---
_id: '1553'
abstract:
- lang: eng
  text: Cell movement has essential functions in development, immunity, and cancer.
    Various cell migration patterns have been reported, but no general rule has emerged
    so far. Here, we show on the basis of experimental data in vitro and in vivo that
    cell persistence, which quantifies the straightness of trajectories, is robustly
    coupled to cell migration speed. We suggest that this universal coupling constitutes
    a generic law of cell migration, which originates in the advection of polarity
    cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis
    relies on a theoretical model that we validate by measuring the persistence of
    cells upon modulation of actin flow speeds and upon optogenetic manipulation of
    the binding of an actin regulator to actin filaments. Beyond the quantitative
    prediction of the coupling, the model yields a generic phase diagram of cellular
    trajectories, which recapitulates the full range of observed migration patterns.
author:
- first_name: Paolo
  full_name: Maiuri, Paolo
  last_name: Maiuri
- first_name: Jean
  full_name: Rupprecht, Jean
  last_name: Rupprecht
- first_name: Stefan
  full_name: Wieser, Stefan
  id: 355AA5A0-F248-11E8-B48F-1D18A9856A87
  last_name: Wieser
  orcid: 0000-0002-2670-2217
- first_name: Verena
  full_name: Ruprecht, Verena
  id: 4D71A03A-F248-11E8-B48F-1D18A9856A87
  last_name: Ruprecht
  orcid: 0000-0003-4088-8633
- first_name: Olivier
  full_name: Bénichou, Olivier
  last_name: Bénichou
- first_name: Nicolas
  full_name: Carpi, Nicolas
  last_name: Carpi
- first_name: Mathieu
  full_name: Coppey, Mathieu
  last_name: Coppey
- first_name: Simon
  full_name: De Beco, Simon
  last_name: De Beco
- first_name: Nir
  full_name: Gov, Nir
  last_name: Gov
- 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: Carolina
  full_name: Lage Crespo, Carolina
  last_name: Lage Crespo
- first_name: Franziska
  full_name: Lautenschlaeger, Franziska
  last_name: Lautenschlaeger
- first_name: Maël
  full_name: Le Berre, Maël
  last_name: Le Berre
- first_name: Ana
  full_name: Lennon Duménil, Ana
  last_name: Lennon Duménil
- first_name: Matthew
  full_name: Raab, Matthew
  last_name: Raab
- first_name: Hawa
  full_name: Thiam, Hawa
  last_name: Thiam
- first_name: Matthieu
  full_name: Piel, Matthieu
  last_name: Piel
- first_name: Michael K
  full_name: Sixt, Michael K
  id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87
  last_name: Sixt
  orcid: 0000-0002-6620-9179
- first_name: Raphaël
  full_name: Voituriez, Raphaël
  last_name: Voituriez
citation:
  ama: Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling
    between cell speed and cell persistence. <i>Cell</i>. 2015;161(2):374-386. doi:<a
    href="https://doi.org/10.1016/j.cell.2015.01.056">10.1016/j.cell.2015.01.056</a>
  apa: Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N.,
    … Voituriez, R. (2015). Actin flows mediate a universal coupling between cell
    speed and cell persistence. <i>Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.cell.2015.01.056">https://doi.org/10.1016/j.cell.2015.01.056</a>
  chicago: Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier
    Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal
    Coupling between Cell Speed and Cell Persistence.” <i>Cell</i>. Cell Press, 2015.
    <a href="https://doi.org/10.1016/j.cell.2015.01.056">https://doi.org/10.1016/j.cell.2015.01.056</a>.
  ieee: P. Maiuri <i>et al.</i>, “Actin flows mediate a universal coupling between
    cell speed and cell persistence,” <i>Cell</i>, vol. 161, no. 2. Cell Press, pp.
    374–386, 2015.
  ista: Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M,
    De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre
    M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin
    flows mediate a universal coupling between cell speed and cell persistence. Cell.
    161(2), 374–386.
  mla: Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell
    Speed and Cell Persistence.” <i>Cell</i>, vol. 161, no. 2, Cell Press, 2015, pp.
    374–86, doi:<a href="https://doi.org/10.1016/j.cell.2015.01.056">10.1016/j.cell.2015.01.056</a>.
  short: P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M.
    Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger,
    M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez,
    Cell 161 (2015) 374–386.
date_created: 2018-12-11T11:52:41Z
date_published: 2015-04-09T00:00:00Z
date_updated: 2021-01-12T06:51:33Z
day: '09'
department:
- _id: MiSi
- _id: CaHe
doi: 10.1016/j.cell.2015.01.056
ec_funded: 1
intvolume: '       161'
issue: '2'
language:
- iso: eng
month: '04'
oa_version: None
page: 374 - 386
project:
- _id: 2529486C-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: T 560-B17
  name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation
- _id: 25A603A2-B435-11E9-9278-68D0E5697425
  call_identifier: FP7
  grant_number: '281556'
  name: Cytoskeletal force generation and force transduction of migrating leukocytes
    (EU)
- _id: 25ABD200-B435-11E9-9278-68D0E5697425
  grant_number: RGP0058/2011
  name: 'Cell migration in complex environments: from in vivo experiments to theoretical
    models'
publication: Cell
publication_status: published
publisher: Cell Press
publist_id: '5618'
quality_controlled: '1'
scopus_import: 1
status: public
title: Actin flows mediate a universal coupling between cell speed and cell persistence
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 161
year: '2015'
...
