---
_id: '7789'
abstract:
- lang: eng
  text: During embryonic and postnatal development, organs and tissues grow steadily
    to achieve their final size at the end of puberty. However, little is known about
    the cellular dynamics that mediate postnatal growth. By combining in vivo clonal
    lineage tracing, proliferation kinetics, single-cell transcriptomics, andin vitro
    micro-pattern experiments, we resolved the cellular dynamics taking place during
    postnatal skin epidermis expansion. Our data revealed that harmonious growth is
    engineered by a single population of developmental progenitors presenting a fixed
    fate imbalance of self-renewing divisions with an ever-decreasing proliferation
    rate. Single-cell RNA sequencing revealed that epidermal developmental progenitors
    form a more uniform population compared with adult stem and progenitor cells.
    Finally, we found that the spatial pattern of cell division orientation is dictated
    locally by the underlying collagen fiber orientation. Our results uncover a simple
    design principle of organ growth where progenitors and differentiated cells expand
    in harmony with their surrounding tissues.
article_processing_charge: No
article_type: original
author:
- first_name: Sophie
  full_name: Dekoninck, Sophie
  last_name: Dekoninck
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Alejandro
  full_name: Sifrim, Alejandro
  last_name: Sifrim
- first_name: Yekaterina A.
  full_name: Miroshnikova, Yekaterina A.
  last_name: Miroshnikova
- first_name: Mariaceleste
  full_name: Aragona, Mariaceleste
  last_name: Aragona
- first_name: Milan
  full_name: Malfait, Milan
  last_name: Malfait
- first_name: Souhir
  full_name: Gargouri, Souhir
  last_name: Gargouri
- first_name: Charlotte
  full_name: De Neunheuser, Charlotte
  last_name: De Neunheuser
- first_name: Christine
  full_name: Dubois, Christine
  last_name: Dubois
- first_name: Thierry
  full_name: Voet, Thierry
  last_name: Voet
- first_name: Sara A.
  full_name: Wickström, Sara A.
  last_name: Wickström
- first_name: Benjamin D.
  full_name: Simons, Benjamin D.
  last_name: Simons
- first_name: Cédric
  full_name: Blanpain, Cédric
  last_name: Blanpain
citation:
  ama: Dekoninck S, Hannezo EB, Sifrim A, et al. Defining the design principles of
    skin epidermis postnatal growth. <i>Cell</i>. 2020;181(3):604-620.e22. doi:<a
    href="https://doi.org/10.1016/j.cell.2020.03.015">10.1016/j.cell.2020.03.015</a>
  apa: Dekoninck, S., Hannezo, E. B., Sifrim, A., Miroshnikova, Y. A., Aragona, M.,
    Malfait, M., … Blanpain, C. (2020). Defining the design principles of skin epidermis
    postnatal growth. <i>Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.cell.2020.03.015">https://doi.org/10.1016/j.cell.2020.03.015</a>
  chicago: Dekoninck, Sophie, Edouard B Hannezo, Alejandro Sifrim, Yekaterina A. Miroshnikova,
    Mariaceleste Aragona, Milan Malfait, Souhir Gargouri, et al. “Defining the Design
    Principles of Skin Epidermis Postnatal Growth.” <i>Cell</i>. Elsevier, 2020. <a
    href="https://doi.org/10.1016/j.cell.2020.03.015">https://doi.org/10.1016/j.cell.2020.03.015</a>.
  ieee: S. Dekoninck <i>et al.</i>, “Defining the design principles of skin epidermis
    postnatal growth,” <i>Cell</i>, vol. 181, no. 3. Elsevier, p. 604–620.e22, 2020.
  ista: Dekoninck S, Hannezo EB, Sifrim A, Miroshnikova YA, Aragona M, Malfait M,
    Gargouri S, De Neunheuser C, Dubois C, Voet T, Wickström SA, Simons BD, Blanpain
    C. 2020. Defining the design principles of skin epidermis postnatal growth. Cell.
    181(3), 604–620.e22.
  mla: Dekoninck, Sophie, et al. “Defining the Design Principles of Skin Epidermis
    Postnatal Growth.” <i>Cell</i>, vol. 181, no. 3, Elsevier, 2020, p. 604–620.e22,
    doi:<a href="https://doi.org/10.1016/j.cell.2020.03.015">10.1016/j.cell.2020.03.015</a>.
  short: S. Dekoninck, E.B. Hannezo, A. Sifrim, Y.A. Miroshnikova, M. Aragona, M.
    Malfait, S. Gargouri, C. De Neunheuser, C. Dubois, T. Voet, S.A. Wickström, B.D.
    Simons, C. Blanpain, Cell 181 (2020) 604–620.e22.
date_created: 2020-05-03T22:00:48Z
date_published: 2020-04-30T00:00:00Z
date_updated: 2023-08-21T06:17:43Z
day: '30'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1016/j.cell.2020.03.015
external_id:
  isi:
  - '000530708400016'
  pmid:
  - '32259486'
file:
- access_level: open_access
  checksum: e2114902f4e9d75a752e9efb5ae06011
  content_type: application/pdf
  creator: dernst
  date_created: 2020-05-04T10:20:55Z
  date_updated: 2020-07-14T12:48:03Z
  file_id: '7795'
  file_name: 2020_Cell_Dekoninck.pdf
  file_size: 17992888
  relation: main_file
file_date_updated: 2020-07-14T12:48:03Z
has_accepted_license: '1'
intvolume: '       181'
isi: 1
issue: '3'
language:
- iso: eng
month: '04'
oa: 1
oa_version: Published Version
page: 604-620.e22
pmid: 1
publication: Cell
publication_identifier:
  eissn:
  - '10974172'
  issn:
  - '00928674'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Defining the design principles of skin epidermis postnatal growth
tmp:
  image: /images/cc_by_nc_nd.png
  legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode
  name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International
    (CC BY-NC-ND 4.0)
  short: CC BY-NC-ND (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 181
year: '2020'
...
---
_id: '8220'
abstract:
- lang: eng
  text: Understanding to what extent stem cell potential is a cell-intrinsic property
    or an emergent behavior coming from global tissue dynamics and geometry is a key
    outstanding question of systems and stem cell biology. Here, we propose a theory
    of stem cell dynamics as a stochastic competition for access to a spatially localized
    niche, giving rise to a stochastic conveyor-belt model. Cell divisions produce
    a steady cellular stream which advects cells away from the niche, while random
    rearrangements enable cells away from the niche to be favorably repositioned.
    Importantly, even when assuming that all cells in a tissue are molecularly equivalent,
    we predict a common (“universal”) functional dependence of the long-term clonal
    survival probability on distance from the niche, as well as the emergence of a
    well-defined number of functional stem cells, dependent only on the rate of random
    movements vs. mitosis-driven advection. We test the predictions of this theory
    on datasets of pubertal mammary gland tips and embryonic kidney tips, as well
    as homeostatic intestinal crypts. Importantly, we find good agreement for the
    predicted functional dependency of the competition as a function of position,
    and thus functional stem cell number in each organ. This argues for a key role
    of positional fluctuations in dictating stem cell number and dynamics, and we
    discuss the applicability of this theory to other settings.
acknowledgement: "We thank all members of the E.H., B.D.S., and J.v.R. groups for
  stimulating discussions. This project was supported by\r\nthe European Research
  Council (648804 to J.v.R. and 851288 to E.H.). It has also received support from
  the CancerGenomics.nl (Netherlands Organization for Scientific Research) program
  (J.v.R.) and the Doctor Josef Steiner Foundation (J.v.R). B.D.S. was supported by
  Royal Society E. P. Abraham Research Professorship RP/R1/180165 and Wellcome Trust
  Grant 098357/Z/12/Z."
article_processing_charge: No
article_type: original
author:
- first_name: Bernat
  full_name: Corominas-Murtra, Bernat
  id: 43BE2298-F248-11E8-B48F-1D18A9856A87
  last_name: Corominas-Murtra
  orcid: 0000-0001-9806-5643
- first_name: Colinda L.G.J.
  full_name: Scheele, Colinda L.G.J.
  last_name: Scheele
- first_name: Kasumi
  full_name: Kishi, Kasumi
  id: 3065DFC4-F248-11E8-B48F-1D18A9856A87
  last_name: Kishi
- first_name: Saskia I.J.
  full_name: Ellenbroek, Saskia I.J.
  last_name: Ellenbroek
- first_name: Benjamin D.
  full_name: Simons, Benjamin D.
  last_name: Simons
- first_name: Jacco
  full_name: Van Rheenen, Jacco
  last_name: Van Rheenen
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
citation:
  ama: Corominas-Murtra B, Scheele CLGJ, Kishi K, et al. Stem cell lineage survival
    as a noisy competition for niche access. <i>Proceedings of the National Academy
    of Sciences of the United States of America</i>. 2020;117(29):16969-16975. doi:<a
    href="https://doi.org/10.1073/pnas.1921205117">10.1073/pnas.1921205117</a>
  apa: Corominas-Murtra, B., Scheele, C. L. G. J., Kishi, K., Ellenbroek, S. I. J.,
    Simons, B. D., Van Rheenen, J., &#38; Hannezo, E. B. (2020). Stem cell lineage
    survival as a noisy competition for niche access. <i>Proceedings of the National
    Academy of Sciences of the United States of America</i>. National Academy of Sciences.
