---
_id: '1566'
abstract:
- lang: eng
text: Deposits of misfolded proteins in the human brain are associated with the
development of many neurodegenerative diseases. Recent studies show that these
proteins have common traits even at the monomer level. Among them, a polyglutamine
region that is present in huntingtin is known to exhibit a correlation between
the length of the chain and the severity as well as the earliness of the onset
of Huntington disease. Here, we apply bias exchange molecular dynamics to generate
structures of polyglutamine expansions of several lengths and characterize the
resulting independent conformations. We compare the properties of these conformations
to those of the standard proteins, as well as to other homopolymeric tracts. We
find that, similar to the previously studied polyvaline chains, the set of possible
transient folds is much broader than the set of known-to-date folds, although
the conformations have different structures. We show that the mechanical stability
is not related to any simple geometrical characteristics of the structures. We
demonstrate that long polyglutamine expansions result in higher mechanical stability
than the shorter ones. They also have a longer life span and are substantially
more prone to form knotted structures. The knotted region has an average length
of 35 residues, similar to the typical threshold for most polyglutamine-related
diseases. Similarly, changes in shape and mechanical stability appear once the
total length of the peptide exceeds this threshold of 35 glutamine residues. We
suggest that knotted conformers may also harm the cellular machinery and thus
lead to disease.
acknowledgement: 'We acknowledge the support by the EU Joint Programme in Neurodegenerative
Diseases (JPND AC14/00037) project. The project is supported through the following
funding organisations under the aegis of JPND—www.jpnd.eu: Ireland, HRB; Poland,
National Science Centre; and Spain, ISCIII. '
article_number: e1004541
author:
- first_name: Àngel
full_name: Gómez Sicilia, Àngel
last_name: Gómez Sicilia
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Marek
full_name: Cieplak, Marek
last_name: Cieplak
- first_name: Mariano
full_name: Carrión Vázquez, Mariano
last_name: Carrión Vázquez
citation:
ama: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. An exploration of
the universe of polyglutamine structures. PLoS Computational Biology. 2015;11(10).
doi:10.1371/journal.pcbi.1004541
apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., & Carrión Vázquez, M. (2015).
An exploration of the universe of polyglutamine structures. PLoS Computational
Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004541
chicago: Gómez Sicilia, Àngel, Mateusz K Sikora, Marek Cieplak, and Mariano Carrión
Vázquez. “An Exploration of the Universe of Polyglutamine Structures.” PLoS
Computational Biology. Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004541.
ieee: À. Gómez Sicilia, M. K. Sikora, M. Cieplak, and M. Carrión Vázquez, “An exploration
of the universe of polyglutamine structures,” PLoS Computational Biology,
vol. 11, no. 10. Public Library of Science, 2015.
ista: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. 2015. An exploration
of the universe of polyglutamine structures. PLoS Computational Biology. 11(10),
e1004541.
mla: Gómez Sicilia, Àngel, et al. “An Exploration of the Universe of Polyglutamine
Structures.” PLoS Computational Biology, vol. 11, no. 10, e1004541, Public
Library of Science, 2015, doi:10.1371/journal.pcbi.1004541.
short: À. Gómez Sicilia, M.K. Sikora, M. Cieplak, M. Carrión Vázquez, PLoS Computational
Biology 11 (2015).
date_created: 2018-12-11T11:52:45Z
date_published: 2015-10-23T00:00:00Z
date_updated: 2023-02-23T14:05:55Z
day: '23'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1371/journal.pcbi.1004541
file:
- access_level: open_access
checksum: 8b67d729be663bfc9af04bfd94459655
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:21Z
date_updated: 2020-07-14T12:45:02Z
file_id: '5207'
file_name: IST-2016-478-v1+1_journal.pcbi.1004541.pdf
file_size: 1412511
relation: main_file
file_date_updated: 2020-07-14T12:45:02Z
has_accepted_license: '1'
intvolume: ' 11'
issue: '10'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
publication: PLoS Computational Biology
publication_status: published
publisher: Public Library of Science
publist_id: '5605'
pubrep_id: '478'
quality_controlled: '1'
related_material:
record:
- id: '9714'
relation: research_data
status: public
scopus_import: 1
status: public
title: An exploration of the universe of polyglutamine structures
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: '2015'
...
---
_id: '1581'
abstract:
- lang: eng
text: In animal embryos, morphogen gradients determine tissue patterning and morphogenesis.
Shyer et al. provide evidence that, during vertebrate gut formation, tissue folding
generates graded activity of signals required for subsequent steps of gut growth
and differentiation, thereby revealing an intriguing link between tissue morphogenesis
and morphogen gradient formation.
article_processing_charge: No
author:
- first_name: Mark Tobias
full_name: Bollenbach, Mark Tobias
id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87
last_name: Bollenbach
orcid: 0000-0003-4398-476X
- 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: Bollenbach MT, Heisenberg C-PJ. Gradients are shaping up. Cell. 2015;161(3):431-432.
doi:10.1016/j.cell.2015.04.009
apa: Bollenbach, M. T., & Heisenberg, C.-P. J. (2015). Gradients are shaping
up. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.04.009
chicago: Bollenbach, Mark Tobias, and Carl-Philipp J Heisenberg. “Gradients Are
Shaping Up.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.04.009.
ieee: M. T. Bollenbach and C.-P. J. Heisenberg, “Gradients are shaping up,” Cell,
vol. 161, no. 3. Cell Press, pp. 431–432, 2015.
ista: Bollenbach MT, Heisenberg C-PJ. 2015. Gradients are shaping up. Cell. 161(3),
431–432.
mla: Bollenbach, Mark Tobias, and Carl-Philipp J. Heisenberg. “Gradients Are Shaping
Up.” Cell, vol. 161, no. 3, Cell Press, 2015, pp. 431–32, doi:10.1016/j.cell.2015.04.009.
short: M.T. Bollenbach, C.-P.J. Heisenberg, Cell 161 (2015) 431–432.
date_created: 2018-12-11T11:52:50Z
date_published: 2015-04-23T00:00:00Z
date_updated: 2022-08-25T13:56:10Z
day: '23'
department:
- _id: ToBo
- _id: CaHe
doi: 10.1016/j.cell.2015.04.009
intvolume: ' 161'
issue: '3'
language:
- iso: eng
month: '04'
oa_version: None
page: 431 - 432
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5590'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Gradients are shaping up
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 161
year: '2015'
...
---
_id: '1817'
abstract:
- lang: eng
text: 'Vertebrates have a unique 3D body shape in which correct tissue and organ
shape and alignment are essential for function. For example, vision requires the
lens to be centred in the eye cup which must in turn be correctly positioned in
the head. Tissue morphogenesis depends on force generation, force transmission
through the tissue, and response of tissues and extracellular matrix to force.
Although a century ago D''Arcy Thompson postulated that terrestrial animal body
shapes are conditioned by gravity, there has been no animal model directly demonstrating
how the aforementioned mechano-morphogenetic processes are coordinated to generate
a body shape that withstands gravity. Here we report a unique medaka fish (Oryzias
latipes) mutant, hirame (hir), which is sensitive to deformation by gravity. hir
embryos display a markedly flattened body caused by mutation of YAP, a nuclear
executor of Hippo signalling that regulates organ size. We show that actomyosin-mediated
tissue tension is reduced in hir embryos, leading to tissue flattening and tissue
misalignment, both of which contribute to body flattening. By analysing YAP function
in 3D spheroids of human cells, we identify the Rho GTPase activating protein
ARHGAP18 as an effector of YAP in controlling tissue tension. Together, these
findings reveal a previously unrecognised function of YAP in regulating tissue
shape and alignment required for proper 3D body shape. Understanding this morphogenetic
function of YAP could facilitate the use of embryonic stem cells to generate complex
organs requiring correct alignment of multiple tissues. '
author:
- first_name: Sean
full_name: Porazinski, Sean
last_name: Porazinski
- first_name: Huijia
full_name: Wang, Huijia
last_name: Wang
- first_name: Yoichi
full_name: Asaoka, Yoichi
last_name: Asaoka
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
- first_name: Tatsuo
full_name: Miyamoto, Tatsuo
last_name: Miyamoto
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Shoji
full_name: Hata, Shoji
last_name: Hata
- first_name: Takashi
full_name: Sasaki, Takashi
last_name: Sasaki
- first_name: Gabriel
full_name: Krens, Gabriel
id: 2B819732-F248-11E8-B48F-1D18A9856A87
last_name: Krens
orcid: 0000-0003-4761-5996
- first_name: Yumi
full_name: Osada, Yumi
last_name: Osada
- first_name: Satoshi
full_name: Asaka, Satoshi
last_name: Asaka
- first_name: Akihiro
full_name: Momoi, Akihiro
last_name: Momoi
- first_name: Sarah
full_name: Linton, Sarah
last_name: Linton
- first_name: Joel
full_name: Miesfeld, Joel
last_name: Miesfeld
- first_name: Brian
full_name: Link, Brian
last_name: Link
- first_name: Takeshi
full_name: Senga, Takeshi
last_name: Senga
- first_name: Atahualpa
full_name: Castillo Morales, Atahualpa
last_name: Castillo Morales
- first_name: Araxi
full_name: Urrutia, Araxi
last_name: Urrutia
- first_name: Nobuyoshi
full_name: Shimizu, Nobuyoshi
last_name: Shimizu
- first_name: Hideaki
full_name: Nagase, Hideaki
last_name: Nagase
- first_name: Shinya
full_name: Matsuura, Shinya
last_name: Matsuura
- first_name: Stefan
full_name: Bagby, Stefan
last_name: Bagby
- first_name: Hisato
full_name: Kondoh, Hisato
last_name: Kondoh
- first_name: Hiroshi
full_name: Nishina, Hiroshi
last_name: Nishina
- 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
- first_name: Makoto
full_name: Furutani Seiki, Makoto
last_name: Furutani Seiki
citation:
ama: Porazinski S, Wang H, Asaoka Y, et al. YAP is essential for tissue tension
to ensure vertebrate 3D body shape. Nature. 2015;521(7551):217-221. doi:10.1038/nature14215
apa: Porazinski, S., Wang, H., Asaoka, Y., Behrndt, M., Miyamoto, T., Morita, H.,
… Furutani Seiki, M. (2015). YAP is essential for tissue tension to ensure vertebrate
3D body shape. Nature. Nature Publishing Group. https://doi.org/10.1038/nature14215
chicago: Porazinski, Sean, Huijia Wang, Yoichi Asaoka, Martin Behrndt, Tatsuo Miyamoto,
Hitoshi Morita, Shoji Hata, et al. “YAP Is Essential for Tissue Tension to Ensure
Vertebrate 3D Body Shape.” Nature. Nature Publishing Group, 2015. https://doi.org/10.1038/nature14215.
