---
_id: '6513'
abstract:
- lang: eng
text: Adult intestinal stem cells are located at the bottom of crypts of Lieberkühn,
where they express markers such as LGR5 1,2 and fuel the constant replenishment
of the intestinal epithelium1. Although fetal LGR5-expressing cells can give rise
to adult intestinal stem cells3,4, it remains unclear whether this population
in the patterned epithelium represents unique intestinal stem-cell precursors.
Here we show, using unbiased quantitative lineage-tracing approaches, biophysical
modelling and intestinal transplantation, that all cells of the mouse intestinal
epithelium—irrespective of their location and pattern of LGR5 expression in the
fetal gut tube—contribute actively to the adult intestinal stem cell pool. Using
3D imaging, we find that during fetal development the villus undergoes gross remodelling
and fission. This brings epithelial cells from the non-proliferative villus into
the proliferative intervillus region, which enables them to contribute to the
adult stem-cell niche. Our results demonstrate that large-scale remodelling of
the intestinal wall and cell-fate specification are closely linked. Moreover,
these findings provide a direct link between the observed plasticity and cellular
reprogramming of differentiating cells in adult tissues following damage5,6,7,8,9,
revealing that stem-cell identity is an induced rather than a hardwired property.
article_processing_charge: No
article_type: original
author:
- first_name: Jordi
full_name: Guiu, Jordi
last_name: Guiu
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Shiro
full_name: Yui, Shiro
last_name: Yui
- first_name: Samuel
full_name: Demharter, Samuel
last_name: Demharter
- first_name: Svetlana
full_name: Ulyanchenko, Svetlana
last_name: Ulyanchenko
- first_name: Martti
full_name: Maimets, Martti
last_name: Maimets
- first_name: Anne
full_name: Jørgensen, Anne
last_name: Jørgensen
- first_name: Signe
full_name: Perlman, Signe
last_name: Perlman
- first_name: Lene
full_name: Lundvall, Lene
last_name: Lundvall
- first_name: Linn Salto
full_name: Mamsen, Linn Salto
last_name: Mamsen
- first_name: Agnete
full_name: Larsen, Agnete
last_name: Larsen
- first_name: Rasmus H.
full_name: Olesen, Rasmus H.
last_name: Olesen
- first_name: Claus Yding
full_name: Andersen, Claus Yding
last_name: Andersen
- first_name: Lea Langhoff
full_name: Thuesen, Lea Langhoff
last_name: Thuesen
- first_name: Kristine Juul
full_name: Hare, Kristine Juul
last_name: Hare
- first_name: Tune H.
full_name: Pers, Tune H.
last_name: Pers
- first_name: Konstantin
full_name: Khodosevich, Konstantin
last_name: Khodosevich
- first_name: Benjamin D.
full_name: Simons, Benjamin D.
last_name: Simons
- first_name: Kim B.
full_name: Jensen, Kim B.
last_name: Jensen
citation:
ama: Guiu J, Hannezo EB, Yui S, et al. Tracing the origin of adult intestinal stem
cells. Nature. 2019;570:107-111. doi:10.1038/s41586-019-1212-5
apa: Guiu, J., Hannezo, E. B., Yui, S., Demharter, S., Ulyanchenko, S., Maimets,
M., … Jensen, K. B. (2019). Tracing the origin of adult intestinal stem cells.
Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1212-5
chicago: Guiu, Jordi, Edouard B Hannezo, Shiro Yui, Samuel Demharter, Svetlana Ulyanchenko,
Martti Maimets, Anne Jørgensen, et al. “Tracing the Origin of Adult Intestinal
Stem Cells.” Nature. Springer Nature, 2019. https://doi.org/10.1038/s41586-019-1212-5.
ieee: J. Guiu et al., “Tracing the origin of adult intestinal stem cells,”
Nature, vol. 570. Springer Nature, pp. 107–111, 2019.
ista: Guiu J, Hannezo EB, Yui S, Demharter S, Ulyanchenko S, Maimets M, Jørgensen
A, Perlman S, Lundvall L, Mamsen LS, Larsen A, Olesen RH, Andersen CY, Thuesen
LL, Hare KJ, Pers TH, Khodosevich K, Simons BD, Jensen KB. 2019. Tracing the origin
of adult intestinal stem cells. Nature. 570, 107–111.
mla: Guiu, Jordi, et al. “Tracing the Origin of Adult Intestinal Stem Cells.” Nature,
vol. 570, Springer Nature, 2019, pp. 107–11, doi:10.1038/s41586-019-1212-5.
short: J. Guiu, E.B. Hannezo, S. Yui, S. Demharter, S. Ulyanchenko, M. Maimets,
A. Jørgensen, S. Perlman, L. Lundvall, L.S. Mamsen, A. Larsen, R.H. Olesen, C.Y.
Andersen, L.L. Thuesen, K.J. Hare, T.H. Pers, K. Khodosevich, B.D. Simons, K.B.
Jensen, Nature 570 (2019) 107–111.
date_created: 2019-06-02T21:59:14Z
date_published: 2019-06-06T00:00:00Z
date_updated: 2025-07-10T11:53:29Z
day: '06'
department:
- _id: EdHa
doi: 10.1038/s41586-019-1212-5
external_id:
isi:
- '000470149000048'
pmid:
- '31092921'
fulldoi: https://doi.org/10.1038/s41586-019-1212-5
intvolume: ' 570'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6986928
month: '06'
oa: 1
oa_version: Submitted Version
page: 107-111
pmid: 1
publication: Nature
publication_identifier:
eissn:
- 1476-4687
issn:
- 0028-0836
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tracing the origin of adult intestinal stem cells
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 570
year: '2019'
...
---
_id: '6559'
abstract:
- lang: eng
text: Branching morphogenesis is a prototypical example of complex three-dimensional
organ sculpting, required in multiple developmental settings to maximize the area
of exchange surfaces. It requires, in particular, the coordinated growth of different
cell types together with complex patterning to lead to robust macroscopic outputs.
In recent years, novel multiscale quantitative biology approaches, together with
biophysical modelling, have begun to shed new light of this topic. Here, we wish
to review some of these recent developments, highlighting the generic design principles
that can be abstracted across different branched organs, as well as the implications
for the broader fields of stem cell, developmental and systems biology.
article_processing_charge: No
article_type: original
author:
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Benjamin D.
full_name: Simons, Benjamin D.
last_name: Simons
citation:
ama: Hannezo EB, Simons BD. Multiscale dynamics of branching morphogenesis. Current
Opinion in Cell Biology. 2019;60:99-105. doi:10.1016/j.ceb.2019.04.008
apa: Hannezo, E. B., & Simons, B. D. (2019). Multiscale dynamics of branching
morphogenesis. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2019.04.008
chicago: Hannezo, Edouard B, and Benjamin D. Simons. “Multiscale Dynamics of Branching
Morphogenesis.” Current Opinion in Cell Biology. Elsevier, 2019. https://doi.org/10.1016/j.ceb.2019.04.008.
ieee: E. B. Hannezo and B. D. Simons, “Multiscale dynamics of branching morphogenesis,”
Current Opinion in Cell Biology, vol. 60. Elsevier, pp. 99–105, 2019.
ista: Hannezo EB, Simons BD. 2019. Multiscale dynamics of branching morphogenesis.
Current Opinion in Cell Biology. 60, 99–105.
mla: Hannezo, Edouard B., and Benjamin D. Simons. “Multiscale Dynamics of Branching
Morphogenesis.” Current Opinion in Cell Biology, vol. 60, Elsevier, 2019,
pp. 99–105, doi:10.1016/j.ceb.2019.04.008.
short: E.B. Hannezo, B.D. Simons, Current Opinion in Cell Biology 60 (2019) 99–105.
date_created: 2019-06-16T21:59:12Z
date_published: 2019-10-01T00:00:00Z
date_updated: 2026-04-03T09:38:46Z
day: '01'
department:
- _id: EdHa
doi: 10.1016/j.ceb.2019.04.008
external_id:
isi:
- '000486545800014'
pmid:
- '31181348'
fulldoi: https://doi.org/10.1016/j.ceb.2019.04.008
intvolume: ' 60'
isi: 1
language:
- iso: eng
month: '10'
oa_version: None
page: 99-105
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
eissn:
- 1879-0410
issn:
- 0955-0674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiscale dynamics of branching morphogenesis
type: journal_article
user_id: ba8df636-2132-11f1-aed0-ed93e2281fdd
volume: 60
year: '2019'
...