    <a href="https://doi.org/10.1073/pnas.1921205117">https://doi.org/10.1073/pnas.1921205117</a>
  chicago: Corominas-Murtra, Bernat, Colinda L.G.J. Scheele, Kasumi Kishi, Saskia
    I.J. Ellenbroek, Benjamin D. Simons, Jacco Van Rheenen, and Edouard B Hannezo.
    “Stem Cell Lineage Survival as a Noisy Competition for Niche Access.” <i>Proceedings
    of the National Academy of Sciences of the United States of America</i>. National
    Academy of Sciences, 2020. <a href="https://doi.org/10.1073/pnas.1921205117">https://doi.org/10.1073/pnas.1921205117</a>.
  ieee: B. Corominas-Murtra <i>et al.</i>, “Stem cell lineage survival as a noisy
    competition for niche access,” <i>Proceedings of the National Academy of Sciences
    of the United States of America</i>, vol. 117, no. 29. National Academy of Sciences,
    pp. 16969–16975, 2020.
  ista: Corominas-Murtra B, Scheele CLGJ, Kishi K, Ellenbroek SIJ, Simons BD, Van
    Rheenen J, Hannezo EB. 2020. Stem cell lineage survival as a noisy competition
    for niche access. Proceedings of the National Academy of Sciences of the United
    States of America. 117(29), 16969–16975.
  mla: Corominas-Murtra, Bernat, et al. “Stem Cell Lineage Survival as a Noisy Competition
    for Niche Access.” <i>Proceedings of the National Academy of Sciences of the United
    States of America</i>, vol. 117, no. 29, National Academy of Sciences, 2020, pp.
    16969–75, doi:<a href="https://doi.org/10.1073/pnas.1921205117">10.1073/pnas.1921205117</a>.
  short: B. Corominas-Murtra, C.L.G.J. Scheele, K. Kishi, S.I.J. Ellenbroek, B.D.
    Simons, J. Van Rheenen, E.B. Hannezo, Proceedings of the National Academy of Sciences
    of the United States of America 117 (2020) 16969–16975.
date_created: 2020-08-09T22:00:52Z
date_published: 2020-07-21T00:00:00Z
date_updated: 2023-08-22T08:29:30Z
day: '21'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1073/pnas.1921205117
ec_funded: 1
external_id:
  isi:
  - '000553292900014'
  pmid:
  - '32611816'
file:
- access_level: open_access
  content_type: application/pdf
  creator: dernst
  date_created: 2020-08-10T06:50:28Z
  date_updated: 2020-08-10T06:50:28Z
  file_id: '8223'
  file_name: 2020_PNAS_Corominas.pdf
  file_size: 1111604
  relation: main_file
  success: 1
file_date_updated: 2020-08-10T06:50:28Z
has_accepted_license: '1'
intvolume: '       117'
isi: 1
issue: '29'
language:
- iso: eng
month: '07'
oa: 1
oa_version: Published Version
page: 16969-16975
pmid: 1
project:
- _id: 05943252-7A3F-11EA-A408-12923DDC885E
  call_identifier: H2020
  grant_number: '851288'
  name: Design Principles of Branching Morphogenesis
publication: Proceedings of the National Academy of Sciences of the United States
  of America
publication_identifier:
  eissn:
  - '10916490'
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
  link:
  - relation: press_release
    url: https://ist.ac.at/en/news/order-from-noise/
scopus_import: '1'
status: public
title: Stem cell lineage survival as a noisy competition for niche access
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 117
year: '2020'
...
---
_id: '8669'
abstract:
- lang: eng
  text: Pancreatic islets play an essential role in regulating blood glucose level.
    Although the molecular pathways underlying islet cell differentiation are beginning
    to be resolved, the cellular basis of islet morphogenesis and fate allocation
    remain unclear. By combining unbiased and targeted lineage tracing, we address
    the events leading to islet formation in the mouse. From the statistical analysis
    of clones induced at multiple embryonic timepoints, here we show that, during
    the secondary transition, islet formation involves the aggregation of multiple
    equipotent endocrine progenitors that transition from a phase of stochastic amplification
    by cell division into a phase of sublineage restriction and limited islet fission.
    Together, these results explain quantitatively the heterogeneous size distribution
    and degree of polyclonality of maturing islets, as well as dispersion of progenitors
    within and between islets. Further, our results show that, during the secondary
    transition, α- and β-cells are generated in a contemporary manner. Together, these
    findings provide insight into the cellular basis of islet development.
article_number: '5037'
article_processing_charge: No
article_type: original
author:
- first_name: Magdalena K.
  full_name: Sznurkowska, Magdalena K.
  last_name: Sznurkowska
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Roberta
  full_name: Azzarelli, Roberta
  last_name: Azzarelli
- first_name: Lemonia
  full_name: Chatzeli, Lemonia
  last_name: Chatzeli
- first_name: Tatsuro
  full_name: Ikeda, Tatsuro
  last_name: Ikeda
- first_name: Shosei
  full_name: Yoshida, Shosei
  last_name: Yoshida
- first_name: Anna
  full_name: Philpott, Anna
  last_name: Philpott
- first_name: Benjamin D
  full_name: Simons, Benjamin D
  last_name: Simons
citation:
  ama: Sznurkowska MK, Hannezo EB, Azzarelli R, et al. Tracing the cellular basis
    of islet specification in mouse pancreas. <i>Nature Communications</i>. 2020;11.
    doi:<a href="https://doi.org/10.1038/s41467-020-18837-3">10.1038/s41467-020-18837-3</a>
  apa: Sznurkowska, M. K., Hannezo, E. B., Azzarelli, R., Chatzeli, L., Ikeda, T.,
    Yoshida, S., … Simons, B. D. (2020). Tracing the cellular basis of islet specification
    in mouse pancreas. <i>Nature Communications</i>. Springer Nature. <a href="https://doi.org/10.1038/s41467-020-18837-3">https://doi.org/10.1038/s41467-020-18837-3</a>
  chicago: Sznurkowska, Magdalena K., Edouard B Hannezo, Roberta Azzarelli, Lemonia
    Chatzeli, Tatsuro Ikeda, Shosei Yoshida, Anna Philpott, and Benjamin D Simons.
    “Tracing the Cellular Basis of Islet Specification in Mouse Pancreas.” <i>Nature
    Communications</i>. Springer Nature, 2020. <a href="https://doi.org/10.1038/s41467-020-18837-3">https://doi.org/10.1038/s41467-020-18837-3</a>.
  ieee: M. K. Sznurkowska <i>et al.</i>, “Tracing the cellular basis of islet specification
    in mouse pancreas,” <i>Nature Communications</i>, vol. 11. Springer Nature, 2020.
  ista: Sznurkowska MK, Hannezo EB, Azzarelli R, Chatzeli L, Ikeda T, Yoshida S, Philpott
    A, Simons BD. 2020. Tracing the cellular basis of islet specification in mouse
    pancreas. Nature Communications. 11, 5037.
  mla: Sznurkowska, Magdalena K., et al. “Tracing the Cellular Basis of Islet Specification
    in Mouse Pancreas.” <i>Nature Communications</i>, vol. 11, 5037, Springer Nature,
    2020, doi:<a href="https://doi.org/10.1038/s41467-020-18837-3">10.1038/s41467-020-18837-3</a>.
  short: M.K. Sznurkowska, E.B. Hannezo, R. Azzarelli, L. Chatzeli, T. Ikeda, S. Yoshida,
    A. Philpott, B.D. Simons, Nature Communications 11 (2020).
date_created: 2020-10-18T22:01:35Z
date_published: 2020-10-07T00:00:00Z
date_updated: 2023-08-22T10:18:17Z
day: '07'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1038/s41467-020-18837-3
external_id:
  isi:
  - '000577244600003'
  pmid:
  - '33028844'
file:
- access_level: open_access
  checksum: 0ecc0eab72d2d50694852579611a6624
  content_type: application/pdf
  creator: dernst
  date_created: 2020-10-19T11:27:46Z
  date_updated: 2020-10-19T11:27:46Z
  file_id: '8677'
  file_name: 2020_NatureComm_Sznurkowska.pdf
  file_size: 5540540
  relation: main_file
  success: 1
file_date_updated: 2020-10-19T11:27:46Z
has_accepted_license: '1'
intvolume: '        11'
isi: 1
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
pmid: 1
publication: Nature Communications
publication_identifier:
  eissn:
  - '20411723'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tracing the cellular basis of islet specification in mouse pancreas
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 11
year: '2020'
...