ieee: S. Porazinski et al., “YAP is essential for tissue tension to ensure
vertebrate 3D body shape,” Nature, vol. 521, no. 7551. Nature Publishing
Group, pp. 217–221, 2015.
ista: Porazinski S, Wang H, Asaoka Y, Behrndt M, Miyamoto T, Morita H, Hata S, Sasaki
T, Krens G, Osada Y, Asaka S, Momoi A, Linton S, Miesfeld J, Link B, Senga T,
Castillo Morales A, Urrutia A, Shimizu N, Nagase H, Matsuura S, Bagby S, Kondoh
H, Nishina H, Heisenberg C-PJ, Furutani Seiki M. 2015. YAP is essential for tissue
tension to ensure vertebrate 3D body shape. Nature. 521(7551), 217–221.
mla: Porazinski, Sean, et al. “YAP Is Essential for Tissue Tension to Ensure Vertebrate
3D Body Shape.” Nature, vol. 521, no. 7551, Nature Publishing Group, 2015,
pp. 217–21, doi:10.1038/nature14215.
short: S. Porazinski, H. Wang, Y. Asaoka, M. Behrndt, T. Miyamoto, H. Morita, S.
Hata, T. Sasaki, G. Krens, Y. Osada, S. Asaka, A. Momoi, S. Linton, J. Miesfeld,
B. Link, T. Senga, A. Castillo Morales, A. Urrutia, N. Shimizu, H. Nagase, S.
Matsuura, S. Bagby, H. Kondoh, H. Nishina, C.-P.J. Heisenberg, M. Furutani Seiki,
Nature 521 (2015) 217–221.
date_created: 2018-12-11T11:54:10Z
date_published: 2015-03-16T00:00:00Z
date_updated: 2021-01-12T06:53:23Z
day: '16'
department:
- _id: CaHe
doi: 10.1038/nature14215
external_id:
pmid:
- '25778702'
intvolume: ' 521'
issue: '7551'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4720436/
month: '03'
oa: 1
oa_version: Submitted Version
page: 217 - 221
pmid: 1
publication: Nature
publication_status: published
publisher: Nature Publishing Group
publist_id: '5289'
quality_controlled: '1'
scopus_import: 1
status: public
title: YAP is essential for tissue tension to ensure vertebrate 3D body shape
type: journal_article
user_id: 2EBD1598-F248-11E8-B48F-1D18A9856A87
volume: 521
year: '2015'
...
---
_id: '9714'
article_processing_charge: No
author:
- first_name: Àngel
full_name: Gómez Sicilia, Àngel
last_name: Gómez Sicilia
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Marek
full_name: Cieplak, Marek
last_name: Cieplak
- first_name: Mariano
full_name: Carrión Vázquez, Mariano
last_name: Carrión Vázquez
citation:
ama: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. An exploration of
the universe of polyglutamine structures - submission to PLOS journals. 2015.
doi:10.1371/journal.pcbi.1004541.s001
apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., & Carrión Vázquez, M. (2015).
An exploration of the universe of polyglutamine structures - submission to PLOS
journals. Public Library of Science . https://doi.org/10.1371/journal.pcbi.1004541.s001
chicago: Gómez Sicilia, Àngel, Mateusz K Sikora, Marek Cieplak, and Mariano Carrión
Vázquez. “An Exploration of the Universe of Polyglutamine Structures - Submission
to PLOS Journals.” Public Library of Science , 2015. https://doi.org/10.1371/journal.pcbi.1004541.s001.
ieee: À. Gómez Sicilia, M. K. Sikora, M. Cieplak, and M. Carrión Vázquez, “An exploration
of the universe of polyglutamine structures - submission to PLOS journals.” Public
Library of Science , 2015.
ista: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. 2015. An exploration
of the universe of polyglutamine structures - submission to PLOS journals, Public
Library of Science , 10.1371/journal.pcbi.1004541.s001.
mla: Gómez Sicilia, Àngel, et al. An Exploration of the Universe of Polyglutamine
Structures - Submission to PLOS Journals. Public Library of Science , 2015,
doi:10.1371/journal.pcbi.1004541.s001.
short: À. Gómez Sicilia, M.K. Sikora, M. Cieplak, M. Carrión Vázquez, (2015).
date_created: 2021-07-23T12:05:28Z
date_published: 2015-10-23T00:00:00Z
date_updated: 2023-02-23T10:04:35Z
day: '23'
department:
- _id: CaHe
doi: 10.1371/journal.pcbi.1004541.s001
month: '10'
oa_version: Published Version
publisher: 'Public Library of Science '
related_material:
record:
- id: '1566'
relation: used_in_publication
status: public
status: public
title: An exploration of the universe of polyglutamine structures - submission to
PLOS journals
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2015'
...
---
_id: '1891'
abstract:
- lang: eng
text: We provide theoretical tests of a novel experimental technique to determine
mechanostability of proteins based on stretching a mechanically protected protein
by single-molecule force spectroscopy. This technique involves stretching a homogeneous
or heterogeneous chain of reference proteins (single-molecule markers) in which
one of them acts as host to the guest protein under study. The guest protein is
grafted into the host through genetic engineering. It is expected that unraveling
of the host precedes the unraveling of the guest removing ambiguities in the reading
of the force-extension patterns of the guest protein. We study examples of such
systems within a coarse-grained structure-based model. We consider systems with
various ratios of mechanostability for the host and guest molecules and compare
them to experimental results involving cohesin I as the guest molecule. For a
comparison, we also study the force-displacement patterns in proteins that are
linked in a serial fashion. We find that the mechanostability of the guest is
similar to that of the isolated or serially linked protein. We also demonstrate
that the ideal configuration of this strategy would be one in which the host is
much more mechanostable than the single-molecule markers. We finally show that
it is troublesome to use the highly stable cystine knot proteins as a host to
graft a guest in stretching studies because this would involve a cleaving procedure.
acknowledgement: Grant Nr. 2011/01/N/ST3/02475
author:
- first_name: Mateusz
full_name: Chwastyk, Mateusz
last_name: Chwastyk
- first_name: Albert
full_name: Galera Prat, Albert
last_name: Galera Prat
- first_name: Mateusz K
full_name: Sikora, Mateusz K
id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87
last_name: Sikora
- first_name: Àngel
full_name: Gómez Sicilia, Àngel
last_name: Gómez Sicilia
- first_name: Mariano
full_name: Carrión Vázquez, Mariano
last_name: Carrión Vázquez
- first_name: Marek
full_name: Cieplak, Marek
last_name: Cieplak
citation:
ama: 'Chwastyk M, Galera Prat A, Sikora MK, Gómez Sicilia À, Carrión Vázquez M,
Cieplak M. Theoretical tests of the mechanical protection strategy in protein
nanomechanics. Proteins: Structure, Function and Bioinformatics. 2014;82(5):717-726.
doi:10.1002/prot.24436'
apa: 'Chwastyk, M., Galera Prat, A., Sikora, M. K., Gómez Sicilia, À., Carrión Vázquez,
M., & Cieplak, M. (2014). Theoretical tests of the mechanical protection strategy
in protein nanomechanics. Proteins: Structure, Function and Bioinformatics.
Wiley-Blackwell. https://doi.org/10.1002/prot.24436'
chicago: 'Chwastyk, Mateusz, Albert Galera Prat, Mateusz K Sikora, Àngel Gómez Sicilia,
Mariano Carrión Vázquez, and Marek Cieplak. “Theoretical Tests of the Mechanical
Protection Strategy in Protein Nanomechanics.” Proteins: Structure, Function
and Bioinformatics. Wiley-Blackwell, 2014. https://doi.org/10.1002/prot.24436.'
ieee: 'M. Chwastyk, A. Galera Prat, M. K. Sikora, À. Gómez Sicilia, M. Carrión Vázquez,
and M. Cieplak, “Theoretical tests of the mechanical protection strategy in protein
nanomechanics,” Proteins: Structure, Function and Bioinformatics, vol.