---
_id: '6601'
abstract:
- lang: eng
text: There is increasing evidence that both mechanical and biochemical signals
play important roles in development and disease. The development of complex organisms,
in particular, has been proposed to rely on the feedback between mechanical and
biochemical patterning events. This feedback occurs at the molecular level via
mechanosensation but can also arise as an emergent property of the system at the
cellular and tissue level. In recent years, dynamic changes in tissue geometry,
flow, rheology, and cell fate specification have emerged as key platforms of mechanochemical
feedback loops in multiple processes. Here, we review recent experimental and
theoretical advances in understanding how these feedbacks function in development
and disease.
article_processing_charge: No
article_type: review
author:
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Hannezo EB, Heisenberg C-PJ. Mechanochemical feedback loops in development
and disease. Cell. 2019;178(1):12-25. doi:10.1016/j.cell.2019.05.052
apa: Hannezo, E. B., & Heisenberg, C.-P. J. (2019). Mechanochemical feedback
loops in development and disease. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.05.052
chicago: Hannezo, Edouard B, and Carl-Philipp J Heisenberg. “Mechanochemical Feedback
Loops in Development and Disease.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.05.052.
ieee: E. B. Hannezo and C.-P. J. Heisenberg, “Mechanochemical feedback loops in
development and disease,” Cell, vol. 178, no. 1. Elsevier, pp. 12–25, 2019.
ista: Hannezo EB, Heisenberg C-PJ. 2019. Mechanochemical feedback loops in development
and disease. Cell. 178(1), 12–25.
mla: Hannezo, Edouard B., and Carl-Philipp J. Heisenberg. “Mechanochemical Feedback
Loops in Development and Disease.” Cell, vol. 178, no. 1, Elsevier, 2019,
pp. 12–25, doi:10.1016/j.cell.2019.05.052.
short: E.B. Hannezo, C.-P.J. Heisenberg, Cell 178 (2019) 12–25.
date_created: 2019-06-30T21:59:11Z
date_published: 2019-07-27T00:00:00Z
date_updated: 2026-06-18T19:09:33Z
day: '27'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
doi: 10.1016/j.cell.2019.05.052
ec_funded: 1
external_id:
isi:
- '000473002700005'
pmid:
- '31251912'
fulldoi: https://doi.org/10.1016/j.cell.2019.05.052
intvolume: ' 178'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cell.2019.05.052
month: '07'
oa: 1
oa_version: Published Version
page: 12-25
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 268294B6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31639
name: Active mechano-chemical description of the cell cytoskeleton
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanochemical feedback loops in development and disease
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 178
year: '2019'
...
---
_id: '6832'
abstract:
- lang: eng
text: Steady-state turnover is a hallmark of epithelial tissues throughout adult
life. Intestinal epithelial turnover is marked by continuous cell migration, which
is assumed to be driven by mitotic pressure from the crypts. However, the balance
of forces in renewal remains ill-defined. Combining biophysical modeling and quantitative
three-dimensional tissue imaging with genetic and physical manipulations, we revealed
the existence of an actin-related protein 2/3 complex–dependent active migratory
force, which explains quantitatively the profiles of cell speed, density, and
tissue tension along the villi. Cells migrate collectively with minimal rearrangements
while displaying dual—apicobasal and front-back—polarity characterized by actin-rich
basal protrusions oriented in the direction of migration. We propose that active
migration is a critical component of gut epithelial turnover.
article_processing_charge: No
author:
- first_name: Denis
full_name: Krndija, Denis
last_name: Krndija
- first_name: Fatima El
full_name: Marjou, Fatima El
last_name: Marjou
- first_name: Boris
full_name: Guirao, Boris
last_name: Guirao
- first_name: Sophie
full_name: Richon, Sophie
last_name: Richon
- first_name: Olivier
full_name: Leroy, Olivier
last_name: Leroy
- first_name: Yohanns
full_name: Bellaiche, Yohanns
last_name: Bellaiche
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Danijela Matic
full_name: Vignjevic, Danijela Matic
last_name: Vignjevic
citation:
ama: Krndija D, Marjou FE, Guirao B, et al. Active cell migration is critical for
steady-state epithelial turnover in the gut. Science. 2019;365(6454):705-710.
doi:10.1126/science.aau3429
apa: Krndija, D., Marjou, F. E., Guirao, B., Richon, S., Leroy, O., Bellaiche, Y.,
… Vignjevic, D. M. (2019). Active cell migration is critical for steady-state
epithelial turnover in the gut. Science. American Association for the Advancement
of Science. https://doi.org/10.1126/science.aau3429
chicago: Krndija, Denis, Fatima El Marjou, Boris Guirao, Sophie Richon, Olivier
Leroy, Yohanns Bellaiche, Edouard B Hannezo, and Danijela Matic Vignjevic. “Active
Cell Migration Is Critical for Steady-State Epithelial Turnover in the Gut.” Science.
American Association for the Advancement of Science, 2019. https://doi.org/10.1126/science.aau3429.
ieee: D. Krndija et al., “Active cell migration is critical for steady-state
epithelial turnover in the gut,” Science, vol. 365, no. 6454. American
Association for the Advancement of Science, pp. 705–710, 2019.
ista: Krndija D, Marjou FE, Guirao B, Richon S, Leroy O, Bellaiche Y, Hannezo EB,
Vignjevic DM. 2019. Active cell migration is critical for steady-state epithelial
turnover in the gut. Science. 365(6454), 705–710.
mla: Krndija, Denis, et al. “Active Cell Migration Is Critical for Steady-State
Epithelial Turnover in the Gut.” Science, vol. 365, no. 6454, American
Association for the Advancement of Science, 2019, pp. 705–10, doi:10.1126/science.aau3429.
short: D. Krndija, F.E. Marjou, B. Guirao, S. Richon, O. Leroy, Y. Bellaiche, E.B.
Hannezo, D.M. Vignjevic, Science 365 (2019) 705–710.
date_created: 2019-08-25T22:00:51Z
date_published: 2019-08-16T00:00:00Z
date_updated: 2023-08-29T07:16:40Z
day: '16'
department:
- _id: EdHa
doi: 10.1126/science.aau3429
external_id:
isi:
- '000481688700050'
pmid:
- '31416964'
fulldoi: https://doi.org/10.1126/science.aau3429
intvolume: ' 365'
isi: 1
issue: '6454'
language:
- iso: eng
month: '08'
oa_version: None
page: 705-710
pmid: 1
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Active cell migration is critical for steady-state epithelial turnover in the
gut
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 365
year: '2019'
...
---
_id: '9726'
abstract:
- lang: eng
text: A detailed description of the two stochastic models, table of parameters,
supplementary data for Figures 4 and 5, parameter dependence of the results, and
an analysis on motors with different force–velocity functions (PDF)
article_processing_charge: No
author:
- first_name: Mehmet C
full_name: Ucar, Mehmet C
id: 50B2A802-6007-11E9-A42B-EB23E6697425
last_name: Ucar
orcid: 0000-0003-0506-4217
- first_name: Reinhard
full_name: Lipowsky, Reinhard
last_name: Lipowsky
citation:
ama: Ucar MC, Lipowsky R. Supplementary information - Collective force generation
by molecular motors is determined by strain-induced unbinding. 2019. doi:10.1021/acs.nanolett.9b04445.s001
apa: Ucar, M. C., & Lipowsky, R. (2019). Supplementary information - Collective
force generation by molecular motors is determined by strain-induced unbinding.
American Chemical Society. https://doi.org/10.1021/acs.nanolett.9b04445.s001
chicago: Ucar, Mehmet C, and Reinhard Lipowsky. “Supplementary Information - Collective
Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.”
