: Molecular Mechanisms of Cerebral Cortex Development
- _id: 260018B0-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '725780'
name: Principles of Neural Stem Cell Lineage Progression in Cerebral Cortex Development
publication: Journal of Neurochemistry
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Epigenetic cues modulating the generation of cell type diversity in the cerebral
cortex
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 149
year: '2019'
...
---
_id: '6091'
abstract:
- lang: eng
text: Cortical networks are characterized by sparse connectivity, with synapses
found at only a subset of axo-dendritic contacts. Yet within these networks, neurons
can exhibit high connection probabilities, suggesting that cell-intrinsic factors,
not proximity, determine connectivity. Here, we identify ephrin-B3 (eB3) as a
factor that determines synapse density by mediating a cell-cell competition that
requires ephrin-B-EphB signaling. In a microisland culture system designed to
isolate cell-cell competition, we find that eB3 determines winning and losing
neurons in a contest for synapses. In a Mosaic Analysis with Double Markers (MADM)
genetic mouse model system in vivo the relative levels of eB3 control spine density
in layer 5 and 6 neurons. MADM cortical neurons in vitro reveal that eB3 controls
synapse density independently of action potential-driven activity. Our findings
illustrate a new class of competitive mechanism mediated by trans-synaptic organizing
proteins which control the number of synapses neurons receive relative to neighboring
neurons.
article_number: e41563
article_processing_charge: No
author:
- first_name: Nathan T.
full_name: Henderson, Nathan T.
last_name: Henderson
- first_name: Sylvain J.
full_name: Le Marchand, Sylvain J.
last_name: Le Marchand
- first_name: Martin
full_name: Hruska, Martin
last_name: Hruska
- first_name: Simon
full_name: Hippenmeyer, Simon
id: 37B36620-F248-11E8-B48F-1D18A9856A87
last_name: Hippenmeyer
orcid: 0000-0003-2279-1061
- first_name: Liqun
full_name: Luo, Liqun
last_name: Luo
- first_name: Matthew B.
full_name: Dalva, Matthew B.
last_name: Dalva
citation:
ama: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. Ephrin-B3
controls excitatory synapse density through cell-cell competition for EphBs. eLife.
2019;8. doi:10.7554/eLife.41563
apa: Henderson, N. T., Le Marchand, S. J., Hruska, M., Hippenmeyer, S., Luo, L.,
& Dalva, M. B. (2019). Ephrin-B3 controls excitatory synapse density through
cell-cell competition for EphBs. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.41563
chicago: Henderson, Nathan T., Sylvain J. Le Marchand, Martin Hruska, Simon Hippenmeyer,
Liqun Luo, and Matthew B. Dalva. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife. eLife Sciences Publications,
2019. https://doi.org/10.7554/eLife.41563.
ieee: N. T. Henderson, S. J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, and
M. B. Dalva, “Ephrin-B3 controls excitatory synapse density through cell-cell
competition for EphBs,” eLife, vol. 8. eLife Sciences Publications, 2019.
ista: Henderson NT, Le Marchand SJ, Hruska M, Hippenmeyer S, Luo L, Dalva MB. 2019.
Ephrin-B3 controls excitatory synapse density through cell-cell competition for
EphBs. eLife. 8, e41563.
mla: Henderson, Nathan T., et al. “Ephrin-B3 Controls Excitatory Synapse Density
through Cell-Cell Competition for EphBs.” ELife, vol. 8, e41563, eLife
Sciences Publications, 2019, doi:10.7554/eLife.41563.
short: N.T. Henderson, S.J. Le Marchand, M. Hruska, S. Hippenmeyer, L. Luo, M.B.
Dalva, ELife 8 (2019).
date_created: 2019-03-10T22:59:20Z
date_published: 2019-02-21T00:00:00Z
date_updated: 2023-08-24T14:50:50Z
day: '21'
ddc:
- '570'
department:
- _id: SiHi
doi: 10.7554/eLife.41563
external_id:
isi:
- '000459380600001'
pmid:
- '30789343'
file:
- access_level: open_access
checksum: 7b0800d003f14cd06b1802dea0c52941
content_type: application/pdf
creator: dernst
date_created: 2019-03-11T16:15:37Z
date_updated: 2020-07-14T12:47:19Z
file_id: '6098'
file_name: 2019_eLife_Henderson.pdf
file_size: 7260753
relation: main_file
file_date_updated: 2020-07-14T12:47:19Z
fulldoi: https://doi.org/10.7554/eLife.41563
has_accepted_license: '1'
intvolume: ' 8'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Published Version
pmid: 1
publication: eLife
publication_status: published
publisher: eLife Sciences Publications
quality_controlled: '1'
scopus_import: '1'
status: public
title: Ephrin-B3 controls excitatory synapse density through cell-cell competition
for EphBs
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 8
year: '2019'
...