82, no. 5. Wiley-Blackwell, pp. 717–726, 2014.'
ista: 'Chwastyk M, Galera Prat A, Sikora MK, Gómez Sicilia À, Carrión Vázquez M,
Cieplak M. 2014. Theoretical tests of the mechanical protection strategy in protein
nanomechanics. Proteins: Structure, Function and Bioinformatics. 82(5), 717–726.'
mla: 'Chwastyk, Mateusz, et al. “Theoretical Tests of the Mechanical Protection
Strategy in Protein Nanomechanics.” Proteins: Structure, Function and Bioinformatics,
vol. 82, no. 5, Wiley-Blackwell, 2014, pp. 717–26, doi:10.1002/prot.24436.'
short: 'M. Chwastyk, A. Galera Prat, M.K. Sikora, À. Gómez Sicilia, M. Carrión Vázquez,
M. Cieplak, Proteins: Structure, Function and Bioinformatics 82 (2014) 717–726.'
date_created: 2018-12-11T11:54:34Z
date_published: 2014-05-01T00:00:00Z
date_updated: 2021-01-12T06:53:52Z
day: '01'
department:
- _id: CaHe
doi: 10.1002/prot.24436
intvolume: ' 82'
issue: '5'
language:
- iso: eng
month: '05'
oa_version: None
page: 717 - 726
publication: 'Proteins: Structure, Function and Bioinformatics'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '5204'
scopus_import: 1
status: public
title: Theoretical tests of the mechanical protection strategy in protein nanomechanics
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 82
year: '2014'
...
---
_id: '1900'
abstract:
- lang: eng
text: Epithelial cell layers need to be tightly regulated to maintain their integrity
and correct function. Cell integration into epithelial sheets is now shown to
depend on the N-WASP-regulated stabilization of cortical F-actin, which generates
distinct patterns of apical-lateral contractility at E-cadherin-based cell-cell
junctions.
author:
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
- 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: Behrndt M, Heisenberg C-PJ. Lateral junction dynamics lead the way out. Nature
Cell Biology. 2014;16(2):127-129. doi:10.1038/ncb2913
apa: Behrndt, M., & Heisenberg, C.-P. J. (2014). Lateral junction dynamics lead
the way out. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb2913
chicago: Behrndt, Martin, and Carl-Philipp J Heisenberg. “Lateral Junction Dynamics
Lead the Way Out.” Nature Cell Biology. Nature Publishing Group, 2014.
https://doi.org/10.1038/ncb2913.
ieee: M. Behrndt and C.-P. J. Heisenberg, “Lateral junction dynamics lead the way
out,” Nature Cell Biology, vol. 16, no. 2. Nature Publishing Group, pp.
127–129, 2014.
ista: Behrndt M, Heisenberg C-PJ. 2014. Lateral junction dynamics lead the way out.
Nature Cell Biology. 16(2), 127–129.
mla: Behrndt, Martin, and Carl-Philipp J. Heisenberg. “Lateral Junction Dynamics
Lead the Way Out.” Nature Cell Biology, vol. 16, no. 2, Nature Publishing
Group, 2014, pp. 127–29, doi:10.1038/ncb2913.
short: M. Behrndt, C.-P.J. Heisenberg, Nature Cell Biology 16 (2014) 127–129.
date_created: 2018-12-11T11:54:37Z
date_published: 2014-01-31T00:00:00Z
date_updated: 2021-01-12T06:53:56Z
day: '31'
department:
- _id: CaHe
doi: 10.1038/ncb2913
intvolume: ' 16'
issue: '2'
language:
- iso: eng
month: '01'
oa_version: None
page: 127 - 129
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '5195'
quality_controlled: '1'
scopus_import: 1
status: public
title: Lateral junction dynamics lead the way out
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '1912'
abstract:
- lang: eng
text: Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the
embryo along its left-right (LR) axis. Regional differences in cell shape within
the lumen-lining KV epithelium are essential for its LR patterning function. However,
the processes by which KV cells acquire their characteristic shapes are largely
unknown. Here, we show that the notochord induces regional differences in cell
shape within KV by triggering extracellular matrix (ECM) accumulation adjacent
to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts
apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen
growth. Our study provides mechanistic insight into the processes by which KV
translates global embryonic patterning into regional cell shape differences required
for its LR symmetry-breaking function.
acknowledgement: We are grateful to members of the C.-P.H. lab, M. Concha, D. Siekhaus,
and J. Vermot for comments on the manuscript and to M. Furutani-Seiki for sharing
reagents. This work was supported by the Institute of Science and Technology Austria
and an Alexander von Humboldt Foundation fellowship to J.C.
article_processing_charge: No
author:
- first_name: Julien
full_name: Compagnon, Julien
id: 2E3E0988-F248-11E8-B48F-1D18A9856A87
last_name: Compagnon
- first_name: Vanessa
full_name: Barone, Vanessa
id: 419EECCC-F248-11E8-B48F-1D18A9856A87
last_name: Barone
orcid: 0000-0003-2676-3367
- first_name: Srivarsha
full_name: Rajshekar, Srivarsha
last_name: Rajshekar
- first_name: Rita
full_name: Kottmeier, Rita
last_name: Kottmeier
- first_name: Kornelija
full_name: Pranjic-Ferscha, Kornelija
id: 4362B3C2-F248-11E8-B48F-1D18A9856A87
last_name: Pranjic-Ferscha
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
- 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: Compagnon J, Barone V, Rajshekar S, et al. The notochord breaks bilateral symmetry
by controlling cell shapes in the Zebrafish laterality organ. Developmental
Cell. 2014;31(6):774-783. doi:10.1016/j.devcel.2014.11.003
apa: Compagnon, J., Barone, V., Rajshekar, S., Kottmeier, R., Pranjic-Ferscha, K.,
Behrndt, M., & Heisenberg, C.-P. J. (2014). The notochord breaks bilateral
symmetry by controlling cell shapes in the Zebrafish laterality organ. Developmental
Cell. Cell Press. https://doi.org/10.1016/j.devcel.2014.11.003
chicago: Compagnon, Julien, Vanessa Barone, Srivarsha Rajshekar, Rita Kottmeier,
Kornelija Pranjic-Ferscha, Martin Behrndt, and Carl-Philipp J Heisenberg. “The
Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish
Laterality Organ.” Developmental Cell. Cell Press, 2014. https://doi.org/10.1016/j.devcel.2014.11.003.
ieee: J. Compagnon et al., “The notochord breaks bilateral symmetry by controlling
cell shapes in the Zebrafish laterality organ,” Developmental Cell, vol.
31, no. 6. Cell Press, pp. 774–783, 2014.
ista: Compagnon J, Barone V, Rajshekar S, Kottmeier R, Pranjic-Ferscha K, Behrndt
M, Heisenberg C-PJ. 2014. The notochord breaks bilateral symmetry by controlling
cell shapes in the Zebrafish laterality organ. Developmental Cell. 31(6), 774–783.
mla: Compagnon, Julien, et al. “The Notochord Breaks Bilateral Symmetry by Controlling
Cell Shapes in the Zebrafish Laterality Organ.” Developmental Cell, vol.
31, no. 6, Cell Press, 2014, pp. 774–83, doi:10.1016/j.devcel.2014.11.003.
short: J. Compagnon, V. Barone, S. Rajshekar, R. Kottmeier, K. Pranjic-Ferscha,
M. Behrndt, C.-P.J. Heisenberg, Developmental Cell 31 (2014) 774–783.
date_created: 2018-12-11T11:54:41Z
date_published: 2014-12-22T00:00:00Z
date_updated: 2023-09-07T12:05:08Z
day: '22'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2014.11.003
external_id:
pmid:
- '25535919'
intvolume: ' 31'
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://www.ncbi.nlm.nih.gov/pubmed/25535919
month: '12'
oa: 1
oa_version: Published Version
page: 774 - 783
pmid: 1
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '5182'
quality_controlled: '1'
related_material:
record:
- id: '961'
relation: dissertation_contains
status: public
scopus_import: '1'
status: public
title: The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish
laterality organ
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 31
year: '2014'
...
---
_id: '1923'
abstract:
- lang: eng
text: We derive the equations for a thin, axisymmetric elastic shell subjected to
an internal active stress giving rise to active tension and moments within the
shell. We discuss the stability of a cylindrical elastic shell and its response
to a localized change in internal active stress. This description is relevant
to describe the cellular actomyosin cortex, a thin shell at the cell surface behaving
elastically at a short timescale and subjected to active internal forces arising
from myosin molecular motor activity. We show that the recent observations of
cell deformation following detachment of adherent cells (Maître J-L et al 2012
Science 338 253-6) are well accounted for by this mechanical description. The
actin cortex elastic and bending moduli can be obtained from a quantitative analysis
of cell shapes observed in these experiments. Our approach thus provides a non-invasive,
imaging-based method for the extraction of cellular physical parameters.
article_number: '065005'
author:
- first_name: Hélène
full_name: Berthoumieux, Hélène
last_name: Berthoumieux
- first_name: Jean-Léon
full_name: Maître, Jean-Léon
id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87
last_name: Maître
orcid: 0000-0002-3688-1474
- 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
- first_name: Ewa
full_name: Paluch, Ewa
last_name: Paluch
- first_name: Frank
full_name: Julicher, Frank
last_name: Julicher
- first_name: Guillaume
full_name: Salbreux, Guillaume
last_name: Salbreux
citation:
ama: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux
G. Active elastic thin shell theory for cellular deformations. New Journal
of Physics. 2014;16. doi:10.1088/1367-2630/16/6/065005
apa: Berthoumieux, H., Maître, J.-L., Heisenberg, C.-P. J., Paluch, E., Julicher,
F., & Salbreux, G. (2014). Active elastic thin shell theory for cellular deformations.