---
_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. <i>PLoS Computational Biology</i>. 2015;11(10).
    doi:<a href="https://doi.org/10.1371/journal.pcbi.1004541">10.1371/journal.pcbi.1004541</a>
  apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., &#38; Carrión Vázquez, M. (2015).
    An exploration of the universe of polyglutamine structures. <i>PLoS Computational
    Biology</i>. Public Library of Science. <a href="https://doi.org/10.1371/journal.pcbi.1004541">https://doi.org/10.1371/journal.pcbi.1004541</a>
  chicago: Gómez Sicilia, Àngel, Mateusz K Sikora, Marek Cieplak, and Mariano Carrión
    Vázquez. “An Exploration of the Universe of Polyglutamine Structures.” <i>PLoS
    Computational Biology</i>. Public Library of Science, 2015. <a href="https://doi.org/10.1371/journal.pcbi.1004541">https://doi.org/10.1371/journal.pcbi.1004541</a>.
  ieee: À. Gómez Sicilia, M. K. Sikora, M. Cieplak, and M. Carrión Vázquez, “An exploration
    of the universe of polyglutamine structures,” <i>PLoS Computational Biology</i>,
    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.” <i>PLoS Computational Biology</i>, vol. 11, no. 10, e1004541, Public
    Library of Science, 2015, doi:<a href="https://doi.org/10.1371/journal.pcbi.1004541">10.1371/journal.pcbi.1004541</a>.
  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. <i>Cell</i>. 2015;161(3):431-432.
    doi:<a href="https://doi.org/10.1016/j.cell.2015.04.009">10.1016/j.cell.2015.04.009</a>
  apa: Bollenbach, M. T., &#38; Heisenberg, C.-P. J. (2015). Gradients are shaping
    up. <i>Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.cell.2015.04.009">https://doi.org/10.1016/j.cell.2015.04.009</a>
  chicago: Bollenbach, Mark Tobias, and Carl-Philipp J Heisenberg. “Gradients Are
    Shaping Up.” <i>Cell</i>. Cell Press, 2015. <a href="https://doi.org/10.1016/j.cell.2015.04.009">https://doi.org/10.1016/j.cell.2015.04.009</a>.
  ieee: M. T. Bollenbach and C.-P. J. Heisenberg, “Gradients are shaping up,” <i>Cell</i>,
    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.” <i>Cell</i>, vol. 161, no. 3, Cell Press, 2015, pp. 431–32, doi:<a href="https://doi.org/10.1016/j.cell.2015.04.009">10.1016/j.cell.2015.04.009</a>.
  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: '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:<a href="https://doi.org/10.1371/journal.pcbi.1004541.s001">10.1371/journal.pcbi.1004541.s001</a>
  apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., &#38; Carrión Vázquez, M. (2015).
    An exploration of the universe of polyglutamine structures - submission to PLOS
    journals. Public Library of Science . <a href="https://doi.org/10.1371/journal.pcbi.1004541.s001">https://doi.org/10.1371/journal.pcbi.1004541.s001</a>
  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. <a href="https://doi.org/10.1371/journal.pcbi.1004541.s001">https://doi.org/10.1371/journal.pcbi.1004541.s001</a>.
  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 , <a href="https://doi.org/10.1371/journal.pcbi.1004541.s001">10.1371/journal.pcbi.1004541.s001</a>.
  mla: Gómez Sicilia, Àngel, et al. <i>An Exploration of the Universe of Polyglutamine
    Structures - Submission to PLOS Journals</i>. Public Library of Science , 2015,
    doi:<a href="https://doi.org/10.1371/journal.pcbi.1004541.s001">10.1371/journal.pcbi.1004541.s001</a>.
  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: '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. <i>Congenital Anomalies</i>. 2014;54(1):1-7. doi:<a
    href="https://doi.org/10.1111/cga.12039">10.1111/cga.12039</a>
  apa: Hashimoto, M., Morita, H., &#38; Ueno, N. (2014). Molecular and cellular mechanisms
    of development underlying congenital diseases. <i>Congenital Anomalies</i>. Wiley.
    <a href="https://doi.org/10.1111/cga.12039">https://doi.org/10.1111/cga.12039</a>
  chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular
    Mechanisms of Development Underlying Congenital Diseases.” <i>Congenital Anomalies</i>.
    Wiley, 2014. <a href="https://doi.org/10.1111/cga.12039">https://doi.org/10.1111/cga.12039</a>.
  ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of
    development underlying congenital diseases,” <i>Congenital Anomalies</i>, 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.” <i>Congenital Anomalies</i>, vol. 54, no. 1,
    Wiley, 2014, pp. 1–7, doi:<a href="https://doi.org/10.1111/cga.12039">10.1111/cga.12039</a>.