---
_id: '8672'
abstract:
- lang: eng
  text: Cell fate transitions are key to development and homeostasis. It is thus essential
    to understand the cellular mechanisms controlling fate transitions. Cell division
    has been implicated in fate decisions in many stem cell types, including neuronal
    and epithelial progenitors. In other stem cells, such as embryonic stem (ES) cells,
    the role of division remains unclear. Here, we show that exit from naive pluripotency
    in mouse ES cells generally occurs after a division. We further show that exit
    timing is strongly correlated between sister cells, which remain connected by
    cytoplasmic bridges long after division, and that bridge abscission progressively
    accelerates as cells exit naive pluripotency. Finally, interfering with abscission
    impairs naive pluripotency exit, and artificially inducing abscission accelerates
    it. Altogether, our data indicate that a switch in the division machinery leading
    to faster abscission regulates pluripotency exit. Our study identifies abscission
    as a key cellular process coupling cell division to fate transitions.
acknowledgement: This work was supported by the Medical Research Council UK (MRC Program
  award MC_UU_12018/5 ), the European Research Council (starting grant 311637 -MorphoCorDiv
  and consolidator grant 820188 -NanoMechShape to E.K.P.), and the Leverhulme Trust
  (Leverhulme Prize in Biological Sciences to E.K.P.). K.J.C. acknowledges support
  from the Royal Society (Royal Society Research Fellowship). A.C. acknowledges support
  from EMBO ( ALTF 2015-563 ), the Wellcome Trust ( 201334/Z/16/Z ), and the Fondation
  Bettencourt-Schueller (Prix Jeune Chercheur, 2015).
article_processing_charge: No
article_type: original
author:
- first_name: Agathe
  full_name: Chaigne, Agathe
  last_name: Chaigne
- first_name: Céline
  full_name: Labouesse, Céline
  last_name: Labouesse
- first_name: Ian J.
  full_name: White, Ian J.
  last_name: White
- first_name: Meghan
  full_name: Agnew, Meghan
  last_name: Agnew
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Kevin J.
  full_name: Chalut, Kevin J.
  last_name: Chalut
- first_name: Ewa K.
  full_name: Paluch, Ewa K.
  last_name: Paluch
citation:
  ama: Chaigne A, Labouesse C, White IJ, et al. Abscission couples cell division to
    embryonic stem cell fate. <i>Developmental Cell</i>. 2020;55(2):195-208. doi:<a
    href="https://doi.org/10.1016/j.devcel.2020.09.001">10.1016/j.devcel.2020.09.001</a>
  apa: Chaigne, A., Labouesse, C., White, I. J., Agnew, M., Hannezo, E. B., Chalut,
    K. J., &#38; Paluch, E. K. (2020). Abscission couples cell division to embryonic
    stem cell fate. <i>Developmental Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.devcel.2020.09.001">https://doi.org/10.1016/j.devcel.2020.09.001</a>
  chicago: Chaigne, Agathe, Céline Labouesse, Ian J. White, Meghan Agnew, Edouard
    B Hannezo, Kevin J. Chalut, and Ewa K. Paluch. “Abscission Couples Cell Division
    to Embryonic Stem Cell Fate.” <i>Developmental Cell</i>. Elsevier, 2020. <a href="https://doi.org/10.1016/j.devcel.2020.09.001">https://doi.org/10.1016/j.devcel.2020.09.001</a>.
  ieee: A. Chaigne <i>et al.</i>, “Abscission couples cell division to embryonic stem
    cell fate,” <i>Developmental Cell</i>, vol. 55, no. 2. Elsevier, pp. 195–208,
    2020.
  ista: Chaigne A, Labouesse C, White IJ, Agnew M, Hannezo EB, Chalut KJ, Paluch EK.
    2020. Abscission couples cell division to embryonic stem cell fate. Developmental
    Cell. 55(2), 195–208.
  mla: Chaigne, Agathe, et al. “Abscission Couples Cell Division to Embryonic Stem
    Cell Fate.” <i>Developmental Cell</i>, vol. 55, no. 2, Elsevier, 2020, pp. 195–208,
    doi:<a href="https://doi.org/10.1016/j.devcel.2020.09.001">10.1016/j.devcel.2020.09.001</a>.
  short: A. Chaigne, C. Labouesse, I.J. White, M. Agnew, E.B. Hannezo, K.J. Chalut,
    E.K. Paluch, Developmental Cell 55 (2020) 195–208.
date_created: 2020-10-18T22:01:37Z
date_published: 2020-10-26T00:00:00Z
date_updated: 2023-08-22T10:16:58Z
day: '26'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1016/j.devcel.2020.09.001
external_id:
  isi:
  - '000582501100012'
  pmid:
  - '32979313'
file:
- access_level: open_access
  checksum: 88e1a031a61689165d19a19c2f16d795
  content_type: application/pdf
  creator: dernst
  date_created: 2021-02-04T10:20:02Z
  date_updated: 2021-02-04T10:20:02Z
  file_id: '9086'
  file_name: 2020_DevelopmCell_Chaigne.pdf
  file_size: 6929686
  relation: main_file
  success: 1
file_date_updated: 2021-02-04T10:20:02Z
has_accepted_license: '1'
intvolume: '        55'
isi: 1
issue: '2'
language:
- iso: eng
month: '10'
oa: 1
oa_version: Published Version
page: 195-208
pmid: 1
publication: Developmental Cell
publication_identifier:
  eissn:
  - '18781551'
  issn:
  - '15345807'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Abscission couples cell division to embryonic stem cell fate
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 55
year: '2020'
...
---
_id: '7166'
abstract:
- lang: eng
  text: In the living cell, we encounter a large variety of motile processes such
    as organelle transport and cytoskeleton remodeling. These processes are driven
    by motor proteins that generate force by transducing chemical free energy into
    mechanical work. In many cases, the molecular motors work in teams to collectively
    generate larger forces. Recent optical trapping experiments on small teams of
    cytoskeletal motors indicated that the collectively generated force increases
    with the size of the motor team but that this increase depends on the motor type
    and on whether the motors are studied in vitro or in vivo. Here, we use the theory
    of stochastic processes to describe the motion of N motors in a stationary optical
    trap and to compute the N-dependence of the collectively generated forces. We
    consider six distinct motor types, two kinesins, two dyneins, and two myosins.
    We show that the force increases always linearly with N but with a prefactor that
    depends on the performance of the single motor. Surprisingly, this prefactor increases
    for weaker motors with a lower stall force. This counter-intuitive behavior reflects
    the increased probability with which stronger motors detach from the filament
    during strain generation. Our theoretical results are in quantitative agreement
    with experimental data on small teams of kinesin-1 motors.
article_processing_charge: No
article_type: letter_note
author:
- first_name: Mehmet C
  full_name: Ucar, Mehmet C
  id: 50B2A802-6007-11E9-A42B-EB23E6697425
  last_name: Ucar
  orcid: 0000-0003-0506-4217
- first_name: Reinhard
  full_name: Lipowsky, Reinhard
  last_name: Lipowsky
citation:
  ama: Ucar MC, Lipowsky R. Collective force generation by molecular motors is determined
    by strain-induced unbinding. <i>Nano Letters</i>. 2020;20(1):669-676. doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445">10.1021/acs.nanolett.9b04445</a>
  apa: Ucar, M. C., &#38; Lipowsky, R. (2020). Collective force generation by molecular
    motors is determined by strain-induced unbinding. <i>Nano Letters</i>. American
    Chemical Society. <a href="https://doi.org/10.1021/acs.nanolett.9b04445">https://doi.org/10.1021/acs.nanolett.9b04445</a>
  chicago: Ucar, Mehmet C, and Reinhard Lipowsky. “Collective Force Generation by
    Molecular Motors Is Determined by Strain-Induced Unbinding.” <i>Nano Letters</i>.
    American Chemical Society, 2020. <a href="https://doi.org/10.1021/acs.nanolett.9b04445">https://doi.org/10.1021/acs.nanolett.9b04445</a>.
  ieee: M. C. Ucar and R. Lipowsky, “Collective force generation by molecular motors
    is determined by strain-induced unbinding,” <i>Nano Letters</i>, vol. 20, no.
    1. American Chemical Society, pp. 669–676, 2020.
  ista: Ucar MC, Lipowsky R. 2020. Collective force generation by molecular motors
    is determined by strain-induced unbinding. Nano Letters. 20(1), 669–676.
  mla: Ucar, Mehmet C., and Reinhard Lipowsky. “Collective Force Generation by Molecular
    Motors Is Determined by Strain-Induced Unbinding.” <i>Nano Letters</i>, vol. 20,
    no. 1, American Chemical Society, 2020, pp. 669–76, doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445">10.1021/acs.nanolett.9b04445</a>.
  short: M.C. Ucar, R. Lipowsky, Nano Letters 20 (2020) 669–676.
date_created: 2019-12-10T15:36:05Z
date_published: 2020-01-08T00:00:00Z
date_updated: 2023-08-17T14:07:52Z
day: '08'
department:
- _id: EdHa
doi: 10.1021/acs.nanolett.9b04445
external_id:
  isi:
  - '000507151600087'
  pmid:
  - '31797672'
intvolume: '        20'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1021/acs.nanolett.9b04445
month: '01'
oa: 1
oa_version: Published Version
page: 669-676
pmid: 1
publication: Nano Letters
publication_identifier:
  eissn:
  - 1530-6992
  issn:
  - 1530-6984
publication_status: published
publisher: American Chemical Society
quality_controlled: '1'
related_material:
  record:
  - id: '9726'
    relation: research_data
    status: public
  - id: '9885'
    relation: research_data
    status: public
scopus_import: '1'
status: public
title: Collective force generation by molecular motors is determined by strain-induced
  unbinding
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 20
year: '2020'
...