New Journal of Physics. IOP Publishing Ltd. https://doi.org/10.1088/1367-2630/16/6/065005
chicago: Berthoumieux, Hélène, Jean-Léon Maître, Carl-Philipp J Heisenberg, Ewa
Paluch, Frank Julicher, and Guillaume Salbreux. “Active Elastic Thin Shell Theory
for Cellular Deformations.” New Journal of Physics. IOP Publishing Ltd.,
2014. https://doi.org/10.1088/1367-2630/16/6/065005.
ieee: H. Berthoumieux, J.-L. Maître, C.-P. J. Heisenberg, E. Paluch, F. Julicher,
and G. Salbreux, “Active elastic thin shell theory for cellular deformations,”
New Journal of Physics, vol. 16. IOP Publishing Ltd., 2014.
ista: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux
G. 2014. Active elastic thin shell theory for cellular deformations. New Journal
of Physics. 16, 065005.
mla: Berthoumieux, Hélène, et al. “Active Elastic Thin Shell Theory for Cellular
Deformations.” New Journal of Physics, vol. 16, 065005, IOP Publishing
Ltd., 2014, doi:10.1088/1367-2630/16/6/065005.
short: H. Berthoumieux, J.-L. Maître, C.-P.J. Heisenberg, E. Paluch, F. Julicher,
G. Salbreux, New Journal of Physics 16 (2014).
date_created: 2018-12-11T11:54:44Z
date_published: 2014-06-01T00:00:00Z
date_updated: 2021-01-12T06:54:06Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1088/1367-2630/16/6/065005
file:
- access_level: open_access
checksum: 8dbe81ec656bf1264d8889bda9b2b985
content_type: application/pdf
creator: system
date_created: 2018-12-12T10:16:16Z
date_updated: 2020-07-14T12:45:21Z
file_id: '5202'
file_name: IST-2016-429-v1+1_document.pdf
file_size: 941387
relation: main_file
file_date_updated: 2020-07-14T12:45:21Z
has_accepted_license: '1'
intvolume: ' 16'
language:
- iso: eng
month: '06'
oa: 1
oa_version: Published Version
publication: New Journal of Physics
publication_status: published
publisher: IOP Publishing Ltd.
publist_id: '5171'
pubrep_id: '429'
quality_controlled: '1'
scopus_import: 1
status: public
title: Active elastic thin shell theory for cellular deformations
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: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 16
year: '2014'
...
---
_id: '1925'
abstract:
- lang: eng
text: In the past decade carbon nanotubes (CNTs) have been widely studied as a potential
drug-delivery system, especially with functionality for cellular targeting. Yet,
little is known about the actual process of docking to cell receptors and transport
dynamics after internalization. Here we performed single-particle studies of folic
acid (FA) mediated CNT binding to human carcinoma cells and their transport inside
the cytosol. In particular, we employed molecular recognition force spectroscopy,
an atomic force microscopy based method, to visualize and quantify docking of
FA functionalized CNTs to FA binding receptors in terms of binding probability
and binding force. We then traced individual fluorescently labeled, FA functionalized
CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed
trajectories of directed diffusion and areas of nanotube confinement in the cytosol.
Our results demonstrate the potential of a single-molecule approach for investigation
of drug-delivery vehicles and their targeting capacity.
acknowledgement: "This work was supported by EC grant Marie Curie RTN-CT-2006-035616,
CARBIO 'Carbon nanotubes for biomedical applications' and Austrian FFG grant mnt-era.net
823980, 'IntelliTip'.\r\n"
article_number: '125704'
article_processing_charge: No
article_type: original
author:
- first_name: Constanze
full_name: Lamprecht, Constanze
last_name: Lamprecht
- first_name: Birgit
full_name: Plochberger, Birgit
last_name: Plochberger
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- first_name: Stefan
full_name: Wieser, Stefan
id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
last_name: Wieser
orcid: 0000-0002-2670-2217
- first_name: Christian
full_name: Rankl, Christian
last_name: Rankl
- first_name: Elena
full_name: Heister, Elena
last_name: Heister
- first_name: Barbara
full_name: Unterauer, Barbara
last_name: Unterauer
- first_name: Mario
full_name: Brameshuber, Mario
last_name: Brameshuber
- first_name: Jürgen
full_name: Danzberger, Jürgen
last_name: Danzberger
- first_name: Petar
full_name: Lukanov, Petar
last_name: Lukanov
- first_name: Emmanuel
full_name: Flahaut, Emmanuel
last_name: Flahaut
- first_name: Gerhard
full_name: Schütz, Gerhard
last_name: Schütz
- first_name: Peter
full_name: Hinterdorfer, Peter
last_name: Hinterdorfer
- first_name: Andreas
full_name: Ebner, Andreas
last_name: Ebner
citation:
ama: Lamprecht C, Plochberger B, Ruprecht V, et al. A single-molecule approach to
explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology.
2014;25(12). doi:10.1088/0957-4484/25/12/125704
apa: Lamprecht, C., Plochberger, B., Ruprecht, V., Wieser, S., Rankl, C., Heister,
E., … Ebner, A. (2014). A single-molecule approach to explore binding uptake and
transport of cancer cell targeting nanotubes. Nanotechnology. IOP Publishing.
https://doi.org/10.1088/0957-4484/25/12/125704
chicago: Lamprecht, Constanze, Birgit Plochberger, Verena Ruprecht, Stefan Wieser,
Christian Rankl, Elena Heister, Barbara Unterauer, et al. “A Single-Molecule Approach
to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology.
IOP Publishing, 2014. https://doi.org/10.1088/0957-4484/25/12/125704.
ieee: C. Lamprecht et al., “A single-molecule approach to explore binding
uptake and transport of cancer cell targeting nanotubes,” Nanotechnology,
vol. 25, no. 12. IOP Publishing, 2014.
ista: Lamprecht C, Plochberger B, Ruprecht V, Wieser S, Rankl C, Heister E, Unterauer
B, Brameshuber M, Danzberger J, Lukanov P, Flahaut E, Schütz G, Hinterdorfer P,
Ebner A. 2014. A single-molecule approach to explore binding uptake and transport
of cancer cell targeting nanotubes. Nanotechnology. 25(12), 125704.
mla: Lamprecht, Constanze, et al. “A Single-Molecule Approach to Explore Binding
Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology,
vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:10.1088/0957-4484/25/12/125704.
short: C. Lamprecht, B. Plochberger, V. Ruprecht, S. Wieser, C. Rankl, E. Heister,
B. Unterauer, M. Brameshuber, J. Danzberger, P. Lukanov, E. Flahaut, G. Schütz,
P. Hinterdorfer, A. Ebner, Nanotechnology 25 (2014).
date_created: 2018-12-11T11:54:45Z
date_published: 2014-03-28T00:00:00Z
date_updated: 2021-01-12T06:54:07Z
day: '28'
ddc:
- '570'
department:
- _id: CaHe
- _id: MiSi
doi: 10.1088/0957-4484/25/12/125704
file:
- access_level: open_access
checksum: df4e03d225a19179e7790f6d87a12332
content_type: application/pdf
creator: dernst
date_created: 2020-05-15T09:21:19Z
date_updated: 2020-07-14T12:45:21Z
file_id: '7856'
file_name: 2014_Nanotechnology_Lamprecht.pdf
file_size: 3804152
relation: main_file
file_date_updated: 2020-07-14T12:45:21Z
has_accepted_license: '1'
intvolume: ' 25'
issue: '12'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Submitted Version
publication: Nanotechnology
publication_status: published
publisher: IOP Publishing
publist_id: '5169'
scopus_import: 1
status: public
title: A single-molecule approach to explore binding uptake and transport of cancer
cell targeting nanotubes
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 25
year: '2014'
...
---
_id: '1403'
abstract:
- lang: eng
text: A variety of developmental and disease related processes depend on epithelial
cell sheet spreading. In order to gain insight into the biophysical mechanism(s)
underlying the tissue morphogenesis we studied the spreading of an epithelium
during the early development of the zebrafish embryo. In zebrafish epiboly the
enveloping cell layer (EVL), a simple squamous epithelium, spreads over the yolk
cell to completely engulf it at the end of gastrulation. Previous studies have
proposed that an actomyosin ring forming within the yolk syncytial layer (YSL)
acts as purse string that through constriction along its circumference pulls on
the margin of the EVL. Direct biophysical evidence for this hypothesis has however
been missing. The aim of the thesis was to understand how the actomyosin ring
may generate pulling forces onto the EVL and what cellular mechanism(s) may facilitate
the spreading of the epithelium. Using laser ablation to measure cortical tension
within the actomyosin ring we found an anisotropic tension distribution, which
was highest along the circumference of the ring. However the low degree of anisotropy
was incompatible with the actomyosin ring functioning as a purse string only.
Additionally, we observed retrograde cortical flow from vegetal parts of the ring
into the EVL margin. Interpreting the experimental data using a theoretical distribution
that models the tissues as active viscous gels led us to proposen that the actomyosin
ring has a twofold contribution to EVL epiboly. It not only acts as a purse string
through constriction along its circumference, but in addition constriction along
the width of the ring generates pulling forces through friction-resisted cortical
flow. Moreover, when rendering the purse string mechanism unproductive EVL epiboly
proceeded normally indicating that the flow-friction mechanism is sufficient to
drive the process. Aiming to understand what cellular mechanism(s) may facilitate
the spreading of the epithelium we found that tension-oriented EVL cell divisions
limit tissue anisotropy by releasing tension along the division axis and promote
epithelial spreading. Notably, EVL cells undergo ectopic cell fusion in conditions
in which oriented-cell division is impaired or the epithelium is mechanically
challenged. Taken together our study of EVL epiboly suggests a novel mechanism
of force generation for actomyosin rings through friction-resisted cortical flow
and highlights the importance of tension-oriented cell divisions in epithelial
morphogenesis.
acknowledged_ssus:
- _id: SSU
alternative_title:
- IST Austria Thesis
author:
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
citation:
ama: Behrndt M. Forces driving epithelial spreading in zebrafish epiboly. 2014.
apa: Behrndt, M. (2014). Forces driving epithelial spreading in zebrafish epiboly.