  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: '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. <i>Proteins: Structure, Function and Bioinformatics</i>. 2014;82(5):717-726.
    doi:<a href="https://doi.org/10.1002/prot.24436">10.1002/prot.24436</a>'
  apa: 'Chwastyk, M., Galera Prat, A., Sikora, M. K., Gómez Sicilia, À., Carrión Vázquez,
    M., &#38; Cieplak, M. (2014). Theoretical tests of the mechanical protection strategy
    in protein nanomechanics. <i>Proteins: Structure, Function and Bioinformatics</i>.
    Wiley-Blackwell. <a href="https://doi.org/10.1002/prot.24436">https://doi.org/10.1002/prot.24436</a>'
  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.” <i>Proteins: Structure, Function
    and Bioinformatics</i>. Wiley-Blackwell, 2014. <a href="https://doi.org/10.1002/prot.24436">https://doi.org/10.1002/prot.24436</a>.'
  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,” <i>Proteins: Structure, Function and Bioinformatics</i>, 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.” <i>Proteins: Structure, Function and Bioinformatics</i>,
    vol. 82, no. 5, Wiley-Blackwell, 2014, pp. 717–26, doi:<a href="https://doi.org/10.1002/prot.24436">10.1002/prot.24436</a>.'
  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. <i>Nature
    Cell Biology</i>. 2014;16(2):127-129. doi:<a href="https://doi.org/10.1038/ncb2913">10.1038/ncb2913</a>
  apa: Behrndt, M., &#38; Heisenberg, C.-P. J. (2014). Lateral junction dynamics lead
    the way out. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncb2913">https://doi.org/10.1038/ncb2913</a>
  chicago: Behrndt, Martin, and Carl-Philipp J Heisenberg. “Lateral Junction Dynamics
    Lead the Way Out.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2014.
    <a href="https://doi.org/10.1038/ncb2913">https://doi.org/10.1038/ncb2913</a>.
  ieee: M. Behrndt and C.-P. J. Heisenberg, “Lateral junction dynamics lead the way
    out,” <i>Nature Cell Biology</i>, 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.” <i>Nature Cell Biology</i>, vol. 16, no. 2, Nature Publishing
    Group, 2014, pp. 127–29, doi:<a href="https://doi.org/10.1038/ncb2913">10.1038/ncb2913</a>.
  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. <i>Developmental
    Cell</i>. 2014;31(6):774-783. doi:<a href="https://doi.org/10.1016/j.devcel.2014.11.003">10.1016/j.devcel.2014.11.003</a>
  apa: Compagnon, J., Barone, V., Rajshekar, S., Kottmeier, R., Pranjic-Ferscha, K.,
    Behrndt, M., &#38; Heisenberg, C.-P. J. (2014). The notochord breaks bilateral
    symmetry by controlling cell shapes in the Zebrafish laterality organ. <i>Developmental
    Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.devcel.2014.11.003">https://doi.org/10.1016/j.devcel.2014.11.003</a>
  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.” <i>Developmental Cell</i>. Cell Press, 2014. <a href="https://doi.org/10.1016/j.devcel.2014.11.003">https://doi.org/10.1016/j.devcel.2014.11.003</a>.
  ieee: J. Compagnon <i>et al.</i>, “The notochord breaks bilateral symmetry by controlling
    cell shapes in the Zebrafish laterality organ,” <i>Developmental Cell</i>, 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.” <i>Developmental Cell</i>, vol.
    31, no. 6, Cell Press, 2014, pp. 774–83, doi:<a href="https://doi.org/10.1016/j.devcel.2014.11.003">10.1016/j.devcel.2014.11.003</a>.
  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. <i>New Journal
    of Physics</i>. 2014;16. doi:<a href="https://doi.org/10.1088/1367-2630/16/6/065005">10.1088/1367-2630/16/6/065005</a>
  apa: Berthoumieux, H., Maître, J.-L., Heisenberg, C.-P. J., Paluch, E., Julicher,
    F., &#38; Salbreux, G. (2014). Active elastic thin shell theory for cellular deformations.
    <i>New Journal of Physics</i>. IOP Publishing Ltd. <a href="https://doi.org/10.1088/1367-2630/16/6/065005">https://doi.org/10.1088/1367-2630/16/6/065005</a>
  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.” <i>New Journal of Physics</i>. IOP Publishing Ltd.,
    2014. <a href="https://doi.org/10.1088/1367-2630/16/6/065005">https://doi.org/10.1088/1367-2630/16/6/065005</a>.
  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,”
    <i>New Journal of Physics</i>, 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.” <i>New Journal of Physics</i>, vol. 16, 065005, IOP Publishing
    Ltd., 2014, doi:<a href="https://doi.org/10.1088/1367-2630/16/6/065005">10.1088/1367-2630/16/6/065005</a>.
  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. <i>Nanotechnology</i>.
    2014;25(12). doi:<a href="https://doi.org/10.1088/0957-4484/25/12/125704">10.1088/0957-4484/25/12/125704</a>
  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. <i>Nanotechnology</i>. IOP Publishing.
    <a href="https://doi.org/10.1088/0957-4484/25/12/125704">https://doi.org/10.1088/0957-4484/25/12/125704</a>
  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.” <i>Nanotechnology</i>.