---
_id: '7431'
abstract:
- lang: eng
  text: 'In many real-world systems, information can be transmitted in two qualitatively
    different ways: by copying or by transformation. Copying occurs when messages
    are transmitted without modification, e.g. when an offspring receives an unaltered
    copy of a gene from its parent. Transformation occurs when messages are modified
    systematically during transmission, e.g. when mutational biases occur during genetic
    replication. Standard information-theoretic measures do not distinguish these
    two modes of information transfer, although they may reflect different mechanisms
    and have different functional consequences. Starting from a few simple axioms,
    we derive a decomposition of mutual information into the information transmitted
    by copying versus the information transmitted by transformation. We begin with
    a decomposition that applies when the source and destination of the channel have
    the same set of messages and a notion of message identity exists. We then generalize
    our decomposition to other kinds of channels, which can involve different source
    and destination sets and broader notions of similarity. In addition, we show that
    copy information can be interpreted as the minimal work needed by a physical copying
    process, which is relevant for understanding the physics of replication. We use
    the proposed decomposition to explore a model of amino acid substitution rates.
    Our results apply to any system in which the fidelity of copying, rather than
    simple predictability, is of critical relevance.'
acknowledgement: "AK was supported by Grant No. FQXi-RFP-1622 from the FQXi foundation,
  and Grant No. CHE-1648973 from the U.S.\r\nNational Science Foundation. AK would
  like to thank the Santa Fe Institute for supporting this research. The authors\r\nthank
  Jordi Fortuny, Rudolf Hanel, Joshua Garland, and Blai Vidiella for helpful discussions,
  as well as the anonymous\r\nreviewers for their insightful suggestions. "
article_number: '0623'
article_processing_charge: No
article_type: original
arxiv: 1
author:
- first_name: Artemy
  full_name: Kolchinsky, Artemy
  last_name: Kolchinsky
- first_name: Bernat
  full_name: Corominas-Murtra, Bernat
  id: 43BE2298-F248-11E8-B48F-1D18A9856A87
  last_name: Corominas-Murtra
  orcid: 0000-0001-9806-5643
citation:
  ama: Kolchinsky A, Corominas-Murtra B. Decomposing information into copying versus
    transformation. <i>Journal of the Royal Society Interface</i>. 2020;17(162). doi:<a
    href="https://doi.org/10.1098/rsif.2019.0623">10.1098/rsif.2019.0623</a>
  apa: Kolchinsky, A., &#38; Corominas-Murtra, B. (2020). Decomposing information
    into copying versus transformation. <i>Journal of the Royal Society Interface</i>.
    The Royal Society. <a href="https://doi.org/10.1098/rsif.2019.0623">https://doi.org/10.1098/rsif.2019.0623</a>
  chicago: Kolchinsky, Artemy, and Bernat Corominas-Murtra. “Decomposing Information
    into Copying versus Transformation.” <i>Journal of the Royal Society Interface</i>.
    The Royal Society, 2020. <a href="https://doi.org/10.1098/rsif.2019.0623">https://doi.org/10.1098/rsif.2019.0623</a>.
  ieee: A. Kolchinsky and B. Corominas-Murtra, “Decomposing information into copying
    versus transformation,” <i>Journal of the Royal Society Interface</i>, vol. 17,
    no. 162. The Royal Society, 2020.
  ista: Kolchinsky A, Corominas-Murtra B. 2020. Decomposing information into copying
    versus transformation. Journal of the Royal Society Interface. 17(162), 0623.
  mla: Kolchinsky, Artemy, and Bernat Corominas-Murtra. “Decomposing Information into
    Copying versus Transformation.” <i>Journal of the Royal Society Interface</i>,
    vol. 17, no. 162, 0623, The Royal Society, 2020, doi:<a href="https://doi.org/10.1098/rsif.2019.0623">10.1098/rsif.2019.0623</a>.
  short: A. Kolchinsky, B. Corominas-Murtra, Journal of the Royal Society Interface
    17 (2020).
date_created: 2020-02-02T23:01:03Z
date_published: 2020-01-29T00:00:00Z
date_updated: 2023-08-17T14:31:28Z
day: '29'
department:
- _id: EdHa
doi: 10.1098/rsif.2019.0623
external_id:
  arxiv:
  - '1903.10693'
  isi:
  - '000538369800002'
  pmid:
  - '31964273'
intvolume: '        17'
isi: 1
issue: '162'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://arxiv.org/abs/1903.10693
month: '01'
oa: 1
oa_version: Preprint
pmid: 1
publication: Journal of the Royal Society Interface
publication_identifier:
  eissn:
  - '17425662'
publication_status: published
publisher: The Royal Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Decomposing information into copying versus transformation
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 17
year: '2020'
...
---
_id: '9885'
abstract:
- lang: eng
  text: Data obtained from the fine-grained simulations used in Figures 2-5, data
    obtained from the coarse-grained numerical calculations used in Figure 6, and
    a sample script for the fine-grained simulation as a Jupyter notebook (ZIP)
article_processing_charge: No
author:
- first_name: Mehmet C
  full_name: Ucar, Mehmet C
  id: 50B2A802-6007-11E9-A42B-EB23E6697425
  last_name: Ucar
  orcid: 0000-0003-0506-4217
- first_name: Reinhard
  full_name: Lipowsky, Reinhard
  last_name: Lipowsky
citation:
  ama: Ucar MC, Lipowsky R. MURL_Dataz. 2020. doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445.s002">10.1021/acs.nanolett.9b04445.s002</a>
  apa: Ucar, M. C., &#38; Lipowsky, R. (2020). MURL_Dataz. American Chemical Society
    . <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s002">https://doi.org/10.1021/acs.nanolett.9b04445.s002</a>
  chicago: Ucar, Mehmet C, and Reinhard Lipowsky. “MURL_Dataz.” American Chemical
    Society , 2020. <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s002">https://doi.org/10.1021/acs.nanolett.9b04445.s002</a>.
  ieee: M. C. Ucar and R. Lipowsky, “MURL_Dataz.” American Chemical Society , 2020.
  ista: Ucar MC, Lipowsky R. 2020. MURL_Dataz, American Chemical Society , <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s002">10.1021/acs.nanolett.9b04445.s002</a>.
  mla: Ucar, Mehmet C., and Reinhard Lipowsky. <i>MURL_Dataz</i>. American Chemical
    Society , 2020, doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445.s002">10.1021/acs.nanolett.9b04445.s002</a>.
  short: M.C. Ucar, R. Lipowsky, (2020).
date_created: 2021-08-11T13:16:03Z
date_published: 2020-01-08T00:00:00Z
date_updated: 2023-08-17T14:07:52Z
day: '08'
department:
- _id: EdHa
doi: 10.1021/acs.nanolett.9b04445.s002
month: '01'
oa_version: Published Version
publisher: 'American Chemical Society '
related_material:
  record:
  - id: '7166'
    relation: used_in_publication
    status: public
status: public
title: MURL_Dataz
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2020'
...
---
_id: '6832'
abstract:
- lang: eng
  text: Steady-state turnover is a hallmark of epithelial tissues throughout adult
    life. Intestinal epithelial turnover is marked by continuous cell migration, which
    is assumed to be driven by mitotic pressure from the crypts. However, the balance
    of forces in renewal remains ill-defined. Combining biophysical modeling and quantitative
    three-dimensional tissue imaging with genetic and physical manipulations, we revealed
    the existence of an actin-related protein 2/3 complex–dependent active migratory
    force, which explains quantitatively the profiles of cell speed, density, and
    tissue tension along the villi. Cells migrate collectively with minimal rearrangements
    while displaying dual—apicobasal and front-back—polarity characterized by actin-rich
    basal protrusions oriented in the direction of migration. We propose that active
    migration is a critical component of gut epithelial turnover.
article_processing_charge: No
author:
- first_name: Denis
  full_name: Krndija, Denis
  last_name: Krndija
- first_name: Fatima El
  full_name: Marjou, Fatima El
  last_name: Marjou
- first_name: Boris
  full_name: Guirao, Boris
  last_name: Guirao
- first_name: Sophie
  full_name: Richon, Sophie
  last_name: Richon
- first_name: Olivier
  full_name: Leroy, Olivier
  last_name: Leroy
- first_name: Yohanns
  full_name: Bellaiche, Yohanns
  last_name: Bellaiche
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Danijela Matic
  full_name: Vignjevic, Danijela Matic
  last_name: Vignjevic
citation:
  ama: Krndija D, Marjou FE, Guirao B, et al. Active cell migration is critical for
    steady-state epithelial turnover in the gut. <i>Science</i>. 2019;365(6454):705-710.
    doi:<a href="https://doi.org/10.1126/science.aau3429">10.1126/science.aau3429</a>
  apa: Krndija, D., Marjou, F. E., Guirao, B., Richon, S., Leroy, O., Bellaiche, Y.,
    … Vignjevic, D. M. (2019). Active cell migration is critical for steady-state
    epithelial turnover in the gut. <i>Science</i>. American Association for the Advancement
    of Science. <a href="https://doi.org/10.1126/science.aau3429">https://doi.org/10.1126/science.aau3429</a>
  chicago: Krndija, Denis, Fatima El Marjou, Boris Guirao, Sophie Richon, Olivier
    Leroy, Yohanns Bellaiche, Edouard B Hannezo, and Danijela Matic Vignjevic. “Active
    Cell Migration Is Critical for Steady-State Epithelial Turnover in the Gut.” <i>Science</i>.