IST Austria.
chicago: Behrndt, Martin. “Forces Driving Epithelial Spreading in Zebrafish Epiboly.”
IST Austria, 2014.
ieee: M. Behrndt, “Forces driving epithelial spreading in zebrafish epiboly,” IST
Austria, 2014.
ista: Behrndt M. 2014. Forces driving epithelial spreading in zebrafish epiboly.
IST Austria.
mla: Behrndt, Martin. Forces Driving Epithelial Spreading in Zebrafish Epiboly.
IST Austria, 2014.
short: M. Behrndt, Forces Driving Epithelial Spreading in Zebrafish Epiboly, IST
Austria, 2014.
date_created: 2018-12-11T11:51:49Z
date_published: 2014-08-01T00:00:00Z
date_updated: 2023-10-17T12:16:58Z
day: '01'
department:
- _id: CaHe
language:
- iso: eng
month: '08'
oa_version: None
page: '91'
publication_status: published
publisher: IST Austria
publist_id: '5804'
related_material:
record:
- id: '2282'
relation: part_of_dissertation
status: public
- id: '2950'
relation: part_of_dissertation
status: public
- id: '3373'
relation: part_of_dissertation
status: public
status: public
supervisor:
- 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
title: Forces driving epithelial spreading in zebrafish epiboly
type: dissertation
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
year: '2014'
...
---
_id: '6178'
abstract:
- lang: eng
text: Mechanically coupled cells can generate forces driving cell and tissue morphogenesis
during development. Visualization and measuring of these forces is of major importance
to better understand the complexity of the biomechanic processes that shape cells
and tissues. Here, we describe how UV laser ablation can be utilized to quantitatively
assess mechanical tension in different tissues of the developing zebrafish and
in cultures of primary germ layer progenitor cells ex vivo.
article_processing_charge: No
author:
- first_name: Michael
full_name: Smutny, Michael
id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87
last_name: Smutny
orcid: 0000-0002-5920-9090
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
- first_name: Pedro
full_name: Campinho, Pedro
id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87
last_name: Campinho
orcid: 0000-0002-8526-5416
- first_name: Verena
full_name: Ruprecht, Verena
id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
last_name: Ruprecht
orcid: 0000-0003-4088-8633
- 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: 'Smutny M, Behrndt M, Campinho P, Ruprecht V, Heisenberg C-PJ. UV laser ablation
to measure cell and tissue-generated forces in the zebrafish embryo in vivo and
ex vivo. In: Nelson C, ed. Tissue Morphogenesis. Vol 1189. Methods in Molecular
Biology. New York, NY: Springer; 2014:219-235. doi:10.1007/978-1-4939-1164-6_15'
apa: 'Smutny, M., Behrndt, M., Campinho, P., Ruprecht, V., & Heisenberg, C.-P.
J. (2014). UV laser ablation to measure cell and tissue-generated forces in the
zebrafish embryo in vivo and ex vivo. In C. Nelson (Ed.), Tissue Morphogenesis
(Vol. 1189, pp. 219–235). New York, NY: Springer. https://doi.org/10.1007/978-1-4939-1164-6_15'
chicago: 'Smutny, Michael, Martin Behrndt, Pedro Campinho, Verena Ruprecht, and
Carl-Philipp J Heisenberg. “UV Laser Ablation to Measure Cell and Tissue-Generated
Forces in the Zebrafish Embryo in Vivo and Ex Vivo.” In Tissue Morphogenesis,
edited by Celeste Nelson, 1189:219–35. Methods in Molecular Biology. New York,
NY: Springer, 2014. https://doi.org/10.1007/978-1-4939-1164-6_15.'
ieee: 'M. Smutny, M. Behrndt, P. Campinho, V. Ruprecht, and C.-P. J. Heisenberg,
“UV laser ablation to measure cell and tissue-generated forces in the zebrafish
embryo in vivo and ex vivo,” in Tissue Morphogenesis, vol. 1189, C. Nelson,
Ed. New York, NY: Springer, 2014, pp. 219–235.'
ista: 'Smutny M, Behrndt M, Campinho P, Ruprecht V, Heisenberg C-PJ. 2014.UV laser
ablation to measure cell and tissue-generated forces in the zebrafish embryo in
vivo and ex vivo. In: Tissue Morphogenesis. vol. 1189, 219–235.'
mla: Smutny, Michael, et al. “UV Laser Ablation to Measure Cell and Tissue-Generated
Forces in the Zebrafish Embryo in Vivo and Ex Vivo.” Tissue Morphogenesis,
edited by Celeste Nelson, vol. 1189, Springer, 2014, pp. 219–35, doi:10.1007/978-1-4939-1164-6_15.
short: M. Smutny, M. Behrndt, P. Campinho, V. Ruprecht, C.-P.J. Heisenberg, in:,
C. Nelson (Ed.), Tissue Morphogenesis, Springer, New York, NY, 2014, pp. 219–235.
date_created: 2019-03-26T08:55:59Z
date_published: 2014-08-22T00:00:00Z
date_updated: 2023-09-05T14:12:00Z
day: '22'
department:
- _id: CaHe
doi: 10.1007/978-1-4939-1164-6_15
editor:
- first_name: Celeste
full_name: Nelson, Celeste
last_name: Nelson
external_id:
pmid:
- '25245697'
intvolume: ' 1189'
language:
- iso: eng
month: '08'
oa_version: None
page: 219-235
place: New York, NY
pmid: 1
publication: Tissue Morphogenesis
publication_identifier:
eissn:
- 1940-6029
isbn:
- '9781493911639'
- '9781493911646'
issn:
- 1064-3745
publication_status: published
publisher: Springer
quality_controlled: '1'
series_title: Methods in Molecular Biology
status: public
title: UV laser ablation to measure cell and tissue-generated forces in the zebrafish
embryo in vivo and ex vivo
type: book_chapter
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 1189
year: '2014'
...
---
_id: '10815'
abstract:
- lang: eng
text: In the last several decades, developmental biology has clarified the molecular
mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated
that the “tool-kit genes” essential for regulating developmental processes are
not only highly conserved among species, but are also used as systems at various
times and places in an organism to control distinct developmental events. Therefore,
mutations in many of these tool-kit genes may cause congenital diseases involving
morphological abnormalities. This link between genes and abnormal morphological
phenotypes underscores the importance of understanding how cells behave and contribute
to morphogenesis as a result of gene function. Recent improvements in live imaging
and in quantitative analyses of cellular dynamics will advance our understanding
of the cellular pathogenesis of congenital diseases associated with aberrant morphologies.
In these studies, it is critical to select an appropriate model organism for the
particular phenomenon of interest.
acknowledgement: The authors thank all the members of the Division of Morphogenesis,
National Institute for Basic Biology, for their contributions to the research, their
encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical
reading of the manuscript. We also thank the Model Animal Research and Spectrography
and Bioimaging Facilities, NIBB Core Research Facilities, for technical support.
M.H. was supported by a research fellowship from the Japan Society for the Promotion
of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid
for Scientific Research on Innovative Areas from the Ministry of Education, Culture,
Sports, Science, and Technology (MEXT), Japan, to N.U.
article_processing_charge: No
article_type: original
author:
- first_name: Masakazu
full_name: Hashimoto, Masakazu
last_name: Hashimoto
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- first_name: Naoto
full_name: Ueno, Naoto
last_name: Ueno
citation:
ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development
underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039
apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms
of development underlying congenital diseases. Congenital Anomalies. Wiley.
https://doi.org/10.1111/cga.12039
chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular
Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies.
Wiley, 2014. https://doi.org/10.1111/cga.12039.
ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of
development underlying congenital diseases,” Congenital Anomalies, vol.
54, no. 1. Wiley, pp. 1–7, 2014.
ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of
development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7.
mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development
Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1,
Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039.
short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7.
date_created: 2022-03-04T08:17:25Z
date_published: 2014-02-01T00:00:00Z
date_updated: 2022-03-04T08:26:05Z
day: '01'
department:
- _id: CaHe
doi: 10.1111/cga.12039
external_id:
pmid:
- '24666178'
intvolume: ' 54'
issue: '1'
keyword:
- Developmental Biology
- Embryology
- General Medicine
- Pediatrics
- Perinatology
- and Child Health
language:
- iso: eng
main_file_link:
- open_access: '1'
url: https://doi.org/10.1111/cga.12039
month: '02'
oa: 1
oa_version: None
page: 1-7
pmid: 1
publication: Congenital Anomalies
publication_identifier:
issn:
- 0914-3505
publication_status: published
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Molecular and cellular mechanisms of development underlying congenital diseases
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 54
year: '2014'
...