American Chemical Society, 2019. https://doi.org/10.1021/acs.nanolett.9b04445.s001.
ieee: M. C. Ucar and R. Lipowsky, “Supplementary information - Collective force
generation by molecular motors is determined by strain-induced unbinding.” American
Chemical Society, 2019.
ista: Ucar MC, Lipowsky R. 2019. Supplementary information - Collective force generation
by molecular motors is determined by strain-induced unbinding, American Chemical
Society, 10.1021/acs.nanolett.9b04445.s001.
mla: Ucar, Mehmet C., and Reinhard Lipowsky. Supplementary Information - Collective
Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.
American Chemical Society, 2019, doi:10.1021/acs.nanolett.9b04445.s001.
short: M.C. Ucar, R. Lipowsky, (2019).
date_created: 2021-07-27T09:51:46Z
date_published: 2019-12-19T00:00:00Z
date_updated: 2026-07-06T12:13:40Z
day: '19'
department:
- _id: EdHa
doi: 10.1021/acs.nanolett.9b04445.s001
fulldoi: https://doi.org/10.1021/acs.nanolett.9b04445.s001
month: '12'
oa_version: Published Version
publisher: American Chemical Society
related_material:
record:
- id: '7166'
relation: used_in_publication
status: public
status: public
title: Supplementary information - Collective force generation by molecular motors
is determined by strain-induced unbinding
type: research_data_reference
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2019'
...
---
_id: '6508'
abstract:
- lang: eng
text: Segregation of maternal determinants within the oocyte constitutes the first
step in embryo patterning. In zebrafish oocytes, extensive ooplasmic streaming
leads to the segregation of ooplasm from yolk granules along the animal-vegetal
axis of the oocyte. Here, we show that this process does not rely on cortical
actin reorganization, as previously thought, but instead on a cell-cycle-dependent
bulk actin polymerization wave traveling from the animal to the vegetal pole of
the oocyte. This wave functions in segregation by both pulling ooplasm animally
and pushing yolk granules vegetally. Using biophysical experimentation and theory,
we show that ooplasm pulling is mediated by bulk actin network flows exerting
friction forces on the ooplasm, while yolk granule pushing is achieved by a mechanism
closely resembling actin comet formation on yolk granules. Our study defines a
novel role of cell-cycle-controlled bulk actin polymerization waves in oocyte
polarization via ooplasmic segregation.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We would like to thank Pierre Recho, Guillaume Salbreux, and Silvia
Grigolon for advice on the theory, Lila Solnica-Krezel for kindly providing us with
zebrafish dachsous mutants, members of the Heisenberg and Hannezo groups for fruitful
discussions, and the Bioimaging and zebrafish facilities at IST Austria for their
continuous support. This project has received funding from the European Union (European
Research Council Advanced Grant 742573 to C.P.H.) and from the Austrian Science
Fund (FWF) (P 31639 to E.H.).
article_processing_charge: No
article_type: original
author:
- first_name: Shayan
full_name: Shamipour, Shayan
id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
last_name: Shamipour
- first_name: Roland
full_name: Kardos, Roland
id: 4039350E-F248-11E8-B48F-1D18A9856A87
last_name: Kardos
- first_name: Shi-lei
full_name: Xue, Shi-lei
id: 31D2C804-F248-11E8-B48F-1D18A9856A87
last_name: Xue
- first_name: Björn
full_name: Hof, Björn
id: 3A374330-F248-11E8-B48F-1D18A9856A87
last_name: Hof
orcid: 0000-0003-2057-2754
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Carl-Philipp J
full_name: Heisenberg, Carl-Philipp J
id: 39427864-F248-11E8-B48F-1D18A9856A87
last_name: Heisenberg
orcid: 0000-0002-0912-4566
citation:
ama: Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. Bulk actin
dynamics drive phase segregation in zebrafish oocytes. Cell. 2019;177(6):1463-1479.e18.
doi:10.1016/j.cell.2019.04.030
apa: Shamipour, S., Kardos, R., Xue, S., Hof, B., Hannezo, E. B., & Heisenberg,
C.-P. J. (2019). Bulk actin dynamics drive phase segregation in zebrafish oocytes.
Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.04.030
chicago: Shamipour, Shayan, Roland Kardos, Shi-lei Xue, Björn Hof, Edouard B Hannezo,
and Carl-Philipp J Heisenberg. “Bulk Actin Dynamics Drive Phase Segregation in
Zebrafish Oocytes.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.04.030.
ieee: S. Shamipour, R. Kardos, S. Xue, B. Hof, E. B. Hannezo, and C.-P. J. Heisenberg,
“Bulk actin dynamics drive phase segregation in zebrafish oocytes,” Cell,
vol. 177, no. 6. Elsevier, p. 1463–1479.e18, 2019.
ista: Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. 2019. Bulk
actin dynamics drive phase segregation in zebrafish oocytes. Cell. 177(6), 1463–1479.e18.
mla: Shamipour, Shayan, et al. “Bulk Actin Dynamics Drive Phase Segregation in Zebrafish
Oocytes.” Cell, vol. 177, no. 6, Elsevier, 2019, p. 1463–1479.e18, doi:10.1016/j.cell.2019.04.030.
short: S. Shamipour, R. Kardos, S. Xue, B. Hof, E.B. Hannezo, C.-P.J. Heisenberg,
Cell 177 (2019) 1463–1479.e18.
date_created: 2019-06-02T21:59:12Z
date_published: 2019-05-30T00:00:00Z
date_updated: 2026-10-23T22:30:23Z
day: '30'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
- _id: BjHo
doi: 10.1016/j.cell.2019.04.030
ec_funded: 1
external_id:
isi:
- '000469415100013'
pmid:
- '31080065'
file:
- access_level: open_access
checksum: aea43726d80e35ce3885073a5f05c3e3
content_type: application/pdf
creator: dernst
date_created: 2020-10-21T07:22:34Z
date_updated: 2020-10-21T07:22:34Z
file_id: '8686'
file_name: 2019_Cell_Shamipour_accepted.pdf
file_size: 3356292
relation: main_file
success: 1
file_date_updated: 2020-10-21T07:22:34Z
fulldoi: https://doi.org/10.1016/j.cell.2019.04.030
has_accepted_license: '1'
intvolume: ' 177'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1016/j.cell.2019.04.030
month: '05'
oa: 1
oa_version: Published Version
page: 1463-1479.e18
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
call_identifier: H2020
grant_number: '742573'
name: Interaction and feedback between cell mechanics and fate specification in
vertebrate gastrulation
- _id: 268294B6-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: P31639
name: Active mechano-chemical description of the cell cytoskeleton
publication: Cell
publication_identifier:
eissn:
- 1097-4172
issn:
- 0092-8674
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/how-the-cytoplasm-separates-from-the-yolk/
record:
- id: '8350'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Bulk actin dynamics drive phase segregation in zebrafish oocytes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 177
year: '2019'
...
---
_id: '288'
abstract:
- lang: eng
text: Recent lineage tracing studies have revealed that mammary gland homeostasis
relies on unipotent stem cells. However, whether and when lineage restriction
occurs during embryonic mammary development, and which signals orchestrate cell
fate specification, remain unknown. Using a combination of in vivo clonal analysis
with whole mount immunofluorescence and mathematical modelling of clonal dynamics,
we found that embryonic multipotent mammary cells become lineage-restricted surprisingly
early in development, with evidence for unipotency as early as E12.5 and no statistically
discernable bipotency after E15.5. To gain insights into the mechanisms governing
the switch from multipotency to unipotency, we used gain-of-function Notch1 mice
and demonstrated that Notch activation cell autonomously dictates luminal cell
fate specification to both embryonic and basally committed mammary cells. These
functional studies have important implications for understanding the signals underlying
cell plasticity and serve to clarify how reactivation of embryonic programs in
adult cells can lead to cancer.