    American Association for the Advancement of Science, 2019. <a href="https://doi.org/10.1126/science.aau3429">https://doi.org/10.1126/science.aau3429</a>.
  ieee: D. Krndija <i>et al.</i>, “Active cell migration is critical for steady-state
    epithelial turnover in the gut,” <i>Science</i>, vol. 365, no. 6454. American
    Association for the Advancement of Science, pp. 705–710, 2019.
  ista: Krndija D, Marjou FE, Guirao B, Richon S, Leroy O, Bellaiche Y, Hannezo EB,
    Vignjevic DM. 2019. Active cell migration is critical for steady-state epithelial
    turnover in the gut. Science. 365(6454), 705–710.
  mla: Krndija, Denis, et al. “Active Cell Migration Is Critical for Steady-State
    Epithelial Turnover in the Gut.” <i>Science</i>, vol. 365, no. 6454, American
    Association for the Advancement of Science, 2019, pp. 705–10, doi:<a href="https://doi.org/10.1126/science.aau3429">10.1126/science.aau3429</a>.
  short: D. Krndija, F.E. Marjou, B. Guirao, S. Richon, O. Leroy, Y. Bellaiche, E.B.
    Hannezo, D.M. Vignjevic, Science 365 (2019) 705–710.
date_created: 2019-08-25T22:00:51Z
date_published: 2019-08-16T00:00:00Z
date_updated: 2023-08-29T07:16:40Z
day: '16'
department:
- _id: EdHa
doi: 10.1126/science.aau3429
external_id:
  isi:
  - '000481688700050'
  pmid:
  - '31416964'
intvolume: '       365'
isi: 1
issue: '6454'
language:
- iso: eng
month: '08'
oa_version: None
page: 705-710
pmid: 1
publication: Science
publication_status: published
publisher: American Association for the Advancement of Science
quality_controlled: '1'
scopus_import: '1'
status: public
title: Active cell migration is critical for steady-state epithelial turnover in the
  gut
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 365
year: '2019'
...
---
_id: '5789'
abstract:
- lang: eng
  text: Tissue morphogenesis is driven by mechanical forces that elicit changes in
    cell size, shape and motion. The extent by which forces deform tissues critically
    depends on the rheological properties of the recipient tissue. Yet, whether and
    how dynamic changes in tissue rheology affect tissue morphogenesis and how they
    are regulated within the developing organism remain unclear. Here, we show that
    blastoderm spreading at the onset of zebrafish morphogenesis relies on a rapid,
    pronounced and spatially patterned tissue fluidization. Blastoderm fluidization
    is temporally controlled by mitotic cell rounding-dependent cell–cell contact
    disassembly during the last rounds of cell cleavages. Moreover, fluidization is
    spatially restricted to the central blastoderm by local activation of non-canonical
    Wnt signalling within the blastoderm margin, increasing cell cohesion and thereby
    counteracting the effect of mitotic rounding on contact disassembly. Overall,
    our results identify a fluidity transition mediated by loss of cell cohesion as
    a critical regulator of embryo morphogenesis.
acknowledged_ssus:
- _id: Bio
article_processing_charge: No
article_type: original
author:
- first_name: Nicoletta
  full_name: Petridou, Nicoletta
  id: 2A003F6C-F248-11E8-B48F-1D18A9856A87
  last_name: Petridou
  orcid: 0000-0002-8451-1195
- first_name: Silvia
  full_name: Grigolon, Silvia
  last_name: Grigolon
- first_name: Guillaume
  full_name: Salbreux, Guillaume
  last_name: Salbreux
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Petridou N, Grigolon S, Salbreux G, Hannezo EB, Heisenberg C-PJ. Fluidization-mediated
    tissue spreading by mitotic cell rounding and non-canonical Wnt signalling. <i>Nature
    Cell Biology</i>. 2019;21:169–178. doi:<a href="https://doi.org/10.1038/s41556-018-0247-4">10.1038/s41556-018-0247-4</a>
  apa: Petridou, N., Grigolon, S., Salbreux, G., Hannezo, E. B., &#38; Heisenberg,
    C.-P. J. (2019). Fluidization-mediated tissue spreading by mitotic cell rounding
    and non-canonical Wnt signalling. <i>Nature Cell Biology</i>. Nature Publishing
    Group. <a href="https://doi.org/10.1038/s41556-018-0247-4">https://doi.org/10.1038/s41556-018-0247-4</a>
  chicago: Petridou, Nicoletta, Silvia Grigolon, Guillaume Salbreux, Edouard B Hannezo,
    and Carl-Philipp J Heisenberg. “Fluidization-Mediated Tissue Spreading by Mitotic
    Cell Rounding and Non-Canonical Wnt Signalling.” <i>Nature Cell Biology</i>. Nature
    Publishing Group, 2019. <a href="https://doi.org/10.1038/s41556-018-0247-4">https://doi.org/10.1038/s41556-018-0247-4</a>.
  ieee: N. Petridou, S. Grigolon, G. Salbreux, E. B. Hannezo, and C.-P. J. Heisenberg,
    “Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical
    Wnt signalling,” <i>Nature Cell Biology</i>, vol. 21. Nature Publishing Group,
    pp. 169–178, 2019.
  ista: Petridou N, Grigolon S, Salbreux G, Hannezo EB, Heisenberg C-PJ. 2019. Fluidization-mediated
    tissue spreading by mitotic cell rounding and non-canonical Wnt signalling. Nature
    Cell Biology. 21, 169–178.
  mla: Petridou, Nicoletta, et al. “Fluidization-Mediated Tissue Spreading by Mitotic
    Cell Rounding and Non-Canonical Wnt Signalling.” <i>Nature Cell Biology</i>, vol.
    21, Nature Publishing Group, 2019, pp. 169–178, doi:<a href="https://doi.org/10.1038/s41556-018-0247-4">10.1038/s41556-018-0247-4</a>.
  short: N. Petridou, S. Grigolon, G. Salbreux, E.B. Hannezo, C.-P.J. Heisenberg,
    Nature Cell Biology 21 (2019) 169–178.
date_created: 2018-12-30T22:59:15Z
date_published: 2019-02-01T00:00:00Z
date_updated: 2023-09-11T14:03:28Z
day: '01'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
doi: 10.1038/s41556-018-0247-4
ec_funded: 1
external_id:
  isi:
  - '000457468300011'
  pmid:
  - '30559456'
file:
- access_level: open_access
  checksum: e38523787b3bc84006f2793de99ad70f
  content_type: application/pdf
  creator: dernst
  date_created: 2020-10-21T07:18:35Z
  date_updated: 2020-10-21T07:18:35Z
  file_id: '8685'
  file_name: 2018_NatureCellBio_Petridou_accepted.pdf
  file_size: 71590590
  relation: main_file
  success: 1
file_date_updated: 2020-10-21T07:18:35Z
has_accepted_license: '1'
intvolume: '        21'
isi: 1
language:
- iso: eng
month: '02'
oa: 1
oa_version: Submitted Version
page: 169–178
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742573'
  name: Interaction and feedback between cell mechanics and fate specification in
    vertebrate gastrulation
- _id: 253E54C8-B435-11E9-9278-68D0E5697425
  grant_number: ALTF710-2016
  name: Molecular mechanism of auxindriven formative divisions delineating lateral
    root organogenesis in plants (EMBO fellowship)
publication: Nature Cell Biology
publication_identifier:
  issn:
  - '14657392'
publication_status: published
publisher: Nature Publishing Group
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/when-a-fish-becomes-fluid/
scopus_import: '1'
status: public
title: Fluidization-mediated tissue spreading by mitotic cell rounding and non-canonical
  Wnt signalling
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 21
year: '2019'
...
---
_id: '5944'
abstract:
- lang: eng
  text: Understanding the thermodynamics of the duplication process is a fundamental
    step towards a comprehensive physical theory of biological systems. However, the
    immense complexity of real cells obscures the fundamental tensions between energy
    gradients and entropic contributions that underlie duplication. The study of synthetic,
    feasible systems reproducing part of the key ingredients of living entities but
    overcoming major sources of biological complexity is of great relevance to deepen
    the comprehension of the fundamental thermodynamic processes underlying life and
    its prevalence. In this paper an abstract—yet realistic—synthetic system made
    of small synthetic protocell aggregates is studied in detail. A fundamental relation
    between free energy and entropic gradients is derived for a general, non-equilibrium
    scenario, setting the thermodynamic conditions for the occurrence and prevalence
    of duplication phenomena. This relation sets explicitly how the energy gradients
    invested in creating and maintaining structural—and eventually, functional—elements
    of the system must always compensate the entropic gradients, whose contributions
    come from changes in the translational, configurational, and macrostate entropies,
    as well as from dissipation due to irreversible transitions. Work/energy relations
    are also derived, defining lower bounds on the energy required for the duplication
    event to take place. A specific example including real ternary emulsions is provided
    in order to grasp the orders of magnitude involved in the problem. It is found
    that the minimal work invested over the system to trigger a duplication event
    is around ~ 10−13J , which results, in the case of duplication of all the vesicles
    contained in a liter of emulsion, in an amount of energy around ~ 1kJ . Without
    aiming to describe a truly biological process of duplication, this theoretical
    contribution seeks to explicitly define and identify the key actors that participate
    in it.