---
_id: '2248'
abstract:
- lang: eng
text: 'Avian forelimb digit homology remains one of the standard themes in comparative
biology and EvoDevo research. In order to resolve the apparent contradictions
between embryological and paleontological evidence a variety of hypotheses have
been presented in recent years. The proposals range from excluding birds from
the dinosaur clade, to assignments of homology by different criteria, or even
assuming a hexadactyl tetrapod limb ground state. At present two approaches prevail:
the frame shift hypothesis and the pyramid reduction hypothesis. While the former
postulates a homeotic shift of digit identities, the latter argues for a gradual
bilateral reduction of phalanges and digits. Here we present a new model that
integrates elements from both hypotheses with the existing experimental and fossil
evidence. We start from the main feature common to both earlier concepts, the
initiating ontogenetic event: reduction and loss of the anterior-most digit. It
is proposed that a concerted mechanism of molecular regulation and developmental
mechanics is capable of shifting the boundaries of hoxD expression in embryonic
forelimb buds as well as changing the digit phenotypes. Based on a distinction
between positional (topological) and compositional (phenotypic) homology criteria,
we argue that the identity of the avian digits is II, III, IV, despite a partially
altered phenotype. Finally, we introduce an alternative digit reduction scheme
that reconciles the current fossil evidence with the presented molecular-morphogenetic
model. Our approach identifies specific experiments that allow to test whether
gene expression can be shifted and digit phenotypes can be altered by induced
digit loss or digit gain.'
author:
- first_name: Daniel
full_name: Capek, Daniel
id: 31C42484-F248-11E8-B48F-1D18A9856A87
last_name: Capek
orcid: 0000-0001-5199-9940
- first_name: Brian
full_name: Metscher, Brian
last_name: Metscher
- first_name: Gerd
full_name: Müller, Gerd
last_name: Müller
citation:
ama: 'Capek D, Metscher B, Müller G. Thumbs down: A molecular-morphogenetic approach
to avian digit homology. Journal of Experimental Zoology Part B: Molecular
and Developmental Evolution. 2014;322(1):1-12. doi:10.1002/jez.b.22545'
apa: 'Capek, D., Metscher, B., & Müller, G. (2014). Thumbs down: A molecular-morphogenetic
approach to avian digit homology. Journal of Experimental Zoology Part B: Molecular
and Developmental Evolution. Wiley-Blackwell. https://doi.org/10.1002/jez.b.22545'
chicago: 'Capek, Daniel, Brian Metscher, and Gerd Müller. “Thumbs down: A Molecular-Morphogenetic
Approach to Avian Digit Homology.” Journal of Experimental Zoology Part B:
Molecular and Developmental Evolution. Wiley-Blackwell, 2014. https://doi.org/10.1002/jez.b.22545.'
ieee: 'D. Capek, B. Metscher, and G. Müller, “Thumbs down: A molecular-morphogenetic
approach to avian digit homology,” Journal of Experimental Zoology Part B:
Molecular and Developmental Evolution, vol. 322, no. 1. Wiley-Blackwell, pp.
1–12, 2014.'
ista: 'Capek D, Metscher B, Müller G. 2014. Thumbs down: A molecular-morphogenetic
approach to avian digit homology. Journal of Experimental Zoology Part B: Molecular
and Developmental Evolution. 322(1), 1–12.'
mla: 'Capek, Daniel, et al. “Thumbs down: A Molecular-Morphogenetic Approach to
Avian Digit Homology.” Journal of Experimental Zoology Part B: Molecular and
Developmental Evolution, vol. 322, no. 1, Wiley-Blackwell, 2014, pp. 1–12,
doi:10.1002/jez.b.22545.'
short: 'D. Capek, B. Metscher, G. Müller, Journal of Experimental Zoology Part B:
Molecular and Developmental Evolution 322 (2014) 1–12.'
date_created: 2018-12-11T11:56:33Z
date_published: 2014-01-01T00:00:00Z
date_updated: 2021-01-12T06:56:16Z
day: '01'
department:
- _id: CaHe
doi: 10.1002/jez.b.22545
intvolume: ' 322'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 1 - 12
publication: 'Journal of Experimental Zoology Part B: Molecular and Developmental
Evolution'
publication_identifier:
issn:
- '15525007'
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4701'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Thumbs down: A molecular-morphogenetic approach to avian digit homology'
type: journal_article
user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87
volume: 322
year: '2014'
...
---
_id: '1406'
abstract:
- lang: eng
text: Epithelial spreading is a critical part of various developmental and wound
repair processes. Here we use zebrafish epiboly as a model system to study the
cellular and molecular mechanisms underlying the spreading of epithelial sheets.
During zebrafish epiboly the enveloping cell layer (EVL), a simple squamous epithelium,
spreads over the embryo to eventually cover the entire yolk cell by the end of
gastrulation. The EVL leading edge is anchored through tight junctions to the
yolk syncytial layer (YSL), where directly adjacent to the EVL margin a contractile
actomyosin ring is formed that is thought to drive EVL epiboly. The prevalent
view in the field was that the contractile ring exerts a pulling force on the
EVL margin, which pulls the EVL towards the vegetal pole. However, how this force
is generated and how it affects EVL morphology still remains elusive. Moreover,
the cellular mechanisms mediating the increase in EVL surface area, while maintaining
tissue integrity and function are still unclear. Here we show that the YSL actomyosin
ring pulls on the EVL margin by two distinct force-generating mechanisms. One
mechanism is based on contraction of the ring around its circumference, as previously
proposed. The second mechanism is based on actomyosin retrogade flows, generating
force through resistance against the substrate. The latter can function at any
epiboly stage even in situations where the contraction-based mechanism is unproductive.
Additionally, we demonstrate that during epiboly the EVL is subjected to anisotropic
tension, which guides the orientation of EVL cell division along the main axis
(animal-vegetal) of tension. The influence of tension in cell division orientation
involves cell elongation and requires myosin-2 activity for proper spindle alignment.
Strikingly, we reveal that tension-oriented cell divisions release anisotropic
tension within the EVL and that in the absence of such divisions, EVL cells undergo
ectopic fusions. We conclude that forces applied to the EVL by the action of the
YSL actomyosin ring generate a tension anisotropy in the EVL that orients cell
divisions, which in turn limit tissue tension increase thereby facilitating tissue
spreading.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
alternative_title:
- ISTA Thesis
article_processing_charge: No
author:
- first_name: Pedro
full_name: Campinho, Pedro
id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87
last_name: Campinho
orcid: 0000-0002-8526-5416
citation:
ama: 'Campinho P. Mechanics of zebrafish epiboly: Tension-oriented cell divisions
limit anisotropic tissue tension in epithelial spreading. 2013.'
apa: 'Campinho, P. (2013). Mechanics of zebrafish epiboly: Tension-oriented cell
divisions limit anisotropic tissue tension in epithelial spreading. Institute
of Science and Technology Austria.'
chicago: 'Campinho, Pedro. “Mechanics of Zebrafish Epiboly: Tension-Oriented Cell
Divisions Limit Anisotropic Tissue Tension in Epithelial Spreading.” Institute
of Science and Technology Austria, 2013.'
ieee: 'P. Campinho, “Mechanics of zebrafish epiboly: Tension-oriented cell divisions
limit anisotropic tissue tension in epithelial spreading,” Institute of Science
and Technology Austria, 2013.'
ista: 'Campinho P. 2013. Mechanics of zebrafish epiboly: Tension-oriented cell divisions
limit anisotropic tissue tension in epithelial spreading. Institute of Science
and Technology Austria.'
mla: 'Campinho, Pedro. Mechanics of Zebrafish Epiboly: Tension-Oriented Cell
Divisions Limit Anisotropic Tissue Tension in Epithelial Spreading. Institute
of Science and Technology Austria, 2013.'
short: 'P. Campinho, Mechanics of Zebrafish Epiboly: Tension-Oriented Cell Divisions
Limit Anisotropic Tissue Tension in Epithelial Spreading, Institute of Science
and Technology Austria, 2013.'
date_created: 2018-12-11T11:51:50Z
date_published: 2013-10-01T00:00:00Z
date_updated: 2023-09-07T11:36:07Z
day: '01'
degree_awarded: PhD
department:
- _id: CaHe
language:
- iso: eng
month: '10'
oa_version: None
page: '123'
publication_identifier:
issn:
- 2663-337X
publication_status: published
publisher: Institute of Science and Technology Austria
publist_id: '5801'
status: public
supervisor:
- 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
title: 'Mechanics of zebrafish epiboly: Tension-oriented cell divisions limit anisotropic
tissue tension in epithelial spreading'
type: dissertation
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
year: '2013'
...
---
_id: '2278'
abstract:
- lang: eng
text: It is firmly established that interactions between neurons and glia are fundamental
across species for the correct establishment of a functional brain. Here, we found
that the glia of the Drosophila larval brain display an essential non-autonomous
role during the development of the optic lobe. The optic lobe develops from neuroepithelial
cells that proliferate by dividing symmetrically until they switch to asymmetric/differentiative
divisions that generate neuroblasts. The proneural gene lethal of scute (l9sc)
is transiently activated by the epidermal growth factor receptor (EGFR)-Ras signal
transduction pathway at the leading edge of a proneural wave that sweeps from
medial to lateral neuroepithelium, promoting this switch. This process is tightly
regulated by the tissue-autonomous function within the neuroepithelium of multiple
signaling pathways, including EGFR-Ras and Notch. This study shows that the Notch
ligand Serrate (Ser) is expressed in the glia and it forms a complex in vivo with
Notch and Canoe, which colocalize at the adherens junctions of neuroepithelial
cells. This complex is crucial for interactions between glia and neuroepithelial
cells during optic lobe development. Ser is tissue-autonomously required in the
glia where it activates Notch to regulate its proliferation, and non-autonomously
in the neuroepithelium where Ser induces Notch signaling to avoid the premature
activation of the EGFR-Ras pathway and hence of L9sc. Interestingly, different
Notch activity reporters showed very different expression patterns in the glia
and in the neuroepithelium, suggesting the existence of tissue-specific factors
that promote the expression of particular Notch target genes or/and a reporter
response dependent on different thresholds of Notch signaling.
author:
- first_name: Raquel
full_name: Pérez Gómez, Raquel
last_name: Pérez Gómez
- first_name: Jana
full_name: Slovakova, Jana
id: 30F3F2F0-F248-11E8-B48F-1D18A9856A87
last_name: Slovakova
- first_name: Noemí
full_name: Rives Quinto, Noemí
last_name: Rives Quinto
- first_name: Alena
full_name: Krejčí, Alena
last_name: Krejčí
- first_name: Ana
full_name: Carmena, Ana
last_name: Carmena
citation:
ama: Pérez Gómez R, Slovakova J, Rives Quinto N, Krejčí A, Carmena A. A serrate-notch-canoe
complex mediates essential interactions between glia and neuroepithelial cells
during Drosophila optic lobe development. Journal of Cell Science. 2013;126(21):4873-4884.
doi:10.1242/jcs.125617
apa: Pérez Gómez, R., Slovakova, J., Rives Quinto, N., Krejčí, A., & Carmena,
A. (2013). A serrate-notch-canoe complex mediates essential interactions between
glia and neuroepithelial cells during Drosophila optic lobe development. Journal
of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.125617
chicago: Pérez Gómez, Raquel, Jana Slovakova, Noemí Rives Quinto, Alena Krejčí,
and Ana Carmena. “A Serrate-Notch-Canoe Complex Mediates Essential Interactions
between Glia and Neuroepithelial Cells during Drosophila Optic Lobe Development.”