    IOP Publishing, 2014. <a href="https://doi.org/10.1088/0957-4484/25/12/125704">https://doi.org/10.1088/0957-4484/25/12/125704</a>.
  ieee: C. Lamprecht <i>et al.</i>, “A single-molecule approach to explore binding
    uptake and transport of cancer cell targeting nanotubes,” <i>Nanotechnology</i>,
    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.” <i>Nanotechnology</i>,
    vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:<a href="https://doi.org/10.1088/0957-4484/25/12/125704">10.1088/0957-4484/25/12/125704</a>.
  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: '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. <i>Journal of Experimental Zoology Part B: Molecular
    and Developmental Evolution</i>. 2014;322(1):1-12. doi:<a href="https://doi.org/10.1002/jez.b.22545">10.1002/jez.b.22545</a>'
  apa: 'Capek, D., Metscher, B., &#38; Müller, G. (2014). Thumbs down: A molecular-morphogenetic
    approach to avian digit homology. <i>Journal of Experimental Zoology Part B: Molecular
    and Developmental Evolution</i>. Wiley-Blackwell. <a href="https://doi.org/10.1002/jez.b.22545">https://doi.org/10.1002/jez.b.22545</a>'
  chicago: 'Capek, Daniel, Brian Metscher, and Gerd Müller. “Thumbs down: A Molecular-Morphogenetic
    Approach to Avian Digit Homology.” <i>Journal of Experimental Zoology Part B:
    Molecular and Developmental Evolution</i>. Wiley-Blackwell, 2014. <a href="https://doi.org/10.1002/jez.b.22545">https://doi.org/10.1002/jez.b.22545</a>.'
  ieee: 'D. Capek, B. Metscher, and G. Müller, “Thumbs down: A molecular-morphogenetic
    approach to avian digit homology,” <i>Journal of Experimental Zoology Part B:
    Molecular and Developmental Evolution</i>, 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.” <i>Journal of Experimental Zoology Part B: Molecular and
    Developmental Evolution</i>, vol. 322, no. 1, Wiley-Blackwell, 2014, pp. 1–12,
    doi:<a href="https://doi.org/10.1002/jez.b.22545">10.1002/jez.b.22545</a>.'
  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: '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. <i>Tissue Morphogenesis</i>. Vol 1189. Methods in Molecular
    Biology. New York, NY: Springer; 2014:219-235. doi:<a href="https://doi.org/10.1007/978-1-4939-1164-6_15">10.1007/978-1-4939-1164-6_15</a>'
  apa: 'Smutny, M., Behrndt, M., Campinho, P., Ruprecht, V., &#38; 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.), <i>Tissue Morphogenesis</i>
    (Vol. 1189, pp. 219–235). New York, NY: Springer. <a href="https://doi.org/10.1007/978-1-4939-1164-6_15">https://doi.org/10.1007/978-1-4939-1164-6_15</a>'
  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 <i>Tissue Morphogenesis</i>,
    edited by Celeste Nelson, 1189:219–35. Methods in Molecular Biology. New York,
    NY: Springer, 2014. <a href="https://doi.org/10.1007/978-1-4939-1164-6_15">https://doi.org/10.1007/978-1-4939-1164-6_15</a>.'
  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 <i>Tissue Morphogenesis</i>, 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.” <i>Tissue Morphogenesis</i>,
    edited by Celeste Nelson, vol. 1189, Springer, 2014, pp. 219–35, doi:<a href="https://doi.org/10.1007/978-1-4939-1164-6_15">10.1007/978-1-4939-1164-6_15</a>.
  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: '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). <i>Forces driving epithelial spreading in zebrafish epiboly</i>.
    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. <i>Forces Driving Epithelial Spreading in Zebrafish Epiboly</i>.
    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: '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.
    <i>Current Biology</i>. 2013;23(14):R626-R633. doi:<a href="https://doi.org/10.1016/j.cub.2013.06.019">10.1016/j.cub.2013.06.019</a>
  apa: Maître, J.-L., &#38; Heisenberg, C.-P. J. (2013). Three functions of cadherins
    in cell adhesion. <i>Current Biology</i>. Cell Press. <a href="https://doi.org/10.1016/j.cub.2013.06.019">https://doi.org/10.1016/j.cub.2013.06.019</a>
  chicago: Maître, Jean-Léon, and Carl-Philipp J Heisenberg. “Three Functions of Cadherins
    in Cell Adhesion.” <i>Current Biology</i>. Cell Press, 2013. <a href="https://doi.org/10.1016/j.cub.2013.06.019">https://doi.org/10.1016/j.cub.2013.06.019</a>.
  ieee: J.-L. Maître and C.-P. J. Heisenberg, “Three functions of cadherins in cell
    adhesion,” <i>Current Biology</i>, 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.” <i>Current Biology</i>, vol. 23, no. 14, Cell Press, 2013,
    pp. R626–33, doi:<a href="https://doi.org/10.1016/j.cub.2013.06.019">10.1016/j.cub.2013.06.019</a>.
  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.