article_processing_charge: No
article_type: original
author:
- first_name: Anna
full_name: Lilja, Anna
last_name: Lilja
- first_name: Veronica
full_name: Rodilla, Veronica
last_name: Rodilla
- first_name: Mathilde
full_name: Huyghe, Mathilde
last_name: Huyghe
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Camille
full_name: Landragin, Camille
last_name: Landragin
- first_name: Olivier
full_name: Renaud, Olivier
last_name: Renaud
- first_name: Olivier
full_name: Leroy, Olivier
last_name: Leroy
- first_name: Steffen
full_name: Rulands, Steffen
last_name: Rulands
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
- first_name: Silvia
full_name: Fré, Silvia
last_name: Fré
citation:
ama: Lilja A, Rodilla V, Huyghe M, et al. Clonal analysis of Notch1-expressing cells
reveals the existence of unipotent stem cells that retain long-term plasticity
in the embryonic mammary gland. Nature Cell Biology. 2018;20(6):677-687.
doi:10.1038/s41556-018-0108-1
apa: Lilja, A., Rodilla, V., Huyghe, M., Hannezo, E. B., Landragin, C., Renaud,
O., … Fré, S. (2018). Clonal analysis of Notch1-expressing cells reveals the existence
of unipotent stem cells that retain long-term plasticity in the embryonic mammary
gland. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/s41556-018-0108-1
chicago: Lilja, Anna, Veronica Rodilla, Mathilde Huyghe, Edouard B Hannezo, Camille
Landragin, Olivier Renaud, Olivier Leroy, Steffen Rulands, Benjamin Simons, and
Silvia Fré. “Clonal Analysis of Notch1-Expressing Cells Reveals the Existence
of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic Mammary
Gland.” Nature Cell Biology. Nature Publishing Group, 2018. https://doi.org/10.1038/s41556-018-0108-1.
ieee: A. Lilja et al., “Clonal analysis of Notch1-expressing cells reveals
the existence of unipotent stem cells that retain long-term plasticity in the
embryonic mammary gland,” Nature Cell Biology, vol. 20, no. 6. Nature Publishing
Group, pp. 677–687, 2018.
ista: Lilja A, Rodilla V, Huyghe M, Hannezo EB, Landragin C, Renaud O, Leroy O,
Rulands S, Simons B, Fré S. 2018. Clonal analysis of Notch1-expressing cells reveals
the existence of unipotent stem cells that retain long-term plasticity in the
embryonic mammary gland. Nature Cell Biology. 20(6), 677–687.
mla: Lilja, Anna, et al. “Clonal Analysis of Notch1-Expressing Cells Reveals the
Existence of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic
Mammary Gland.” Nature Cell Biology, vol. 20, no. 6, Nature Publishing
Group, 2018, pp. 677–87, doi:10.1038/s41556-018-0108-1.
short: A. Lilja, V. Rodilla, M. Huyghe, E.B. Hannezo, C. Landragin, O. Renaud, O.
Leroy, S. Rulands, B. Simons, S. Fré, Nature Cell Biology 20 (2018) 677–687.
date_created: 2018-12-11T11:45:38Z
date_published: 2018-05-21T00:00:00Z
date_updated: 2023-09-11T12:44:08Z
day: '21'
department:
- _id: EdHa
doi: 10.1038/s41556-018-0108-1
external_id:
isi:
- '000433237300003'
pmid:
- '29784917'
fulldoi: https://doi.org/10.1038/s41556-018-0108-1
intvolume: ' 20'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984964
month: '05'
oa: 1
oa_version: Submitted Version
page: 677 - 687
pmid: 1
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '7594'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Clonal analysis of Notch1-expressing cells reveals the existence of unipotent
stem cells that retain long-term plasticity in the embryonic mammary gland
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 20
year: '2018'
...
---
_id: '132'
abstract:
- lang: eng
text: Pancreas development involves a coordinated process in which an early phase
of cell segregation is followed by a longer phase of lineage restriction, expansion,
and tissue remodeling. By combining clonal tracing and whole-mount reconstruction
with proliferation kinetics and single-cell transcriptional profiling, we define
the functional basis of pancreas morphogenesis. We show that the large-scale organization
of mouse pancreas can be traced to the activity of self-renewing precursors positioned
at the termini of growing ducts, which act collectively to drive serial rounds
of stochastic ductal bifurcation balanced by termination. During this phase of
branching morphogenesis, multipotent precursors become progressively fate-restricted,
giving rise to self-renewing acinar-committed precursors that are conveyed with
growing ducts, as well as ductal progenitors that expand the trailing ducts and
give rise to delaminating endocrine cells. These findings define quantitatively
how the functional behavior and lineage progression of precursor pools determine
the large-scale patterning of pancreatic sub-compartments.
acknowledgement: E.H. is funded by a Junior Research Fellowship from Trinity College,
Cam-bridge, a Sir Henry Wellcome Fellowship from the Wellcome Trust, and theBettencourt-Schueller
Young Researcher Prize for support.
article_processing_charge: No
article_type: original
author:
- first_name: Magdalena
full_name: Sznurkowska, Magdalena
last_name: Sznurkowska
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Roberta
full_name: Azzarelli, Roberta
last_name: Azzarelli
- first_name: Steffen
full_name: Rulands, Steffen
last_name: Rulands
- first_name: Sonia
full_name: Nestorowa, Sonia
last_name: Nestorowa
- first_name: Christopher
full_name: Hindley, Christopher
last_name: Hindley
- first_name: Jennifer
full_name: Nichols, Jennifer
last_name: Nichols
- first_name: Berthold
full_name: Göttgens, Berthold
last_name: Göttgens
- first_name: Meritxell
full_name: Huch, Meritxell
last_name: Huch
- first_name: Anna
full_name: Philpott, Anna
last_name: Philpott
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
citation:
ama: Sznurkowska M, Hannezo EB, Azzarelli R, et al. Defining lineage potential and
fate behavior of precursors during pancreas development. Developmental Cell.
2018;46(3):360-375. doi:10.1016/j.devcel.2018.06.028
apa: Sznurkowska, M., Hannezo, E. B., Azzarelli, R., Rulands, S., Nestorowa, S.,
Hindley, C., … Simons, B. (2018). Defining lineage potential and fate behavior
of precursors during pancreas development. Developmental Cell. Cell Press.
https://doi.org/10.1016/j.devcel.2018.06.028
chicago: Sznurkowska, Magdalena, Edouard B Hannezo, Roberta Azzarelli, Steffen Rulands,
Sonia Nestorowa, Christopher Hindley, Jennifer Nichols, et al. “Defining Lineage
Potential and Fate Behavior of Precursors during Pancreas Development.” Developmental
Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.06.028.
ieee: M. Sznurkowska et al., “Defining lineage potential and fate behavior
of precursors during pancreas development,” Developmental Cell, vol. 46,
no. 3. Cell Press, pp. 360–375, 2018.
ista: Sznurkowska M, Hannezo EB, Azzarelli R, Rulands S, Nestorowa S, Hindley C,
Nichols J, Göttgens B, Huch M, Philpott A, Simons B. 2018. Defining lineage potential
and fate behavior of precursors during pancreas development. Developmental Cell.
46(3), 360–375.
mla: Sznurkowska, Magdalena, et al. “Defining Lineage Potential and Fate Behavior
of Precursors during Pancreas Development.” Developmental Cell, vol. 46,
no. 3, Cell Press, 2018, pp. 360–75, doi:10.1016/j.devcel.2018.06.028.
short: M. Sznurkowska, E.B. Hannezo, R. Azzarelli, S. Rulands, S. Nestorowa, C.
Hindley, J. Nichols, B. Göttgens, M. Huch, A. Philpott, B. Simons, Developmental
Cell 46 (2018) 360–375.
date_created: 2018-12-11T11:44:48Z
date_published: 2018-08-06T00:00:00Z
date_updated: 2023-09-11T12:52:41Z
day: '06'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1016/j.devcel.2018.06.028
external_id:
isi:
- '000441327300012'
file:
- access_level: open_access
checksum: 78d2062b9e3c3b90fe71545aeb6d2f65
content_type: application/pdf
creator: dernst
date_created: 2018-12-17T10:49:49Z
date_updated: 2020-07-14T12:44:43Z
file_id: '5694'
file_name: 2018_DevelopmentalCell_Sznurkowska.pdf
file_size: 8948384
relation: main_file
file_date_updated: 2020-07-14T12:44:43Z
fulldoi: https://doi.org/10.1016/j.devcel.2018.06.028
has_accepted_license: '1'
intvolume: ' 46'
isi: 1
issue: '3'
language:
- iso: eng
month: '08'
oa: 1
oa_version: Published Version
page: 360 - 375
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '7791'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Defining lineage potential and fate behavior of precursors during pancreas
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: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 46
year: '2018'
...