Journal of Cell Science. Company of Biologists, 2013. https://doi.org/10.1242/jcs.125617.
ieee: R. Pérez Gómez, J. Slovakova, N. Rives Quinto, A. Krejčí, and A. Carmena,
“A serrate-notch-canoe complex mediates essential interactions between glia and
neuroepithelial cells during Drosophila optic lobe development,” Journal of
Cell Science, vol. 126, no. 21. Company of Biologists, pp. 4873–4884, 2013.
ista: Pérez Gómez R, Slovakova J, Rives Quinto N, Krejčí A, Carmena A. 2013. A serrate-notch-canoe
complex mediates essential interactions between glia and neuroepithelial cells
during Drosophila optic lobe development. Journal of Cell Science. 126(21), 4873–4884.
mla: Pérez Gómez, Raquel, et al. “A Serrate-Notch-Canoe Complex Mediates Essential
Interactions between Glia and Neuroepithelial Cells during Drosophila Optic Lobe
Development.” Journal of Cell Science, vol. 126, no. 21, Company of Biologists,
2013, pp. 4873–84, doi:10.1242/jcs.125617.
short: R. Pérez Gómez, J. Slovakova, N. Rives Quinto, A. Krejčí, A. Carmena, Journal
of Cell Science 126 (2013) 4873–4884.
date_created: 2018-12-11T11:56:43Z
date_published: 2013-11-01T00:00:00Z
date_updated: 2021-01-12T06:56:29Z
day: '01'
department:
- _id: CaHe
doi: 10.1242/jcs.125617
intvolume: ' 126'
issue: '21'
language:
- iso: eng
month: '11'
oa_version: None
page: 4873 - 4884
publication: Journal of Cell Science
publication_status: published
publisher: Company of Biologists
publist_id: '4658'
quality_controlled: '1'
scopus_import: 1
status: public
title: A serrate-notch-canoe complex mediates essential interactions between glia
and neuroepithelial cells during Drosophila optic lobe development
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 126
year: '2013'
...
---
_id: '2282'
abstract:
- lang: eng
text: Epithelial spreading is a common and fundamental aspect of various developmental
and disease-related processes such as epithelial closure and wound healing. A
key challenge for epithelial tissues undergoing spreading is to increase their
surface area without disrupting epithelial integrity. Here we show that orienting
cell divisions by tension constitutes an efficient mechanism by which the enveloping
cell layer (EVL) releases anisotropic tension while undergoing spreading during
zebrafish epiboly. The control of EVL cell-division orientation by tension involves
cell elongation and requires myosin II activity to align the mitotic spindle with
the main tension axis. We also found that in the absence of tension-oriented cell
divisions and in the presence of increased tissue tension, EVL cells undergo ectopic
fusions, suggesting that the reduction of tension anisotropy by oriented cell
divisions is required to prevent EVL cells from fusing. We conclude that cell-division
orientation by tension constitutes a key mechanism for limiting tension anisotropy
and thus promoting tissue spreading during EVL epiboly.
acknowledged_ssus:
- _id: PreCl
- _id: Bio
acknowledgement: 'This work was supported by the IST Austria and MPI-CBG '
author:
- first_name: Pedro
full_name: Campinho, Pedro
id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87
last_name: Campinho
orcid: 0000-0002-8526-5416
- first_name: Martin
full_name: Behrndt, Martin
id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87
last_name: Behrndt
- first_name: Jonas
full_name: Ranft, Jonas
last_name: Ranft
- first_name: Thomas
full_name: Risler, Thomas
last_name: Risler
- first_name: Nicolas
full_name: Minc, Nicolas
last_name: Minc
- 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: Campinho P, Behrndt M, Ranft J, Risler T, Minc N, Heisenberg C-PJ. Tension-oriented
cell divisions limit anisotropic tissue tension in epithelial spreading during
zebrafish epiboly. Nature Cell Biology. 2013;15:1405-1414. doi:10.1038/ncb2869
apa: Campinho, P., Behrndt, M., Ranft, J., Risler, T., Minc, N., & Heisenberg,
C.-P. J. (2013). Tension-oriented cell divisions limit anisotropic tissue tension
in epithelial spreading during zebrafish epiboly. Nature Cell Biology.
Nature Publishing Group. https://doi.org/10.1038/ncb2869
chicago: Campinho, Pedro, Martin Behrndt, Jonas Ranft, Thomas Risler, Nicolas Minc,
and Carl-Philipp J Heisenberg. “Tension-Oriented Cell Divisions Limit Anisotropic
Tissue Tension in Epithelial Spreading during Zebrafish Epiboly.” Nature Cell
Biology. Nature Publishing Group, 2013. https://doi.org/10.1038/ncb2869.
ieee: P. Campinho, M. Behrndt, J. Ranft, T. Risler, N. Minc, and C.-P. J. Heisenberg,
“Tension-oriented cell divisions limit anisotropic tissue tension in epithelial
spreading during zebrafish epiboly,” Nature Cell Biology, vol. 15. Nature
Publishing Group, pp. 1405–1414, 2013.
ista: Campinho P, Behrndt M, Ranft J, Risler T, Minc N, Heisenberg C-PJ. 2013. Tension-oriented
cell divisions limit anisotropic tissue tension in epithelial spreading during
zebrafish epiboly. Nature Cell Biology. 15, 1405–1414.
mla: Campinho, Pedro, et al. “Tension-Oriented Cell Divisions Limit Anisotropic
Tissue Tension in Epithelial Spreading during Zebrafish Epiboly.” Nature Cell
Biology, vol. 15, Nature Publishing Group, 2013, pp. 1405–14, doi:10.1038/ncb2869.
short: P. Campinho, M. Behrndt, J. Ranft, T. Risler, N. Minc, C.-P.J. Heisenberg,
Nature Cell Biology 15 (2013) 1405–1414.
date_created: 2018-12-11T11:56:45Z
date_published: 2013-11-10T00:00:00Z
date_updated: 2023-02-21T17:02:44Z
day: '10'
department:
- _id: CaHe
doi: 10.1038/ncb2869
intvolume: ' 15'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://hal.upmc.fr/hal-00983313/
month: '11'
oa: 1
oa_version: Submitted Version
page: 1405 - 1414
project:
- _id: 252ABD0A-B435-11E9-9278-68D0E5697425
call_identifier: FWF
grant_number: I 930-B20
name: Control of Epithelial Cell Layer Spreading in Zebrafish
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '4652'
quality_controlled: '1'
related_material:
record:
- id: '1403'
relation: dissertation_contains
status: public
scopus_import: 1
status: public
title: Tension-oriented cell divisions limit anisotropic tissue tension in epithelial
spreading during zebrafish epiboly
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2013'
...
---
_id: '2286'
abstract:
- lang: eng
text: The spatiotemporal control of cell divisions is a key factor in epithelial
morphogenesis and patterning. Mao et al (2013) now describe how differential rates
of proliferation within the Drosophila wing disc epithelium give rise to anisotropic
tissue tension in peripheral/proximal regions of the disc. Such global tissue
tension anisotropy in turn determines the orientation of cell divisions by controlling
epithelial cell elongation.
author:
- first_name: Pedro
full_name: Campinho, Pedro
id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87
last_name: Campinho
orcid: 0000-0002-8526-5416
- 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: Campinho P, Heisenberg C-PJ. The force and effect of cell proliferation. EMBO
Journal. 2013;32(21):2783-2784. doi:10.1038/emboj.2013.225
apa: Campinho, P., & Heisenberg, C.-P. J. (2013). The force and effect of cell
proliferation. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2013.225
chicago: Campinho, Pedro, and Carl-Philipp J Heisenberg. “The Force and Effect of
Cell Proliferation.” EMBO Journal. Wiley-Blackwell, 2013. https://doi.org/10.1038/emboj.2013.225.
ieee: P. Campinho and C.-P. J. Heisenberg, “The force and effect of cell proliferation,”
EMBO Journal, vol. 32, no. 21. Wiley-Blackwell, pp. 2783–2784, 2013.
ista: Campinho P, Heisenberg C-PJ. 2013. The force and effect of cell proliferation.
EMBO Journal. 32(21), 2783–2784.
mla: Campinho, Pedro, and Carl-Philipp J. Heisenberg. “The Force and Effect of Cell
Proliferation.” EMBO Journal, vol. 32, no. 21, Wiley-Blackwell, 2013, pp.