    <i>Cell</i>. 2013;153(5):948-962. doi:<a href="https://doi.org/10.1016/j.cell.2013.05.008">10.1016/j.cell.2013.05.008</a>
  apa: Heisenberg, C.-P. J., &#38; Bellaïche, Y. (2013). Forces in tissue morphogenesis
    and patterning. <i>Cell</i>. Cell Press. <a href="https://doi.org/10.1016/j.cell.2013.05.008">https://doi.org/10.1016/j.cell.2013.05.008</a>
  chicago: Heisenberg, Carl-Philipp J, and Yohanns Bellaïche. “Forces in Tissue Morphogenesis
    and Patterning.” <i>Cell</i>. Cell Press, 2013. <a href="https://doi.org/10.1016/j.cell.2013.05.008">https://doi.org/10.1016/j.cell.2013.05.008</a>.
  ieee: C.-P. J. Heisenberg and Y. Bellaïche, “Forces in tissue morphogenesis and
    patterning,” <i>Cell</i>, 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.” <i>Cell</i>, vol. 153, no. 5, Cell Press, 2013, pp. 948–62, doi:<a
    href="https://doi.org/10.1016/j.cell.2013.05.008">10.1016/j.cell.2013.05.008</a>.
  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. <i>Developmental Cell</i>. 2013;24(6):567-569. doi:<a href="https://doi.org/10.1016/j.devcel.2013.03.007">10.1016/j.devcel.2013.03.007</a>'
  apa: 'Morita, H., &#38; Heisenberg, C.-P. J. (2013). Holding on and letting go:
    Cadherin turnover in cell intercalation. <i>Developmental Cell</i>. Cell Press.
    <a href="https://doi.org/10.1016/j.devcel.2013.03.007">https://doi.org/10.1016/j.devcel.2013.03.007</a>'
  chicago: 'Morita, Hitoshi, and Carl-Philipp J Heisenberg. “Holding on and Letting
    Go: Cadherin Turnover in Cell Intercalation.” <i>Developmental Cell</i>. Cell
    Press, 2013. <a href="https://doi.org/10.1016/j.devcel.2013.03.007">https://doi.org/10.1016/j.devcel.2013.03.007</a>.'
  ieee: 'H. Morita and C.-P. J. Heisenberg, “Holding on and letting go: Cadherin turnover
    in cell intercalation,” <i>Developmental Cell</i>, 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.” <i>Developmental Cell</i>, vol. 24,
    no. 6, Cell Press, 2013, pp. 567–69, doi:<a href="https://doi.org/10.1016/j.devcel.2013.03.007">10.1016/j.devcel.2013.03.007</a>.'
  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'
...
---
_id: '2862'
abstract:
- lang: eng
  text: Motile cilia perform crucial functions during embryonic development and throughout
    adult life. Development of organs containing motile cilia involves regulation
    of cilia formation (ciliogenesis) and formation of a luminal space (lumenogenesis)
    in which cilia generate fluid flows. Control of ciliogenesis and lumenogenesis
    is not yet fully understood, and it remains unclear whether these processes are
    coupled. In the zebrafish embryo, lethal giant larvae 2 (lgl2) is expressed prominently
    in ciliated organs. Lgl proteins are involved in establishing cell polarity and
    have been implicated in vesicle trafficking. Here, we identified a role for Lgl2
    in development of ciliated epithelia in Kupffer's vesicle, which directs left-right
    asymmetry of the embryo; the otic vesicles, which give rise to the inner ear;
    and the pronephric ducts of the kidney. Using Kupffer's vesicle as a model ciliated
    organ, we found that depletion of Lgl2 disrupted lumen formation and reduced cilia
    number and length. Immunofluorescence and time-lapse imaging of Kupffer's vesicle
    morphogenesis in Lgl2-deficient embryos suggested cell adhesion defects and revealed
    loss of the adherens junction component E-cadherin at lateral membranes. Genetic
    interaction experiments indicate that Lgl2 interacts with Rab11a to regulate E-cadherin
    and mediate lumen formation that is uncoupled from cilia formation. These results
    uncover new roles and interactions for Lgl2 that are crucial for both lumenogenesis
    and ciliogenesis and indicate that these processes are genetically separable in
    zebrafish.
acknowledgement: Deposited in PMC for release after 12 months. We thank members of
  the Amack lab for helpful discussions and Mahendra Sonawane for donating reagents.
author:
- first_name: Hwee
  full_name: Tay, Hwee
  last_name: Tay
- first_name: Sabrina
  full_name: Schulze, Sabrina
  last_name: Schulze
- first_name: Julien
  full_name: Compagnon, Julien
  id: 2E3E0988-F248-11E8-B48F-1D18A9856A87
  last_name: Compagnon
- first_name: Fiona
  full_name: Foley, Fiona
  last_name: Foley
- 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: H Joseph
  full_name: Yost, H Joseph
  last_name: Yost
- first_name: Salim
  full_name: Abdelilah Seyfried, Salim
  last_name: Abdelilah Seyfried
- first_name: Jeffrey
  full_name: Amack, Jeffrey
  last_name: Amack
citation:
  ama: Tay H, Schulze S, Compagnon J, et al. Lethal giant larvae 2 regulates development
    of the ciliated organ Kupffer’s vesicle. <i>Development</i>. 2013;140(7):1550-1559.
    doi:<a href="https://doi.org/10.1242/dev.087130">10.1242/dev.087130</a>
  apa: Tay, H., Schulze, S., Compagnon, J., Foley, F., Heisenberg, C.-P. J., Yost,
    H. J., … Amack, J. (2013). Lethal giant larvae 2 regulates development of the
    ciliated organ Kupffer’s vesicle. <i>Development</i>. Company of Biologists. <a
    href="https://doi.org/10.1242/dev.087130">https://doi.org/10.1242/dev.087130</a>
  chicago: Tay, Hwee, Sabrina Schulze, Julien Compagnon, Fiona Foley, Carl-Philipp
    J Heisenberg, H Joseph Yost, Salim Abdelilah Seyfried, and Jeffrey Amack. “Lethal
    Giant Larvae 2 Regulates Development of the Ciliated Organ Kupffer’s Vesicle.”