---
_id: '5787'
abstract:
- lang: eng
text: "Branching morphogenesis remains a subject of abiding interest. Although
\ much is \r\nknown about the gene regulatory programs and signaling pathways
that operate at \r\nthe cellular scale, it has remained unclear how the macroscopic
features of branched \r\norgans, including their size, network topology and
\ spatial patterning, are encoded. \r\nLately, it has been proposed that,
these features can be explained quantitatively in \r\nseveral organs within a
single unifying framework. Based on large-\r\nscale organ recon\r\n-\r\nstructions
\ and cell lineage tracing, it has been argued that morphogenesis follows
\ \r\nfrom the collective dynamics of sublineage- \r\nrestricted self- \r\nrenewing
progenitor cells, \r\nlocalized at ductal tips, that act cooperatively to drive
a serial process of ductal elon\r\n-\r\ngation and stochastic tip bifurcation.
By correlating differentiation or cell cycle exit \r\nwith proximity to maturing
ducts, this dynamic results in the specification of a com-\r\nplex network of
\ defined density and statistical organization. These results suggest \r\nthat,
for several mammalian tissues, branched epithelial structures develop as a self-
\r\norganized process, reliant upon a strikingly simple, but generic,
\ set of local rules, \r\nwithout recourse to a rigid and deterministic
\ sequence of genetically programmed \r\nevents. Here, we review the basis
of these findings and discuss their implications."
article_processing_charge: No
author:
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Benjamin D.
full_name: Simons, Benjamin D.
last_name: Simons
citation:
ama: Hannezo EB, Simons BD. Statistical theory of branching morphogenesis. Development
Growth and Differentiation. 2018;60(9):512-521. doi:10.1111/dgd.12570
apa: Hannezo, E. B., & Simons, B. D. (2018). Statistical theory of branching
morphogenesis. Development Growth and Differentiation. Wiley. https://doi.org/10.1111/dgd.12570
chicago: Hannezo, Edouard B, and Benjamin D. Simons. “Statistical Theory of Branching
Morphogenesis.” Development Growth and Differentiation. Wiley, 2018. https://doi.org/10.1111/dgd.12570.
ieee: E. B. Hannezo and B. D. Simons, “Statistical theory of branching morphogenesis,”
Development Growth and Differentiation, vol. 60, no. 9. Wiley, pp. 512–521,
2018.
ista: Hannezo EB, Simons BD. 2018. Statistical theory of branching morphogenesis.
Development Growth and Differentiation. 60(9), 512–521.
mla: Hannezo, Edouard B., and Benjamin D. Simons. “Statistical Theory of Branching
Morphogenesis.” Development Growth and Differentiation, vol. 60, no. 9,
Wiley, 2018, pp. 512–21, doi:10.1111/dgd.12570.
short: E.B. Hannezo, B.D. Simons, Development Growth and Differentiation 60 (2018)
512–521.
date_created: 2018-12-30T22:59:14Z
date_published: 2018-12-09T00:00:00Z
date_updated: 2025-07-10T11:52:59Z
day: '09'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1111/dgd.12570
external_id:
isi:
- '000453555100002'
file:
- access_level: open_access
checksum: a6d30b0785db902c734a84fecb2eadd9
content_type: application/pdf
creator: dernst
date_created: 2019-02-06T10:40:46Z
date_updated: 2020-07-14T12:47:11Z
file_id: '5933'
file_name: 2018_DevGrowh_Hannezo.pdf
file_size: 1313606
relation: main_file
file_date_updated: 2020-07-14T12:47:11Z
fulldoi: https://doi.org/10.1111/dgd.12570
has_accepted_license: '1'
intvolume: ' 60'
isi: 1
issue: '9'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 512-521
publication: Development Growth and Differentiation
publication_identifier:
issn:
- 0012-1592
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Statistical theory of branching morphogenesis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 60
year: '2018'
...
---
_id: '5859'
abstract:
- lang: eng
text: The emergence of syntax during childhood is a remarkable example of how complex
correlations unfold in nonlinear ways through development. In particular, rapid
transitions seem to occur as children reach the age of two, which seems to separate
a two-word, tree-like network of syntactic relations among words from the scale-free
graphs associated with the adult, complex grammar. Here, we explore the evolution
of syntax networks through language acquisition using the chromatic number, which
captures the transition and provides a natural link to standard theories on syntactic
structures. The data analysis is compared to a null model of network growth dynamics
which is shown to display non-trivial and sensible differences. At a more general
level, we observe that the chromatic classes define independent regions of the
graph, and thus, can be interpreted as the footprints of incompatibility relations,
somewhat as opposed to modularity considerations.
acknowledgement: This work was supported by the James McDonnell Foundation (B.C-M.,
S.V. and R.S.)
article_number: '181286'
article_processing_charge: No
article_type: original
author:
- first_name: Bernat
full_name: Corominas-Murtra, Bernat
id: 43BE2298-F248-11E8-B48F-1D18A9856A87
last_name: Corominas-Murtra
orcid: 0000-0001-9806-5643
- first_name: Martí Sànchez
full_name: Fibla, Martí Sànchez
last_name: Fibla
- first_name: Sergi
full_name: Valverde, Sergi
last_name: Valverde
- first_name: Ricard
full_name: Solé, Ricard
last_name: Solé
citation:
ama: Corominas-Murtra B, Fibla MS, Valverde S, Solé R. Chromatic transitions in
the emergence of syntax networks. Royal Society Open Science. 2018;5(12).
doi:10.1098/rsos.181286
apa: Corominas-Murtra, B., Fibla, M. S., Valverde, S., & Solé, R. (2018). Chromatic
transitions in the emergence of syntax networks. Royal Society Open Science.
The Royal Society. https://doi.org/10.1098/rsos.181286
chicago: Corominas-Murtra, Bernat, Martí Sànchez Fibla, Sergi Valverde, and Ricard
Solé. “Chromatic Transitions in the Emergence of Syntax Networks.” Royal Society
Open Science. The Royal Society, 2018. https://doi.org/10.1098/rsos.181286.
ieee: B. Corominas-Murtra, M. S. Fibla, S. Valverde, and R. Solé, “Chromatic transitions
in the emergence of syntax networks,” Royal Society Open Science, vol.
5, no. 12. The Royal Society, 2018.
ista: Corominas-Murtra B, Fibla MS, Valverde S, Solé R. 2018. Chromatic transitions
in the emergence of syntax networks. Royal Society Open Science. 5(12), 181286.
mla: Corominas-Murtra, Bernat, et al. “Chromatic Transitions in the Emergence of
Syntax Networks.” Royal Society Open Science, vol. 5, no. 12, 181286, The
Royal Society, 2018, doi:10.1098/rsos.181286.
short: B. Corominas-Murtra, M.S. Fibla, S. Valverde, R. Solé, Royal Society Open
Science 5 (2018).
date_created: 2019-01-20T22:59:18Z
date_published: 2018-12-12T00:00:00Z
date_updated: 2023-10-18T06:41:12Z
day: '12'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1098/rsos.181286
external_id:
isi:
- '000456566500027'
pmid:
- '30662738'
file:
- access_level: open_access
checksum: 9664d4417f6b792242e31eea77ce9501
content_type: application/pdf
creator: dernst
date_created: 2019-02-05T14:38:09Z
date_updated: 2020-07-14T12:47:13Z
file_id: '5924'
file_name: 2018_RoyalSocOS_Corominas.pdf
file_size: 646732
relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
fulldoi: https://doi.org/10.1098/rsos.181286
has_accepted_license: '1'
intvolume: ' 5'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: Royal Society Open Science
publication_identifier:
issn:
- 2054-5703
publication_status: published
publisher: The Royal Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Chromatic transitions in the emergence of syntax networks
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2018'
...