article_number: '9'
article_processing_charge: No
author:
- first_name: Bernat
  full_name: Corominas-Murtra, Bernat
  id: 43BE2298-F248-11E8-B48F-1D18A9856A87
  last_name: Corominas-Murtra
  orcid: 0000-0001-9806-5643
citation:
  ama: Corominas-Murtra B. Thermodynamics of duplication thresholds in synthetic protocell
    systems. <i>Life</i>. 2019;9(1). doi:<a href="https://doi.org/10.3390/life9010009">10.3390/life9010009</a>
  apa: Corominas-Murtra, B. (2019). Thermodynamics of duplication thresholds in synthetic
    protocell systems. <i>Life</i>. MDPI. <a href="https://doi.org/10.3390/life9010009">https://doi.org/10.3390/life9010009</a>
  chicago: Corominas-Murtra, Bernat. “Thermodynamics of Duplication Thresholds in
    Synthetic Protocell Systems.” <i>Life</i>. MDPI, 2019. <a href="https://doi.org/10.3390/life9010009">https://doi.org/10.3390/life9010009</a>.
  ieee: B. Corominas-Murtra, “Thermodynamics of duplication thresholds in synthetic
    protocell systems,” <i>Life</i>, vol. 9, no. 1. MDPI, 2019.
  ista: Corominas-Murtra B. 2019. Thermodynamics of duplication thresholds in synthetic
    protocell systems. Life. 9(1), 9.
  mla: Corominas-Murtra, Bernat. “Thermodynamics of Duplication Thresholds in Synthetic
    Protocell Systems.” <i>Life</i>, vol. 9, no. 1, 9, MDPI, 2019, doi:<a href="https://doi.org/10.3390/life9010009">10.3390/life9010009</a>.
  short: B. Corominas-Murtra, Life 9 (2019).
date_created: 2019-02-10T22:59:15Z
date_published: 2019-01-15T00:00:00Z
date_updated: 2023-08-24T14:43:41Z
day: '15'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.3390/life9010009
external_id:
  isi:
  - '000464125500001'
file:
- access_level: open_access
  checksum: 7d2322cd96ace41959909b66702d5cf4
  content_type: application/pdf
  creator: dernst
  date_created: 2019-02-11T10:45:27Z
  date_updated: 2020-07-14T12:47:13Z
  file_id: '5951'
  file_name: 2019_Life_Corominas.pdf
  file_size: 963454
  relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: '         9'
isi: 1
issue: '1'
language:
- iso: eng
month: '01'
oa: 1
oa_version: Published Version
publication: Life
publication_identifier:
  eissn:
  - '20751729'
publication_status: published
publisher: MDPI
quality_controlled: '1'
scopus_import: '1'
status: public
title: Thermodynamics of duplication thresholds in synthetic protocell systems
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 9
year: '2019'
...
---
_id: '6191'
abstract:
- lang: eng
  text: The formation of self-organized patterns is key to the morphogenesis of multicellular
    organisms, although a comprehensive theory of biological pattern formation is
    still lacking. Here, we propose a minimal model combining tissue mechanics with
    morphogen turnover and transport to explore routes to patterning. Our active description
    couples morphogen reaction and diffusion, which impact cell differentiation and
    tissue mechanics, to a two-phase poroelastic rheology, where one tissue phase
    consists of a poroelastic cell network and the other one of a permeating extracellular
    fluid, which provides a feedback by actively transporting morphogens. While this
    model encompasses previous theories approximating tissues to inert monophasic
    media, such as Turing’s reaction–diffusion model, it overcomes some of their key
    limitations permitting pattern formation via any two-species biochemical kinetics
    due to mechanically induced cross-diffusion flows. Moreover, we describe a qualitatively
    different advection-driven Keller–Segel instability which allows for the formation
    of patterns with a single morphogen and whose fundamental mode pattern robustly
    scales with tissue size. We discuss the potential relevance of these findings
    for tissue morphogenesis.
article_processing_charge: No
author:
- first_name: Pierre
  full_name: Recho, Pierre
  last_name: Recho
- first_name: Adrien
  full_name: Hallou, Adrien
  last_name: Hallou
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
citation:
  ama: Recho P, Hallou A, Hannezo EB. Theory of mechanochemical patterning in biphasic
    biological tissues. <i>Proceedings of the National Academy of Sciences of the
    United States of America</i>. 2019;116(12):5344-5349. doi:<a href="https://doi.org/10.1073/pnas.1813255116">10.1073/pnas.1813255116</a>
  apa: Recho, P., Hallou, A., &#38; Hannezo, E. B. (2019). Theory of mechanochemical
    patterning in biphasic biological tissues. <i>Proceedings of the National Academy
    of Sciences of the United States of America</i>. National Academy of Sciences.
    <a href="https://doi.org/10.1073/pnas.1813255116">https://doi.org/10.1073/pnas.1813255116</a>
  chicago: Recho, Pierre, Adrien Hallou, and Edouard B Hannezo. “Theory of Mechanochemical
    Patterning in Biphasic Biological Tissues.” <i>Proceedings of the National Academy
    of Sciences of the United States of America</i>. National Academy of Sciences,
    2019. <a href="https://doi.org/10.1073/pnas.1813255116">https://doi.org/10.1073/pnas.1813255116</a>.
  ieee: P. Recho, A. Hallou, and E. B. Hannezo, “Theory of mechanochemical patterning
    in biphasic biological tissues,” <i>Proceedings of the National Academy of Sciences
    of the United States of America</i>, vol. 116, no. 12. National Academy of Sciences,
    pp. 5344–5349, 2019.
  ista: Recho P, Hallou A, Hannezo EB. 2019. Theory of mechanochemical patterning
    in biphasic biological tissues. Proceedings of the National Academy of Sciences
    of the United States of America. 116(12), 5344–5349.
  mla: Recho, Pierre, et al. “Theory of Mechanochemical Patterning in Biphasic Biological
    Tissues.” <i>Proceedings of the National Academy of Sciences of the United States
    of America</i>, vol. 116, no. 12, National Academy of Sciences, 2019, pp. 5344–49,
    doi:<a href="https://doi.org/10.1073/pnas.1813255116">10.1073/pnas.1813255116</a>.
  short: P. Recho, A. Hallou, E.B. Hannezo, Proceedings of the National Academy of
    Sciences of the United States of America 116 (2019) 5344–5349.
date_created: 2019-03-31T21:59:13Z
date_published: 2019-03-19T00:00:00Z
date_updated: 2023-08-25T08:57:30Z
day: '19'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1073/pnas.1813255116
external_id:
  isi:
  - '000461679000027'
  pmid:
  - '30819884'
file:
- access_level: open_access
  checksum: 8b67eee0ea8e5db61583e4d485215258
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-03T14:10:30Z
  date_updated: 2020-07-14T12:47:23Z
  file_id: '6193'
  file_name: 2019_PNAS_Recho.pdf
  file_size: 3456045
  relation: main_file
file_date_updated: 2020-07-14T12:47:23Z
has_accepted_license: '1'
intvolume: '       116'
isi: 1
issue: '12'
language:
- iso: eng
month: '03'
oa: 1
oa_version: Published Version
page: 5344-5349
pmid: 1
project:
- _id: 268294B6-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P31639
  name: Active mechano-chemical description of the cell cytoskeleton
publication: Proceedings of the National Academy of Sciences of the United States
  of America
publication_identifier:
  eissn:
  - '10916490'
  issn:
  - '00278424'
publication_status: published
publisher: National Academy of Sciences
quality_controlled: '1'
related_material:
  link:
  - relation: supplementary_material
    url: www.pnas.org/lookup/suppl/doi:10.1073/pnas.1813255116/-/DCSupplemental
scopus_import: '1'
status: public
title: Theory of mechanochemical patterning in biphasic biological tissues
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 116
year: '2019'
...
---
_id: '6508'
abstract:
- lang: eng
  text: Segregation of maternal determinants within the oocyte constitutes the first
    step in embryo patterning. In zebrafish oocytes, extensive ooplasmic streaming
    leads to the segregation of ooplasm from yolk granules along the animal-vegetal
    axis of the oocyte. Here, we show that this process does not rely on cortical
    actin reorganization, as previously thought, but instead on a cell-cycle-dependent
    bulk actin polymerization wave traveling from the animal to the vegetal pole of
    the oocyte. This wave functions in segregation by both pulling ooplasm animally
    and pushing yolk granules vegetally. Using biophysical experimentation and theory,
    we show that ooplasm pulling is mediated by bulk actin network flows exerting
    friction forces on the ooplasm, while yolk granule pushing is achieved by a mechanism
    closely resembling actin comet formation on yolk granules. Our study defines a
    novel role of cell-cycle-controlled bulk actin polymerization waves in oocyte
    polarization via ooplasmic segregation.
acknowledged_ssus:
- _id: Bio
- _id: PreCl
acknowledgement: We would like to thank Pierre Recho, Guillaume Salbreux, and Silvia
  Grigolon for advice on the theory, Lila Solnica-Krezel for kindly providing us with
  zebrafish dachsous mutants, members of the Heisenberg and Hannezo groups for fruitful
  discussions, and the Bioimaging and zebrafish facilities at IST Austria for their
  continuous support. This project has received funding from the European Union (European
  Research Council Advanced Grant 742573 to C.P.H.) and from the Austrian Science
  Fund (FWF) (P 31639 to E.H.).
article_processing_charge: No
article_type: original
author:
- first_name: Shayan
  full_name: Shamipour, Shayan
  id: 40B34FE2-F248-11E8-B48F-1D18A9856A87
  last_name: Shamipour
- first_name: Roland
  full_name: Kardos, Roland
  id: 4039350E-F248-11E8-B48F-1D18A9856A87
  last_name: Kardos
- first_name: Shi-lei
  full_name: Xue, Shi-lei
  id: 31D2C804-F248-11E8-B48F-1D18A9856A87
  last_name: Xue
- first_name: Björn
  full_name: Hof, Björn
  id: 3A374330-F248-11E8-B48F-1D18A9856A87
  last_name: Hof
  orcid: 0000-0003-2057-2754
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. Bulk actin
    dynamics drive phase segregation in zebrafish oocytes. <i>Cell</i>. 2019;177(6):1463-1479.e18.
    doi:<a href="https://doi.org/10.1016/j.cell.2019.04.030">10.1016/j.cell.2019.04.030</a>
  apa: Shamipour, S., Kardos, R., Xue, S., Hof, B., Hannezo, E. B., &#38; Heisenberg,
    C.-P. J. (2019). Bulk actin dynamics drive phase segregation in zebrafish oocytes.