    <i>Development</i>. Company of Biologists, 2013. <a href="https://doi.org/10.1242/dev.087130">https://doi.org/10.1242/dev.087130</a>.
  ieee: H. Tay <i>et al.</i>, “Lethal giant larvae 2 regulates development of the
    ciliated organ Kupffer’s vesicle,” <i>Development</i>, vol. 140, no. 7. Company
    of Biologists, pp. 1550–1559, 2013.
  ista: Tay H, Schulze S, Compagnon J, Foley F, Heisenberg C-PJ, Yost HJ, Abdelilah
    Seyfried S, Amack J. 2013. Lethal giant larvae 2 regulates development of the
    ciliated organ Kupffer’s vesicle. Development. 140(7), 1550–1559.
  mla: Tay, Hwee, et al. “Lethal Giant Larvae 2 Regulates Development of the Ciliated
    Organ Kupffer’s Vesicle.” <i>Development</i>, vol. 140, no. 7, Company of Biologists,
    2013, pp. 1550–59, doi:<a href="https://doi.org/10.1242/dev.087130">10.1242/dev.087130</a>.
  short: H. Tay, S. Schulze, J. Compagnon, F. Foley, C.-P.J. Heisenberg, H.J. Yost,
    S. Abdelilah Seyfried, J. Amack, Development 140 (2013) 1550–1559.
date_created: 2018-12-11T11:59:59Z
date_published: 2013-04-01T00:00:00Z
date_updated: 2021-01-12T07:00:20Z
day: '01'
department:
- _id: CaHe
doi: 10.1242/dev.087130
external_id:
  pmid:
  - '23482490'
intvolume: '       140'
issue: '7'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596994/
month: '04'
oa: 1
oa_version: Submitted Version
page: 1550 - 1559
pmid: 1
publication: Development
publication_status: published
publisher: Company of Biologists
publist_id: '3927'
quality_controlled: '1'
scopus_import: 1
status: public
title: Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s
  vesicle
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 140
year: '2013'
...
---
_id: '2884'
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: Hélène
  full_name: Berthoumieux, Hélène
  last_name: Berthoumieux
- first_name: Gabriel
  full_name: Krens, Gabriel
  id: 2B819732-F248-11E8-B48F-1D18A9856A87
  last_name: Krens
  orcid: 0000-0003-4761-5996
- first_name: Guillaume
  full_name: Salbreux, Guillaume
  last_name: Salbreux
- first_name: Frank
  full_name: Julicher, Frank
  last_name: Julicher
- first_name: Ewa
  full_name: Paluch, Ewa
  last_name: Paluch
- 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, Berthoumieux H, Krens G, et al. Cell adhesion mechanics of zebrafish
    gastrulation. <i>Medecine Sciences</i>. 2013;29(2):147-150. doi:<a href="https://doi.org/10.1051/medsci/2013292011">10.1051/medsci/2013292011</a>
  apa: Maître, J.-L., Berthoumieux, H., Krens, G., Salbreux, G., Julicher, F., Paluch,
    E., &#38; Heisenberg, C.-P. J. (2013). Cell adhesion mechanics of zebrafish gastrulation.
    <i>Medecine Sciences</i>. Éditions Médicales et Scientifiques. <a href="https://doi.org/10.1051/medsci/2013292011">https://doi.org/10.1051/medsci/2013292011</a>
  chicago: Maître, Jean-Léon, Hélène Berthoumieux, Gabriel Krens, Guillaume Salbreux,
    Frank Julicher, Ewa Paluch, and Carl-Philipp J Heisenberg. “Cell Adhesion Mechanics
    of Zebrafish Gastrulation.” <i>Medecine Sciences</i>. Éditions Médicales et Scientifiques,
    2013. <a href="https://doi.org/10.1051/medsci/2013292011">https://doi.org/10.1051/medsci/2013292011</a>.
  ieee: J.-L. Maître <i>et al.</i>, “Cell adhesion mechanics of zebrafish gastrulation,”
    <i>Medecine Sciences</i>, vol. 29, no. 2. Éditions Médicales et Scientifiques,
    pp. 147–150, 2013.
  ista: Maître J-L, Berthoumieux H, Krens G, Salbreux G, Julicher F, Paluch E, Heisenberg
    C-PJ. 2013. Cell adhesion mechanics of zebrafish gastrulation. Medecine Sciences.
    29(2), 147–150.
  mla: Maître, Jean-Léon, et al. “Cell Adhesion Mechanics of Zebrafish Gastrulation.”