---
_id: '401'
abstract:
- lang: eng
text: The actomyosin cytoskeleton, a key stress-producing unit in epithelial cells,
oscillates spontaneously in a wide variety of systems. Although much of the signal
cascade regulating myosin activity has been characterized, the origin of such
oscillatory behavior is still unclear. Here, we show that basal myosin II oscillation
in Drosophila ovarian epithelium is not controlled by actomyosin cortical tension,
but instead relies on a biochemical oscillator involving ROCK and myosin phosphatase.
Key to this oscillation is a diffusive ROCK flow, linking junctional Rho1 to medial
actomyosin cortex, and dynamically maintained by a self-activation loop reliant
on ROCK kinase activity. In response to the resulting myosin II recruitment, myosin
phosphatase is locally enriched and shuts off ROCK and myosin II signals. Coupling
Drosophila genetics, live imaging, modeling, and optogenetics, we uncover an intrinsic
biochemical oscillator at the core of myosin II regulatory network, shedding light
on the spatio-temporal dynamics of force generation.
article_number: '1210'
article_processing_charge: No
author:
- first_name: Xiang
full_name: Qin, Xiang
last_name: Qin
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Thomas
full_name: Mangeat, Thomas
last_name: Mangeat
- first_name: Chang
full_name: Liu, Chang
last_name: Liu
- first_name: Pralay
full_name: Majumder, Pralay
last_name: Majumder
- first_name: Jjiaying
full_name: Liu, Jjiaying
last_name: Liu
- first_name: Valerie
full_name: Choesmel Cadamuro, Valerie
last_name: Choesmel Cadamuro
- first_name: Jocelyn
full_name: Mcdonald, Jocelyn
last_name: Mcdonald
- first_name: Yinyao
full_name: Liu, Yinyao
last_name: Liu
- first_name: Bin
full_name: Yi, Bin
last_name: Yi
- first_name: Xiaobo
full_name: Wang, Xiaobo
last_name: Wang
citation:
ama: Qin X, Hannezo EB, Mangeat T, et al. A biochemical network controlling basal
myosin oscillation. Nature Communications. 2018;9(1). doi:10.1038/s41467-018-03574-5
apa: Qin, X., Hannezo, E. B., Mangeat, T., Liu, C., Majumder, P., Liu, J., … Wang,
X. (2018). A biochemical network controlling basal myosin oscillation. Nature
Communications. Nature Publishing Group. https://doi.org/10.1038/s41467-018-03574-5
chicago: Qin, Xiang, Edouard B Hannezo, Thomas Mangeat, Chang Liu, Pralay Majumder,
Jjiaying Liu, Valerie Choesmel Cadamuro, et al. “A Biochemical Network Controlling
Basal Myosin Oscillation.” Nature Communications. Nature Publishing Group,
2018. https://doi.org/10.1038/s41467-018-03574-5.
ieee: X. Qin et al., “A biochemical network controlling basal myosin oscillation,”
Nature Communications, vol. 9, no. 1. Nature Publishing Group, 2018.
ista: Qin X, Hannezo EB, Mangeat T, Liu C, Majumder P, Liu J, Choesmel Cadamuro
V, Mcdonald J, Liu Y, Yi B, Wang X. 2018. A biochemical network controlling basal
myosin oscillation. Nature Communications. 9(1), 1210.
mla: Qin, Xiang, et al. “A Biochemical Network Controlling Basal Myosin Oscillation.”
Nature Communications, vol. 9, no. 1, 1210, Nature Publishing Group, 2018,
doi:10.1038/s41467-018-03574-5.
short: X. Qin, E.B. Hannezo, T. Mangeat, C. Liu, P. Majumder, J. Liu, V. Choesmel
Cadamuro, J. Mcdonald, Y. Liu, B. Yi, X. Wang, Nature Communications 9 (2018).
date_created: 2018-12-11T11:46:16Z
date_published: 2018-03-23T00:00:00Z
date_updated: 2023-09-08T11:41:45Z
day: '23'
ddc:
- '539'
- '570'
department:
- _id: EdHa
doi: 10.1038/s41467-018-03574-5
external_id:
isi:
- '000428165400009'
file:
- access_level: open_access
checksum: 87a427bc2e8724be3dd22a4efdd21a33
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:45Z
date_updated: 2020-07-14T12:46:22Z
file_id: '4902'
file_name: IST-2018-996-v1+1_2018_Hannezo_A-biochemical.pdf
file_size: 3780491
relation: main_file
file_date_updated: 2020-07-14T12:46:22Z
fulldoi: https://doi.org/10.1038/s41467-018-03574-5
has_accepted_license: '1'
intvolume: ' 9'
isi: 1
issue: '1'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
publication: Nature Communications
publication_status: published
publisher: Nature Publishing Group
publist_id: '7427'
pubrep_id: '996'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A biochemical network controlling basal myosin oscillation
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: 9
year: '2018'
...
---
_id: '421'
abstract:
- lang: eng
text: Cell shape is determined by a balance of intrinsic properties of the cell
as well as its mechanochemical environment. Inhomogeneous shape changes underlie
many morphogenetic events and involve spatial gradients in active cellular forces
induced by complex chemical signaling. Here, we introduce a mechanochemical model
based on the notion that cell shape changes may be induced by external diffusible
biomolecules that influence cellular contractility (or equivalently, adhesions)
in a concentration-dependent manner—and whose spatial profile in turn is affected
by cell shape. We map out theoretically the possible interplay between chemical
concentration and cellular structure. Besides providing a direct route to spatial
gradients in cell shape profiles in tissues, we show that the dependence on cell
shape helps create robust mechanochemical gradients.
article_processing_charge: No
arxiv: 1
author:
- first_name: Kinjal
full_name: Dasbiswas, Kinjal
last_name: Dasbiswas
- first_name: Claude-Edouard B
full_name: Hannezo, Claude-Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Nir
full_name: Gov, Nir
last_name: Gov
citation:
ama: Dasbiswas K, Hannezo EB, Gov N. Theory of eppithelial cell shape transitions
induced by mechanoactive chemical gradients. Biophysical Journal. 2018;114(4):968-977.
doi:10.1016/j.bpj.2017.12.022
apa: Dasbiswas, K., Hannezo, E. B., & Gov, N. (2018). Theory of eppithelial
cell shape transitions induced by mechanoactive chemical gradients. Biophysical
Journal. Biophysical Society. https://doi.org/10.1016/j.bpj.2017.12.022
chicago: Dasbiswas, Kinjal, Edouard B Hannezo, and Nir Gov. “Theory of Eppithelial
Cell Shape Transitions Induced by Mechanoactive Chemical Gradients.” Biophysical
Journal. Biophysical Society, 2018. https://doi.org/10.1016/j.bpj.2017.12.022.
ieee: K. Dasbiswas, E. B. Hannezo, and N. Gov, “Theory of eppithelial cell shape
transitions induced by mechanoactive chemical gradients,” Biophysical Journal,
vol. 114, no. 4. Biophysical Society, pp. 968–977, 2018.
ista: Dasbiswas K, Hannezo EB, Gov N. 2018. Theory of eppithelial cell shape transitions
induced by mechanoactive chemical gradients. Biophysical Journal. 114(4), 968–977.
mla: Dasbiswas, Kinjal, et al. “Theory of Eppithelial Cell Shape Transitions Induced
by Mechanoactive Chemical Gradients.” Biophysical Journal, vol. 114, no.
4, Biophysical Society, 2018, pp. 968–77, doi:10.1016/j.bpj.2017.12.022.
short: K. Dasbiswas, E.B. Hannezo, N. Gov, Biophysical Journal 114 (2018) 968–977.
date_created: 2018-12-11T11:46:23Z
date_published: 2018-02-27T00:00:00Z
date_updated: 2023-09-19T10:13:55Z
day: '27'
department:
- _id: EdHa
doi: 10.1016/j.bpj.2017.12.022
external_id:
arxiv:
- '1709.01486'
isi:
- '000428016700021'
fulldoi: https://doi.org/10.1016/j.bpj.2017.12.022
intvolume: ' 114'
isi: 1
issue: '4'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1709.01486
month: '02'
oa: 1
oa_version: Submitted Version
page: 968 - 977
publication: Biophysical Journal
publication_status: published
publisher: Biophysical Society
publist_id: '7403'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Theory of eppithelial cell shape transitions induced by mechanoactive chemical
gradients
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 114
year: '2018'
...