2783–84, doi:10.1038/emboj.2013.225.
short: P. Campinho, C.-P.J. Heisenberg, EMBO Journal 32 (2013) 2783–2784.
date_created: 2018-12-11T11:56:46Z
date_published: 2013-10-04T00:00:00Z
date_updated: 2021-01-12T06:56:32Z
day: '04'
department:
- _id: CaHe
doi: 10.1038/emboj.2013.225
external_id:
pmid:
- '24097062'
intvolume: ' 32'
issue: '21'
language:
- iso: eng
main_file_link:
- open_access: '1'
url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817470/
month: '10'
oa: 1
oa_version: Submitted Version
page: 2783 - 2784
pmid: 1
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '4645'
quality_controlled: '1'
scopus_import: 1
status: public
title: The force and effect of cell proliferation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2013'
...
---
_id: '2469'
abstract:
- lang: eng
text: Cadherins are transmembrane proteins that mediate cell–cell adhesion in animals.
By regulating contact formation and stability, cadherins play a crucial role in
tissue morphogenesis and homeostasis. Here, we review the three major unctions
of cadherins in cell–cell contact formation and stability. Two of those functions
lead to a decrease in interfacial ension at the forming cell–cell contact, thereby
promoting contact expansion — first, by providing adhesion tension that lowers
interfacial tension at the cell–cell contact, and second, by signaling to the
actomyosin cytoskeleton in order to reduce cortex tension and thus interfacial
tension at the contact. The third function of cadherins in cell–cell contact formation
is to stabilize the contact by resisting mechanical forces that pull on the contact.
author:
- first_name: Jean-Léon
full_name: Maître, Jean-Léon
id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87
last_name: Maître
orcid: 0000-0002-3688-1474
- 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: Maître J-L, Heisenberg C-PJ. Three functions of cadherins in cell adhesion.
Current Biology. 2013;23(14):R626-R633. doi:10.1016/j.cub.2013.06.019
apa: Maître, J.-L., & Heisenberg, C.-P. J. (2013). Three functions of cadherins
in cell adhesion. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2013.06.019
chicago: Maître, Jean-Léon, and Carl-Philipp J Heisenberg. “Three Functions of Cadherins
in Cell Adhesion.” Current Biology. Cell Press, 2013. https://doi.org/10.1016/j.cub.2013.06.019.
ieee: J.-L. Maître and C.-P. J. Heisenberg, “Three functions of cadherins in cell
adhesion,” Current Biology, vol. 23, no. 14. Cell Press, pp. R626–R633,
2013.
ista: Maître J-L, Heisenberg C-PJ. 2013. Three functions of cadherins in cell adhesion.
Current Biology. 23(14), R626–R633.
mla: Maître, Jean-Léon, and Carl-Philipp J. Heisenberg. “Three Functions of Cadherins
in Cell Adhesion.” Current Biology, vol. 23, no. 14, Cell Press, 2013,
pp. R626–33, doi:10.1016/j.cub.2013.06.019.
short: J.-L. Maître, C.-P.J. Heisenberg, Current Biology 23 (2013) R626–R633.
date_created: 2018-12-11T11:57:51Z
date_published: 2013-07-22T00:00:00Z
date_updated: 2021-01-12T06:57:40Z
day: '22'
ddc:
- '570'
department:
- _id: CaHe
doi: 10.1016/j.cub.2013.06.019
external_id:
pmid:
- '23885883'
file:
- access_level: open_access
checksum: 6a424b2f007b41d4955a9135793b2162
content_type: application/pdf
creator: dernst
date_created: 2019-01-24T15:40:22Z
date_updated: 2020-07-14T12:45:41Z
file_id: '5881'
file_name: 2013_CurrentBiology_Maitre.pdf
file_size: 247320
relation: main_file
file_date_updated: 2020-07-14T12:45:41Z
has_accepted_license: '1'
intvolume: ' 23'
issue: '14'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: R626 - R633
pmid: 1
publication: Current Biology
publication_status: published
publisher: Cell Press
publist_id: '4433'
quality_controlled: '1'
scopus_import: 1
status: public
title: Three functions of cadherins in cell adhesion
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: 23
year: '2013'
...
---
_id: '2833'
abstract:
- lang: eng
text: During development, mechanical forces cause changes in size, shape, number,
position, and gene expression of cells. They are therefore integral to any morphogenetic
processes. Force generation by actin-myosin networks and force transmission through
adhesive complexes are two self-organizing phenomena driving tissue morphogenesis.
Coordination and integration of forces by long-range force transmission and mechanosensing
of cells within tissues produce large-scale tissue shape changes. Extrinsic mechanical
forces also control tissue patterning by modulating cell fate specification and
differentiation. Thus, the interplay between tissue mechanics and biochemical
signaling orchestrates tissue morphogenesis and patterning in development.
acknowledgement: C.-P.H. is supported by the Institute of Science and Technology Austria
and grants from the Deutsche Forschungsgemeinschaft (DFG) and Fonds zur Förderung
der wissenschaftlichen Forschung (FWF).
author:
- 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
- first_name: Yohanns
full_name: Bellaïche, Yohanns
last_name: Bellaïche
citation:
ama: Heisenberg C-PJ, Bellaïche Y. Forces in tissue morphogenesis and patterning.
Cell. 2013;153(5):948-962. doi:10.1016/j.cell.2013.05.008
apa: Heisenberg, C.-P. J., & Bellaïche, Y. (2013). Forces in tissue morphogenesis
and patterning. Cell. Cell Press. https://doi.org/10.1016/j.cell.2013.05.008
chicago: Heisenberg, Carl-Philipp J, and Yohanns Bellaïche. “Forces in Tissue Morphogenesis
and Patterning.” Cell. Cell Press, 2013. https://doi.org/10.1016/j.cell.2013.05.008.
ieee: C.-P. J. Heisenberg and Y. Bellaïche, “Forces in tissue morphogenesis and
patterning,” Cell, vol. 153, no. 5. Cell Press, pp. 948–962, 2013.
ista: Heisenberg C-PJ, Bellaïche Y. 2013. Forces in tissue morphogenesis and patterning.
Cell. 153(5), 948–962.
mla: Heisenberg, Carl-Philipp J., and Yohanns Bellaïche. “Forces in Tissue Morphogenesis
and Patterning.” Cell, vol. 153, no. 5, Cell Press, 2013, pp. 948–62, doi:10.1016/j.cell.2013.05.008.
short: C.-P.J. Heisenberg, Y. Bellaïche, Cell 153 (2013) 948–962.
date_created: 2018-12-11T11:59:50Z
date_published: 2013-05-23T00:00:00Z
date_updated: 2021-01-12T07:00:04Z
day: '23'
department:
- _id: CaHe
doi: 10.1016/j.cell.2013.05.008
intvolume: ' 153'
issue: '5'
language:
- iso: eng
month: '05'
oa_version: None
page: 948 - 962
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '3966'
quality_controlled: '1'
scopus_import: 1
status: public
title: Forces in tissue morphogenesis and patterning
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 153
year: '2013'
...
---
_id: '2841'
abstract:
- lang: eng
text: In zebrafish early development, blastoderm cells undergo extensive radial
intercalations, triggering the spreading of the blastoderm over the yolk cell
and thereby initiating embryonic body axis formation. Now reporting in Developmental
Cell, Song et al. (2013) demonstrate a critical function for EGF-dependent E-cadherin
endocytosis in promoting blastoderm cell intercalations.
author:
- first_name: Hitoshi
full_name: Morita, Hitoshi
id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87
last_name: Morita
- 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: 'Morita H, Heisenberg C-PJ. Holding on and letting go: Cadherin turnover in
cell intercalation. Developmental Cell. 2013;24(6):567-569. doi:10.1016/j.devcel.2013.03.007'
apa: 'Morita, H., & Heisenberg, C.-P. J. (2013). Holding on and letting go:
Cadherin turnover in cell intercalation. Developmental Cell. Cell Press.
https://doi.org/10.1016/j.devcel.2013.03.007'
chicago: 'Morita, Hitoshi, and Carl-Philipp J Heisenberg. “Holding on and Letting
Go: Cadherin Turnover in Cell Intercalation.” Developmental Cell. Cell
Press, 2013. https://doi.org/10.1016/j.devcel.2013.03.007.'
ieee: 'H. Morita and C.-P. J. Heisenberg, “Holding on and letting go: Cadherin turnover
in cell intercalation,” Developmental Cell, vol. 24, no. 6. Cell Press,
pp. 567–569, 2013.'
ista: 'Morita H, Heisenberg C-PJ. 2013. Holding on and letting go: Cadherin turnover
in cell intercalation. Developmental Cell. 24(6), 567–569.'
mla: 'Morita, Hitoshi, and Carl-Philipp J. Heisenberg. “Holding on and Letting Go:
Cadherin Turnover in Cell Intercalation.” Developmental Cell, vol. 24,
no. 6, Cell Press, 2013, pp. 567–69, doi:10.1016/j.devcel.2013.03.007.'
short: H. Morita, C.-P.J. Heisenberg, Developmental Cell 24 (2013) 567–569.
date_created: 2018-12-11T11:59:52Z
date_published: 2013-05-25T00:00:00Z
date_updated: 2021-01-12T07:00:09Z
day: '25'
department:
- _id: CaHe
doi: 10.1016/j.devcel.2013.03.007
intvolume: ' 24'
issue: '6'
language:
- iso: eng
month: '05'
oa_version: None
page: 567 - 569
publication: Developmental Cell
publication_status: published
publisher: Cell Press
publist_id: '3956'
quality_controlled: '1'
scopus_import: 1
status: public
title: 'Holding on and letting go: Cadherin turnover in cell intercalation'
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 24
year: '2013'
...