    <i>Medecine Sciences</i>, vol. 29, no. 2, Éditions Médicales et Scientifiques,
    2013, pp. 147–50, doi:<a href="https://doi.org/10.1051/medsci/2013292011">10.1051/medsci/2013292011</a>.
  short: J.-L. Maître, H. Berthoumieux, G. Krens, G. Salbreux, F. Julicher, E. Paluch,
    C.-P.J. Heisenberg, Medecine Sciences 29 (2013) 147–150.
date_created: 2018-12-11T12:00:08Z
date_published: 2013-02-01T00:00:00Z
date_updated: 2021-01-12T07:00:28Z
day: '01'
department:
- _id: CaHe
doi: 10.1051/medsci/2013292011
intvolume: '        29'
issue: '2'
language:
- iso: eng
month: '02'
oa_version: None
page: 147 - 150
project:
- _id: 252064B8-B435-11E9-9278-68D0E5697425
  grant_number: HE_3231/6-1
  name: Analysis of the Formation and Function of Different Cell Protusion Types During
    Cell Migration in Vivo
- _id: 2527D5CC-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: I 812-B12
  name: Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation
publication: Medecine Sciences
publication_status: published
publisher: Éditions Médicales et Scientifiques
publist_id: '3877'
quality_controlled: '1'
scopus_import: 1
status: public
title: Cell adhesion mechanics of zebrafish gastrulation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 29
year: '2013'
...
---
_id: '2918'
abstract:
- lang: eng
  text: "Oriented mitosis is essential during tissue morphogenesis. The Wnt/planar
    cell polarity (Wnt/PCP) pathway orients mitosis in a number of developmental systems,
    including dorsal epiblast cell divisions along the animal-vegetal (A-V) axis during
    zebrafish gastrulation. How Wnt signalling orients the mitotic plane is, however,
    unknown. Here we show that, in dorsal epiblast cells, anthrax toxin receptor 2a
    (Antxr2a) accumulates in a polarized cortical cap, which is aligned with the embryonic
    A-V axis and forecasts the division plane. Filamentous actin (F-actin) also forms
    an A-V polarized cap, which depends on Wnt/PCP and its effectors RhoA and Rock2.
    Antxr2a is recruited to the cap by interacting with actin. Antxr2a also interacts
    with RhoA and together they activate the diaphanous-related formin zDia2. Mechanistically,
    Antxr2a functions as a Wnt-dependent polarized determinant, which, through the
    action of RhoA and zDia2, exerts torque on the spindle to align it with the A-V
    axis.\r\n"
acknowledgement: This work was supported by the SNSF, the Swiss SystemsX.ch initiative
  and LipidX-2008/011 (M.G-G. and F.G.v.d.G.), by the Fondation SANTE-Vaduz/Aide au
  Soutien des Nouvelles Thérapies (F.G.v.d.G.) and by the ERC, the NCCR Frontiers
  in Genetics and Chemical Biology programmes and the Polish–Swiss research program
  (M.G-G.).
author:
- first_name: Irinka
  full_name: Castanon, Irinka
  last_name: Castanon
- first_name: Laurence
  full_name: Abrami, Laurence
  last_name: Abrami
- first_name: Laurent
  full_name: Holtzer, Laurent
  last_name: Holtzer
- 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: Françoise
  full_name: Van Der Goot, Françoise
  last_name: Van Der Goot
- first_name: Marcos
  full_name: González Gaitán, Marcos
  last_name: González Gaitán
citation:
  ama: Castanon I, Abrami L, Holtzer L, Heisenberg C-PJ, Van Der Goot F, González
    Gaitán M. Anthrax toxin receptor 2a controls mitotic spindle positioning. <i>Nature
    Cell Biology</i>. 2013;15(1):28-39. doi:<a href="https://doi.org/10.1038/ncb2632">10.1038/ncb2632</a>
  apa: Castanon, I., Abrami, L., Holtzer, L., Heisenberg, C.-P. J., Van Der Goot,
    F., &#38; González Gaitán, M. (2013). Anthrax toxin receptor 2a controls mitotic
    spindle positioning. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/ncb2632">https://doi.org/10.1038/ncb2632</a>
  chicago: Castanon, Irinka, Laurence Abrami, Laurent Holtzer, Carl-Philipp J Heisenberg,
    Françoise Van Der Goot, and Marcos González Gaitán. “Anthrax Toxin Receptor 2a
    Controls Mitotic Spindle Positioning.” <i>Nature Cell Biology</i>. Nature Publishing
    Group, 2013. <a href="https://doi.org/10.1038/ncb2632">https://doi.org/10.1038/ncb2632</a>.
  ieee: I. Castanon, L. Abrami, L. Holtzer, C.-P. J. Heisenberg, F. Van Der Goot,
    and M. González Gaitán, “Anthrax toxin receptor 2a controls mitotic spindle positioning,”
    <i>Nature Cell Biology</i>, vol. 15, no. 1. Nature Publishing Group, pp. 28–39,
    2013.
  ista: Castanon I, Abrami L, Holtzer L, Heisenberg C-PJ, Van Der Goot F, González
    Gaitán M. 2013. Anthrax toxin receptor 2a controls mitotic spindle positioning.