---
_id: '5860'
abstract:
- lang: eng
text: 'A major problem for evolutionary theory is understanding the so-called open-ended
nature of evolutionary change, from its definition to its origins. Open-ended
evolution (OEE) refers to the unbounded increase in complexity that seems to characterize
evolution on multiple scales. This property seems to be a characteristic feature
of biological and technological evolution and is strongly tied to the generative
potential associated with combinatorics, which allows the system to grow and expand
their available state spaces. Interestingly, many complex systems presumably displaying
OEE, from language to proteins, share a common statistical property: the presence
of Zipf''s Law. Given an inventory of basic items (such as words or protein domains)
required to build more complex structures (sentences or proteins) Zipf''s Law
tells us that most of these elements are rare whereas a few of them are extremely
common. Using algorithmic information theory, in this paper we provide a fundamental
definition for open-endedness, which can be understood as postulates. Its statistical
counterpart, based on standard Shannon information theory, has the structure of
a variational problem which is shown to lead to Zipf''s Law as the expected consequence
of an evolutionary process displaying OEE. We further explore the problem of information
conservation through an OEE process and we conclude that statistical information
(standard Shannon information) is not conserved, resulting in the paradoxical
situation in which the increase of information content has the effect of erasing
itself. We prove that this paradox is solved if we consider non-statistical forms
of information. This last result implies that standard information theory may
not be a suitable theoretical framework to explore the persistence and increase
of the information content in OEE systems.'
article_number: '20180395'
article_processing_charge: No
arxiv: 1
author:
- first_name: Bernat
full_name: Corominas-Murtra, Bernat
id: 43BE2298-F248-11E8-B48F-1D18A9856A87
last_name: Corominas-Murtra
orcid: 0000-0001-9806-5643
- first_name: Luís F.
full_name: Seoane, Luís F.
last_name: Seoane
- first_name: Ricard
full_name: Solé, Ricard
last_name: Solé
citation:
ama: Corominas-Murtra B, Seoane LF, Solé R. Zipf’s Law, unbounded complexity and
open-ended evolution. Journal of the Royal Society Interface. 2018;15(149).
doi:10.1098/rsif.2018.0395
apa: Corominas-Murtra, B., Seoane, L. F., & Solé, R. (2018). Zipf’s Law, unbounded
complexity and open-ended evolution. Journal of the Royal Society Interface.
Royal Society. https://doi.org/10.1098/rsif.2018.0395
chicago: Corominas-Murtra, Bernat, Luís F. Seoane, and Ricard Solé. “Zipf’s Law,
Unbounded Complexity and Open-Ended Evolution.” Journal of the Royal Society
Interface. Royal Society, 2018. https://doi.org/10.1098/rsif.2018.0395.
ieee: B. Corominas-Murtra, L. F. Seoane, and R. Solé, “Zipf’s Law, unbounded complexity
and open-ended evolution,” Journal of the Royal Society Interface, vol.
15, no. 149. Royal Society, 2018.
ista: Corominas-Murtra B, Seoane LF, Solé R. 2018. Zipf’s Law, unbounded complexity
and open-ended evolution. Journal of the Royal Society Interface. 15(149), 20180395.
mla: Corominas-Murtra, Bernat, et al. “Zipf’s Law, Unbounded Complexity and Open-Ended
Evolution.” Journal of the Royal Society Interface, vol. 15, no. 149, 20180395,
Royal Society, 2018, doi:10.1098/rsif.2018.0395.
short: B. Corominas-Murtra, L.F. Seoane, R. Solé, Journal of the Royal Society Interface
15 (2018).
date_created: 2019-01-20T22:59:19Z
date_published: 2018-12-12T00:00:00Z
date_updated: 2026-08-12T06:28:34Z
day: '12'
department:
- _id: EdHa
doi: 10.1098/rsif.2018.0395
external_id:
arxiv:
- '1612.01605'
isi:
- '000456783800002'
fulldoi: https://doi.org/10.1098/rsif.2018.0395
intvolume: ' 15'
isi: 1
issue: '149'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://arxiv.org/abs/1612.01605
month: '12'
oa: 1
oa_version: Preprint
publication: Journal of the Royal Society Interface
publication_identifier:
issn:
- 1742-5689
publication_status: published
publisher: Royal Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Zipf's Law, unbounded complexity and open-ended evolution
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2018'
...
---
_id: '3'
abstract:
- lang: eng
text: SETD5 gene mutations have been identified as a frequent cause of idiopathic
intellectual disability. Here we show that Setd5-haploinsufficient mice present
developmental defects such as abnormal brain-to-body weight ratios and neural
crest defect-associated phenotypes. Furthermore, Setd5-mutant mice show impairments
in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile
of ultrasonic vocalization, and behavioral inflexibility. Behavioral issues are
accompanied by abnormal expression of postsynaptic density proteins previously
associated with cognition. Our data additionally indicate that Setd5 regulates
RNA polymerase II dynamics and gene transcription via its interaction with the
Hdac3 and Paf1 complexes, findings potentially explaining the gene expression
defects observed in Setd5-haploinsufficient mice. Our results emphasize the decisive
role of Setd5 in a biological pathway found to be disrupted in humans with intellectual
disability and autism spectrum disorder.
acknowledged_ssus:
- _id: M-Shop
- _id: PreCl
acknowledgement: This work was supported by the Simons Foundation Autism Research
Initiative (grant 401299) to G.N. and the DFG (SPP1738 grant NO 1249) to K.-M.N.
article_processing_charge: No
article_type: original
author:
- first_name: Elena
full_name: Deliu, Elena
id: 37A40D7E-F248-11E8-B48F-1D18A9856A87
last_name: Deliu
orcid: 0000-0002-7370-5293
- first_name: Niccoló
full_name: Arecco, Niccoló
last_name: Arecco
- first_name: Jasmin
full_name: Morandell, Jasmin
id: 4739D480-F248-11E8-B48F-1D18A9856A87
last_name: Morandell
- first_name: Christoph
full_name: Dotter, Christoph
id: 4C66542E-F248-11E8-B48F-1D18A9856A87
last_name: Dotter
orcid: 0000-0002-9033-9096
- first_name: Ximena
full_name: Contreras, Ximena
id: 475990FE-F248-11E8-B48F-1D18A9856A87
last_name: Contreras
- first_name: Charles
full_name: Girardot, Charles
last_name: Girardot
- first_name: Eva
full_name: Käsper, Eva
last_name: Käsper
- first_name: Alena
full_name: Kozlova, Alena
id: C50A9596-02D0-11E9-976E-E38CFE5CBC1D
last_name: Kozlova
- first_name: Kasumi
full_name: Kishi, Kasumi
id: 3065DFC4-F248-11E8-B48F-1D18A9856A87
last_name: Kishi
orcid: 0000-0001-6060-4795
- first_name: Ilaria
full_name: Chiaradia, Ilaria
id: B6467F20-02D0-11E9-BDA5-E960C241894A
last_name: Chiaradia
orcid: 0000-0002-9529-4464
- first_name: Kyung
full_name: Noh, Kyung
last_name: Noh
- first_name: Gaia
full_name: Novarino, Gaia
id: 3E57A680-F248-11E8-B48F-1D18A9856A87
last_name: Novarino
orcid: 0000-0002-7673-7178
citation:
ama: Deliu E, Arecco N, Morandell J, et al. Haploinsufficiency of the intellectual
disability gene SETD5 disturbs developmental gene expression and cognition. Nature
Neuroscience. 2018;21(12):1717-1727. doi:10.1038/s41593-018-0266-2
apa: Deliu, E., Arecco, N., Morandell, J., Dotter, C., Contreras, X., Girardot,
C., … Novarino, G. (2018). Haploinsufficiency of the intellectual disability gene
SETD5 disturbs developmental gene expression and cognition. Nature Neuroscience.