    <i>Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.cell.2019.04.030">https://doi.org/10.1016/j.cell.2019.04.030</a>
  chicago: Shamipour, Shayan, Roland Kardos, Shi-lei Xue, Björn Hof, Edouard B Hannezo,
    and Carl-Philipp J Heisenberg. “Bulk Actin Dynamics Drive Phase Segregation in
    Zebrafish Oocytes.” <i>Cell</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.cell.2019.04.030">https://doi.org/10.1016/j.cell.2019.04.030</a>.
  ieee: S. Shamipour, R. Kardos, S. Xue, B. Hof, E. B. Hannezo, and C.-P. J. Heisenberg,
    “Bulk actin dynamics drive phase segregation in zebrafish oocytes,” <i>Cell</i>,
    vol. 177, no. 6. Elsevier, p. 1463–1479.e18, 2019.
  ista: Shamipour S, Kardos R, Xue S, Hof B, Hannezo EB, Heisenberg C-PJ. 2019. Bulk
    actin dynamics drive phase segregation in zebrafish oocytes. Cell. 177(6), 1463–1479.e18.
  mla: Shamipour, Shayan, et al. “Bulk Actin Dynamics Drive Phase Segregation in Zebrafish
    Oocytes.” <i>Cell</i>, vol. 177, no. 6, Elsevier, 2019, p. 1463–1479.e18, doi:<a
    href="https://doi.org/10.1016/j.cell.2019.04.030">10.1016/j.cell.2019.04.030</a>.
  short: S. Shamipour, R. Kardos, S. Xue, B. Hof, E.B. Hannezo, C.-P.J. Heisenberg,
    Cell 177 (2019) 1463–1479.e18.
date_created: 2019-06-02T21:59:12Z
date_published: 2019-05-30T00:00:00Z
date_updated: 2024-03-25T23:30:21Z
day: '30'
ddc:
- '570'
department:
- _id: CaHe
- _id: EdHa
- _id: BjHo
doi: 10.1016/j.cell.2019.04.030
ec_funded: 1
external_id:
  isi:
  - '000469415100013'
  pmid:
  - '31080065'
file:
- access_level: open_access
  checksum: aea43726d80e35ce3885073a5f05c3e3
  content_type: application/pdf
  creator: dernst
  date_created: 2020-10-21T07:22:34Z
  date_updated: 2020-10-21T07:22:34Z
  file_id: '8686'
  file_name: 2019_Cell_Shamipour_accepted.pdf
  file_size: 3356292
  relation: main_file
  success: 1
file_date_updated: 2020-10-21T07:22:34Z
has_accepted_license: '1'
intvolume: '       177'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.cell.2019.04.030
month: '05'
oa: 1
oa_version: Published Version
page: 1463-1479.e18
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742573'
  name: Interaction and feedback between cell mechanics and fate specification in
    vertebrate gastrulation
- _id: 268294B6-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P31639
  name: Active mechano-chemical description of the cell cytoskeleton
publication: Cell
publication_identifier:
  eissn:
  - '10974172'
  issn:
  - '00928674'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/how-the-cytoplasm-separates-from-the-yolk/
  record:
  - id: '8350'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Bulk actin dynamics drive phase segregation in zebrafish oocytes
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 177
year: '2019'
...
---
_id: '6513'
abstract:
- lang: eng
  text: Adult intestinal stem cells are located at the bottom of crypts of Lieberkühn,
    where they express markers such as LGR5 1,2 and fuel the constant replenishment
    of the intestinal epithelium1. Although fetal LGR5-expressing cells can give rise
    to adult intestinal stem cells3,4, it remains unclear whether this population
    in the patterned epithelium represents unique intestinal stem-cell precursors.
    Here we show, using unbiased quantitative lineage-tracing approaches, biophysical
    modelling and intestinal transplantation, that all cells of the mouse intestinal
    epithelium—irrespective of their location and pattern of LGR5 expression in the
    fetal gut tube—contribute actively to the adult intestinal stem cell pool. Using
    3D imaging, we find that during fetal development the villus undergoes gross remodelling
    and fission. This brings epithelial cells from the non-proliferative villus into
    the proliferative intervillus region, which enables them to contribute to the
    adult stem-cell niche. Our results demonstrate that large-scale remodelling of
    the intestinal wall and cell-fate specification are closely linked. Moreover,
    these findings provide a direct link between the observed plasticity and cellular
    reprogramming of differentiating cells in adult tissues following damage5,6,7,8,9,
    revealing that stem-cell identity is an induced rather than a hardwired property.
article_processing_charge: No
article_type: original
author:
- first_name: Jordi
  full_name: Guiu, Jordi
  last_name: Guiu
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Shiro
  full_name: Yui, Shiro
  last_name: Yui
- first_name: Samuel
  full_name: Demharter, Samuel
  last_name: Demharter
- first_name: Svetlana
  full_name: Ulyanchenko, Svetlana
  last_name: Ulyanchenko
- first_name: Martti
  full_name: Maimets, Martti
  last_name: Maimets
- first_name: Anne
  full_name: Jørgensen, Anne
  last_name: Jørgensen
- first_name: Signe
  full_name: Perlman, Signe
  last_name: Perlman
- first_name: Lene
  full_name: Lundvall, Lene
  last_name: Lundvall
- first_name: Linn Salto
  full_name: Mamsen, Linn Salto
  last_name: Mamsen
- first_name: Agnete
  full_name: Larsen, Agnete
  last_name: Larsen
- first_name: Rasmus H.
  full_name: Olesen, Rasmus H.
  last_name: Olesen
- first_name: Claus Yding
  full_name: Andersen, Claus Yding
  last_name: Andersen
- first_name: Lea Langhoff
  full_name: Thuesen, Lea Langhoff
  last_name: Thuesen
- first_name: Kristine Juul
  full_name: Hare, Kristine Juul
  last_name: Hare
- first_name: Tune H.
  full_name: Pers, Tune H.
  last_name: Pers
- first_name: Konstantin
  full_name: Khodosevich, Konstantin
  last_name: Khodosevich
- first_name: Benjamin D.
  full_name: Simons, Benjamin D.
  last_name: Simons
- first_name: Kim B.
  full_name: Jensen, Kim B.
  last_name: Jensen
citation:
  ama: Guiu J, Hannezo EB, Yui S, et al. Tracing the origin of adult intestinal stem
    cells. <i>Nature</i>. 2019;570:107-111. doi:<a href="https://doi.org/10.1038/s41586-019-1212-5">10.1038/s41586-019-1212-5</a>
  apa: Guiu, J., Hannezo, E. B., Yui, S., Demharter, S., Ulyanchenko, S., Maimets,
    M., … Jensen, K. B. (2019). Tracing the origin of adult intestinal stem cells.
    <i>Nature</i>. Springer Nature. <a href="https://doi.org/10.1038/s41586-019-1212-5">https://doi.org/10.1038/s41586-019-1212-5</a>
  chicago: Guiu, Jordi, Edouard B Hannezo, Shiro Yui, Samuel Demharter, Svetlana Ulyanchenko,
    Martti Maimets, Anne Jørgensen, et al. “Tracing the Origin of Adult Intestinal
    Stem Cells.” <i>Nature</i>. Springer Nature, 2019. <a href="https://doi.org/10.1038/s41586-019-1212-5">https://doi.org/10.1038/s41586-019-1212-5</a>.
  ieee: J. Guiu <i>et al.</i>, “Tracing the origin of adult intestinal stem cells,”
    <i>Nature</i>, vol. 570. Springer Nature, pp. 107–111, 2019.
  ista: Guiu J, Hannezo EB, Yui S, Demharter S, Ulyanchenko S, Maimets M, Jørgensen
    A, Perlman S, Lundvall L, Mamsen LS, Larsen A, Olesen RH, Andersen CY, Thuesen
    LL, Hare KJ, Pers TH, Khodosevich K, Simons BD, Jensen KB. 2019. Tracing the origin
    of adult intestinal stem cells. Nature. 570, 107–111.
  mla: Guiu, Jordi, et al. “Tracing the Origin of Adult Intestinal Stem Cells.” <i>Nature</i>,
    vol. 570, Springer Nature, 2019, pp. 107–11, doi:<a href="https://doi.org/10.1038/s41586-019-1212-5">10.1038/s41586-019-1212-5</a>.
  short: J. Guiu, E.B. Hannezo, S. Yui, S. Demharter, S. Ulyanchenko, M. Maimets,
    A. Jørgensen, S. Perlman, L. Lundvall, L.S. Mamsen, A. Larsen, R.H. Olesen, C.Y.
    Andersen, L.L. Thuesen, K.J. Hare, T.H. Pers, K. Khodosevich, B.D. Simons, K.B.