---
_id: '6451'
abstract:
- lang: eng
text: Epidermal growth factor receptor (EGFR) signaling controls skin development
and homeostasis inmice and humans, and its deficiency causes severe skin inflammation,
which might affect epidermalstem cell behavior. Here, we describe the inflammation-independent
effects of EGFR deficiency dur-ing skin morphogenesis and in adult hair follicle
stem cells. Expression and alternative splicing analysisof RNA sequencing data
from interfollicular epidermis and outer root sheath indicate that EGFR con-trols
genes involved in epidermal differentiation and also in centrosome function, DNA
damage, cellcycle, and apoptosis. Genetic experiments employingp53deletion in
EGFR-deficient epidermis revealthat EGFR signaling exhibitsp53-dependent functions
in proliferative epidermal compartments, aswell asp53-independent functions in
differentiated hair shaft keratinocytes. Loss of EGFR leads toabsence of LEF1
protein specifically in the innermost epithelial hair layers, resulting in disorganizationof
medulla cells. Thus, our results uncover important spatial and temporal features
of cell-autonomousEGFR functions in the epidermis.
article_processing_charge: No
author:
- first_name: Nicole
full_name: Amberg, Nicole
id: 4CD6AAC6-F248-11E8-B48F-1D18A9856A87
last_name: Amberg
orcid: 0000-0002-3183-8207
- first_name: Panagiota A.
full_name: Sotiropoulou, Panagiota A.
last_name: Sotiropoulou
- first_name: Gerwin
full_name: Heller, Gerwin
last_name: Heller
- first_name: Beate M.
full_name: Lichtenberger, Beate M.
last_name: Lichtenberger
- first_name: Martin
full_name: Holcmann, Martin
last_name: Holcmann
- first_name: Bahar
full_name: Camurdanoglu, Bahar
last_name: Camurdanoglu
- first_name: Temenuschka
full_name: Baykuscheva-Gentscheva, Temenuschka
last_name: Baykuscheva-Gentscheva
- first_name: Cedric
full_name: Blanpain, Cedric
last_name: Blanpain
- first_name: Maria
full_name: Sibilia, Maria
last_name: Sibilia
citation:
ama: Amberg N, Sotiropoulou PA, Heller G, et al. EGFR controls hair shaft differentiation
in a p53-independent manner. iScience. 2019;15:243-256. doi:10.1016/j.isci.2019.04.018
apa: Amberg, N., Sotiropoulou, P. A., Heller, G., Lichtenberger, B. M., Holcmann,
M., Camurdanoglu, B., … Sibilia, M. (2019). EGFR controls hair shaft differentiation
in a p53-independent manner. IScience. Elsevier. https://doi.org/10.1016/j.isci.2019.04.018
chicago: Amberg, Nicole, Panagiota A. Sotiropoulou, Gerwin Heller, Beate M. Lichtenberger,
Martin Holcmann, Bahar Camurdanoglu, Temenuschka Baykuscheva-Gentscheva, Cedric
Blanpain, and Maria Sibilia. “EGFR Controls Hair Shaft Differentiation in a P53-Independent
Manner.” IScience. Elsevier, 2019. https://doi.org/10.1016/j.isci.2019.04.018.
ieee: N. Amberg et al., “EGFR controls hair shaft differentiation in a p53-independent
manner,” iScience, vol. 15. Elsevier, pp. 243–256, 2019.
ista: Amberg N, Sotiropoulou PA, Heller G, Lichtenberger BM, Holcmann M, Camurdanoglu
B, Baykuscheva-Gentscheva T, Blanpain C, Sibilia M. 2019. EGFR controls hair shaft
differentiation in a p53-independent manner. iScience. 15, 243–256.
mla: Amberg, Nicole, et al. “EGFR Controls Hair Shaft Differentiation in a P53-Independent
Manner.” IScience, vol. 15, Elsevier, 2019, pp. 243–56, doi:10.1016/j.isci.2019.04.018.
short: N. Amberg, P.A. Sotiropoulou, G. Heller, B.M. Lichtenberger, M. Holcmann,
B. Camurdanoglu, T. Baykuscheva-Gentscheva, C. Blanpain, M. Sibilia, IScience
15 (2019) 243–256.
date_created: 2019-05-14T11:47:40Z
date_published: 2019-05-31T00:00:00Z
date_updated: 2023-09-08T11:38:04Z
day: '31'
ddc:
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department:
- _id: SiHi
doi: 10.1016/j.isci.2019.04.018
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language:
- iso: eng
month: '05'
oa: 1
oa_version: Published Version
page: 243-256
publication: iScience
publication_identifier:
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publication_status: published
publisher: Elsevier
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title: EGFR controls hair shaft differentiation in a p53-independent manner
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...