Nature Publishing Group. https://doi.org/10.1038/s41593-018-0266-2
chicago: Deliu, Elena, Niccoló Arecco, Jasmin Morandell, Christoph Dotter, Ximena
Contreras, Charles Girardot, Eva Käsper, et al. “Haploinsufficiency of the Intellectual
Disability Gene SETD5 Disturbs Developmental Gene Expression and Cognition.” Nature
Neuroscience. Nature Publishing Group, 2018. https://doi.org/10.1038/s41593-018-0266-2.
ieee: E. Deliu et al., “Haploinsufficiency of the intellectual disability
gene SETD5 disturbs developmental gene expression and cognition,” Nature Neuroscience,
vol. 21, no. 12. Nature Publishing Group, pp. 1717–1727, 2018.
ista: Deliu E, Arecco N, Morandell J, Dotter C, Contreras X, Girardot C, Käsper
E, Kozlova A, Kishi K, Chiaradia I, Noh K, Novarino G. 2018. Haploinsufficiency
of the intellectual disability gene SETD5 disturbs developmental gene expression
and cognition. Nature Neuroscience. 21(12), 1717–1727.
mla: Deliu, Elena, et al. “Haploinsufficiency of the Intellectual Disability Gene
SETD5 Disturbs Developmental Gene Expression and Cognition.” Nature Neuroscience,
vol. 21, no. 12, Nature Publishing Group, 2018, pp. 1717–27, doi:10.1038/s41593-018-0266-2.
short: E. Deliu, N. Arecco, J. Morandell, C. Dotter, X. Contreras, C. Girardot,
E. Käsper, A. Kozlova, K. Kishi, I. Chiaradia, K. Noh, G. Novarino, Nature Neuroscience
21 (2018) 1717–1727.
corr_author: '1'
date_created: 2018-12-11T11:44:05Z
date_published: 2018-11-19T00:00:00Z
date_updated: 2026-10-23T22:30:09Z
day: '19'
ddc:
- '570'
department:
- _id: GaNo
- _id: EdHa
doi: 10.1038/s41593-018-0266-2
external_id:
isi:
- '000451324700010'
file:
- access_level: open_access
checksum: 60abd0f05b7cdc08a6b0ec460884084f
content_type: application/pdf
creator: dernst
date_created: 2019-04-09T07:41:57Z
date_updated: 2020-07-14T12:45:58Z
file_id: '6255'
file_name: 2017_NatureNeuroscience_Deliu.pdf
file_size: 8167169
relation: main_file
file_date_updated: 2020-07-14T12:45:58Z
fulldoi: https://doi.org/10.1038/s41593-018-0266-2
has_accepted_license: '1'
intvolume: ' 21'
isi: 1
issue: '12'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Submitted Version
page: 1717 - 1727
project:
- _id: 254BA948-B435-11E9-9278-68D0E5697425
grant_number: '401299'
name: Probing development and reversibility of autism spectrum disorders
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '8054'
pubrep_id: '1071'
quality_controlled: '1'
related_material:
link:
- description: News on IST Homepage
relation: press_release
url: https://ist.ac.at/en/news/mutation-that-causes-autism-and-intellectual-disability-makes-brain-less-flexible/
record:
- id: '6074'
relation: popular_science
status: public
- id: '12364'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental
gene expression and cognition
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 21
year: '2018'
...
---
_id: '726'
abstract:
- lang: eng
text: The morphogenesis of branched organs remains a subject of abiding interest.
Although much is known about the underlying signaling pathways, it remains unclear
how macroscopic features of branched organs, including their size, network topology,
and spatial patterning, are encoded. Here, we show that, in mouse mammary gland,
kidney, and human prostate, these features can be explained quantitatively within
a single unifying framework of branching and annihilating random walks. Based
on quantitative analyses of large-scale organ reconstructions and proliferation
kinetics measurements, we propose that morphogenesis follows from the proliferative
activity of equipotent tips that stochastically branch and randomly explore their
environment but compete neutrally for space, becoming proliferatively inactive
when in proximity with neighboring ducts. These results show that complex branched
epithelial structures develop as a self-organized process, reliant upon a strikingly
simple but generic rule, without recourse to a rigid and deterministic sequence
of genetically programmed events.
article_processing_charge: No
author:
- first_name: Edouard B
full_name: Hannezo, Edouard B
id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
last_name: Hannezo
orcid: 0000-0001-6005-1561
- first_name: Colinda
full_name: Scheele, Colinda
last_name: Scheele
- first_name: Mohammad
full_name: Moad, Mohammad
last_name: Moad
- first_name: Nicholas
full_name: Drogo, Nicholas
last_name: Drogo
- first_name: Rakesh
full_name: Heer, Rakesh
last_name: Heer
- first_name: Rosemary
full_name: Sampogna, Rosemary
last_name: Sampogna
- first_name: Jacco
full_name: Van Rheenen, Jacco
last_name: Van Rheenen
- first_name: Benjamin
full_name: Simons, Benjamin
last_name: Simons
citation:
ama: Hannezo EB, Scheele C, Moad M, et al. A unifying theory of branching morphogenesis.
Cell. 2017;171(1):242-255. doi:10.1016/j.cell.2017.08.026
apa: Hannezo, E. B., Scheele, C., Moad, M., Drogo, N., Heer, R., Sampogna, R., …
Simons, B. (2017). A unifying theory of branching morphogenesis. Cell.
Cell Press. https://doi.org/10.1016/j.cell.2017.08.026
chicago: Hannezo, Edouard B, Colinda Scheele, Mohammad Moad, Nicholas Drogo, Rakesh
Heer, Rosemary Sampogna, Jacco Van Rheenen, and Benjamin Simons. “A Unifying Theory
of Branching Morphogenesis.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.08.026.
ieee: E. B. Hannezo et al., “A unifying theory of branching morphogenesis,”
Cell, vol. 171, no. 1. Cell Press, pp. 242–255, 2017.
ista: Hannezo EB, Scheele C, Moad M, Drogo N, Heer R, Sampogna R, Van Rheenen J,
Simons B. 2017. A unifying theory of branching morphogenesis. Cell. 171(1), 242–255.
mla: Hannezo, Edouard B., et al. “A Unifying Theory of Branching Morphogenesis.”
Cell, vol. 171, no. 1, Cell Press, 2017, pp. 242–55, doi:10.1016/j.cell.2017.08.026.
short: E.B. Hannezo, C. Scheele, M. Moad, N. Drogo, R. Heer, R. Sampogna, J. Van
Rheenen, B. Simons, Cell 171 (2017) 242–255.
corr_author: '1'
date_created: 2018-12-11T11:48:10Z
date_published: 2017-09-21T00:00:00Z
date_updated: 2025-07-10T11:54:27Z
day: '21'
ddc:
- '539'
department:
- _id: EdHa
doi: 10.1016/j.cell.2017.08.026
external_id:
isi:
- '000411331800024'
file:
- access_level: open_access
checksum: 7a036d93a9e2e597af9bb504d6133aca
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:11:17Z
date_updated: 2020-07-14T12:47:55Z
file_id: '4870'
file_name: IST-2017-883-v1+1_PIIS0092867417309510.pdf
file_size: 12670204
relation: main_file
file_date_updated: 2020-07-14T12:47:55Z
fulldoi: https://doi.org/10.1016/j.cell.2017.08.026
has_accepted_license: '1'
intvolume: ' 171'
isi: 1
issue: '1'
language:
- iso: eng
month: '09'
oa: 1
oa_version: Published Version
page: 242 - 255
publication: Cell
publication_identifier:
issn:
- 0092-8674
publication_status: published
publisher: Cell Press
publist_id: '6952'
pubrep_id: '883'
quality_controlled: '1'
scopus_import: '1'
status: public
title: A unifying theory of branching morphogenesis
tmp:
image: /images/cc_by.png
legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 171
year: '2017'
...