    Nature Cell Biology. 15(1), 28–39.
  mla: Castanon, Irinka, et al. “Anthrax Toxin Receptor 2a Controls Mitotic Spindle
    Positioning.” <i>Nature Cell Biology</i>, vol. 15, no. 1, Nature Publishing Group,
    2013, pp. 28–39, doi:<a href="https://doi.org/10.1038/ncb2632">10.1038/ncb2632</a>.
  short: I. Castanon, L. Abrami, L. Holtzer, C.-P.J. Heisenberg, F. Van Der Goot,
    M. González Gaitán, Nature Cell Biology 15 (2013) 28–39.
date_created: 2018-12-11T12:00:20Z
date_published: 2013-01-01T00:00:00Z
date_updated: 2021-01-12T07:00:41Z
day: '01'
department:
- _id: CaHe
doi: 10.1038/ncb2632
intvolume: '        15'
issue: '1'
language:
- iso: eng
month: '01'
oa_version: None
page: 28 - 39
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '3819'
quality_controlled: '1'
scopus_import: 1
status: public
title: Anthrax toxin receptor 2a controls mitotic spindle positioning
type: journal_article
user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87
volume: 15
year: '2013'
...
---
_id: '2920'
abstract:
- lang: eng
  text: Cell polarisation in development is a common and fundamental process underlying
    embryo patterning and morphogenesis, and has been extensively studied over the
    past years. Our current knowledge of cell polarisation in development is predominantly
    based on studies that have analysed polarisation of single cells, such as eggs,
    or cellular aggregates with a stable polarising interface, such as cultured epithelial
    cells (St Johnston and Ahringer, 2010). However, in embryonic development, particularly
    of vertebrates, cell polarisation processes often encompass large numbers of cells
    that are placed within moving and proliferating tissues, and undergo mesenchymal-to-epithelial
    transitions with a highly complex spatiotemporal choreography. How such intricate
    cell polarisation processes in embryonic development are achieved has only started
    to be analysed. By using live imaging of neurulation in the transparent zebrafish
    embryo, Buckley et al (2012) now describe a novel polarisation strategy by which
    cells assemble an apical domain in the part of their cell body that intersects
    with the midline of the forming neural rod. This mechanism, along with the previously
    described mirror-symmetric divisions (Tawk et al, 2007), is thought to trigger
    formation of both neural rod midline and lumen.
author:
- first_name: Julien
  full_name: Compagnon, Julien
  id: 2E3E0988-F248-11E8-B48F-1D18A9856A87
  last_name: Compagnon
- 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, Heisenberg C-PJ. Neurulation coordinating cell polarisation and
    lumen formation. <i>EMBO Journal</i>. 2013;32(1):1-3. doi:<a href="https://doi.org/10.1038/emboj.2012.325">10.1038/emboj.2012.325</a>
  apa: Compagnon, J., &#38; Heisenberg, C.-P. J. (2013). Neurulation coordinating
    cell polarisation and lumen formation. <i>EMBO Journal</i>. Wiley-Blackwell. <a
    href="https://doi.org/10.1038/emboj.2012.325">https://doi.org/10.1038/emboj.2012.325</a>
  chicago: Compagnon, Julien, and Carl-Philipp J Heisenberg. “Neurulation Coordinating
    Cell Polarisation and Lumen Formation.” <i>EMBO Journal</i>. Wiley-Blackwell,
    2013. <a href="https://doi.org/10.1038/emboj.2012.325">https://doi.org/10.1038/emboj.2012.325</a>.
  ieee: J. Compagnon and C.-P. J. Heisenberg, “Neurulation coordinating cell polarisation
    and lumen formation,” <i>EMBO Journal</i>, vol. 32, no. 1. Wiley-Blackwell, pp.
    1–3, 2013.
  ista: Compagnon J, Heisenberg C-PJ. 2013. Neurulation coordinating cell polarisation
    and lumen formation. EMBO Journal. 32(1), 1–3.
  mla: Compagnon, Julien, and Carl-Philipp J. Heisenberg. “Neurulation Coordinating
    Cell Polarisation and Lumen Formation.” <i>EMBO Journal</i>, vol. 32, no. 1, Wiley-Blackwell,
    2013, pp. 1–3, doi:<a href="https://doi.org/10.1038/emboj.2012.325">10.1038/emboj.2012.325</a>.
  short: J. Compagnon, C.-P.J. Heisenberg, EMBO Journal 32 (2013) 1–3.
date_created: 2018-12-11T12:00:20Z
date_published: 2013-01-09T00:00:00Z
date_updated: 2021-01-12T07:00:42Z
day: '09'
department:
- _id: CaHe
doi: 10.1038/emboj.2012.325
external_id:
  pmid:
  - '23211745'
intvolume: '        32'
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3545307/
month: '01'
oa: 1
oa_version: Submitted Version
page: 1 - 3
pmid: 1
publication: EMBO Journal
publication_status: published
publisher: Wiley-Blackwell
publist_id: '3817'
quality_controlled: '1'
scopus_import: 1
status: public
title: Neurulation coordinating cell polarisation and lumen formation
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 32
year: '2013'
...