    Jensen, Nature 570 (2019) 107–111.
date_created: 2019-06-02T21:59:14Z
date_published: 2019-06-06T00:00:00Z
date_updated: 2023-08-28T09:30:23Z
day: '06'
department:
- _id: EdHa
doi: 10.1038/s41586-019-1212-5
external_id:
  isi:
  - '000470149000048'
  pmid:
  - '31092921'
intvolume: '       570'
isi: 1
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6986928
month: '06'
oa: 1
oa_version: Submitted Version
page: 107-111
pmid: 1
publication: Nature
publication_identifier:
  eissn:
  - '14764687'
  issn:
  - '00280836'
publication_status: published
publisher: Springer Nature
quality_controlled: '1'
scopus_import: '1'
status: public
title: Tracing the origin of adult intestinal stem cells
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 570
year: '2019'
...
---
_id: '6559'
abstract:
- lang: eng
  text: Branching morphogenesis is a prototypical example of complex three-dimensional
    organ sculpting, required in multiple developmental settings to maximize the area
    of exchange surfaces. It requires, in particular, the coordinated growth of different
    cell types together with complex patterning to lead to robust macroscopic outputs.
    In recent years, novel multiscale quantitative biology approaches, together with
    biophysical modelling, have begun to shed new light of this topic. Here, we wish
    to review some of these recent developments, highlighting the generic design principles
    that can be abstracted across different branched organs, as well as the implications
    for the broader fields of stem cell, developmental and systems biology.
article_processing_charge: No
article_type: original
author:
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Benjamin D.
  full_name: Simons, Benjamin D.
  last_name: Simons
citation:
  ama: Hannezo EB, Simons BD. Multiscale dynamics of branching morphogenesis. <i>Current
    Opinion in Cell Biology</i>. 2019;60:99-105. doi:<a href="https://doi.org/10.1016/j.ceb.2019.04.008">10.1016/j.ceb.2019.04.008</a>
  apa: Hannezo, E. B., &#38; Simons, B. D. (2019). Multiscale dynamics of branching
    morphogenesis. <i>Current Opinion in Cell Biology</i>. Elsevier. <a href="https://doi.org/10.1016/j.ceb.2019.04.008">https://doi.org/10.1016/j.ceb.2019.04.008</a>
  chicago: Hannezo, Edouard B, and Benjamin D. Simons. “Multiscale Dynamics of Branching
    Morphogenesis.” <i>Current Opinion in Cell Biology</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.ceb.2019.04.008">https://doi.org/10.1016/j.ceb.2019.04.008</a>.
  ieee: E. B. Hannezo and B. D. Simons, “Multiscale dynamics of branching morphogenesis,”
    <i>Current Opinion in Cell Biology</i>, vol. 60. Elsevier, pp. 99–105, 2019.
  ista: Hannezo EB, Simons BD. 2019. Multiscale dynamics of branching morphogenesis.
    Current Opinion in Cell Biology. 60, 99–105.
  mla: Hannezo, Edouard B., and Benjamin D. Simons. “Multiscale Dynamics of Branching
    Morphogenesis.” <i>Current Opinion in Cell Biology</i>, vol. 60, Elsevier, 2019,
    pp. 99–105, doi:<a href="https://doi.org/10.1016/j.ceb.2019.04.008">10.1016/j.ceb.2019.04.008</a>.
  short: E.B. Hannezo, B.D. Simons, Current Opinion in Cell Biology 60 (2019) 99–105.
date_created: 2019-06-16T21:59:12Z
date_published: 2019-10-01T00:00:00Z
date_updated: 2023-08-28T09:38:57Z
day: '01'
department:
- _id: EdHa
doi: 10.1016/j.ceb.2019.04.008
external_id:
  isi:
  - '000486545800014'
  pmid:
  - '31181348'
intvolume: '        60'
isi: 1
language:
- iso: eng
month: '10'
oa_version: None
page: 99-105
pmid: 1
publication: Current Opinion in Cell Biology
publication_identifier:
  eissn:
  - '18790410'
  issn:
  - '09550674'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Multiscale dynamics of branching morphogenesis
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 60
year: '2019'
...
---
_id: '6601'
abstract:
- lang: eng
  text: There is increasing evidence that both mechanical and biochemical signals
    play important roles in development and disease. The development of complex organisms,
    in particular, has been proposed to rely on the feedback between mechanical and
    biochemical patterning events. This feedback occurs at the molecular level via
    mechanosensation but can also arise as an emergent property of the system at the
    cellular and tissue level. In recent years, dynamic changes in tissue geometry,
    flow, rheology, and cell fate specification have emerged as key platforms of mechanochemical
    feedback loops in multiple processes. Here, we review recent experimental and
    theoretical advances in understanding how these feedbacks function in development
    and disease.
article_processing_charge: No
article_type: review
author:
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Carl-Philipp J
  full_name: Heisenberg, Carl-Philipp J
  id: 39427864-F248-11E8-B48F-1D18A9856A87
  last_name: Heisenberg
  orcid: 0000-0002-0912-4566
citation:
  ama: Hannezo EB, Heisenberg C-PJ. Mechanochemical feedback loops in development
    and disease. <i>Cell</i>. 2019;178(1):12-25. doi:<a href="https://doi.org/10.1016/j.cell.2019.05.052">10.1016/j.cell.2019.05.052</a>
  apa: Hannezo, E. B., &#38; Heisenberg, C.-P. J. (2019). Mechanochemical feedback
    loops in development and disease. <i>Cell</i>. Elsevier. <a href="https://doi.org/10.1016/j.cell.2019.05.052">https://doi.org/10.1016/j.cell.2019.05.052</a>
  chicago: Hannezo, Edouard B, and Carl-Philipp J Heisenberg. “Mechanochemical Feedback
    Loops in Development and Disease.” <i>Cell</i>. Elsevier, 2019. <a href="https://doi.org/10.1016/j.cell.2019.05.052">https://doi.org/10.1016/j.cell.2019.05.052</a>.
  ieee: E. B. Hannezo and C.-P. J. Heisenberg, “Mechanochemical feedback loops in
    development and disease,” <i>Cell</i>, vol. 178, no. 1. Elsevier, pp. 12–25, 2019.
  ista: Hannezo EB, Heisenberg C-PJ. 2019. Mechanochemical feedback loops in development
    and disease. Cell. 178(1), 12–25.
  mla: Hannezo, Edouard B., and Carl-Philipp J. Heisenberg. “Mechanochemical Feedback
    Loops in Development and Disease.” <i>Cell</i>, vol. 178, no. 1, Elsevier, 2019,
    pp. 12–25, doi:<a href="https://doi.org/10.1016/j.cell.2019.05.052">10.1016/j.cell.2019.05.052</a>.
  short: E.B. Hannezo, C.-P.J. Heisenberg, Cell 178 (2019) 12–25.
date_created: 2019-06-30T21:59:11Z
date_published: 2019-07-27T00:00:00Z
date_updated: 2023-08-28T12:25:21Z
day: '27'
department:
- _id: CaHe
- _id: EdHa
doi: 10.1016/j.cell.2019.05.052
ec_funded: 1
external_id:
  isi:
  - '000473002700005'
  pmid:
  - '31251912'
intvolume: '       178'
isi: 1
issue: '1'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://doi.org/10.1016/j.cell.2019.05.052
month: '07'
oa: 1
oa_version: Published Version
page: 12-25
pmid: 1
project:
- _id: 260F1432-B435-11E9-9278-68D0E5697425
  call_identifier: H2020
  grant_number: '742573'
  name: Interaction and feedback between cell mechanics and fate specification in
    vertebrate gastrulation
- _id: 268294B6-B435-11E9-9278-68D0E5697425
  call_identifier: FWF
  grant_number: P31639
  name: Active mechano-chemical description of the cell cytoskeleton
publication: Cell
publication_identifier:
  issn:
  - '00928674'
publication_status: published
publisher: Elsevier
quality_controlled: '1'
scopus_import: '1'
status: public
title: Mechanochemical feedback loops in development and disease
type: journal_article
user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8
volume: 178
year: '2019'
...
---
_id: '9726'
abstract:
- lang: eng
  text: A detailed description of the two stochastic models, table of parameters,
    supplementary data for Figures 4 and 5, parameter dependence of the results, and
    an analysis on motors with different force–velocity functions (PDF)
article_processing_charge: No
author:
- first_name: Mehmet C
  full_name: Ucar, Mehmet C
  id: 50B2A802-6007-11E9-A42B-EB23E6697425
  last_name: Ucar
  orcid: 0000-0003-0506-4217
- first_name: Reinhard
  full_name: Lipowsky, Reinhard
  last_name: Lipowsky
citation:
  ama: Ucar MC, Lipowsky R. Supplementary information - Collective force generation
    by molecular motors is determined by strain-induced unbinding. 2019. doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445.s001">10.1021/acs.nanolett.9b04445.s001</a>
  apa: Ucar, M. C., &#38; Lipowsky, R. (2019). Supplementary information - Collective
    force generation by molecular motors is determined by strain-induced unbinding.
    American Chemical Society . <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s001">https://doi.org/10.1021/acs.nanolett.9b04445.s001</a>
  chicago: Ucar, Mehmet C, and Reinhard Lipowsky. “Supplementary Information - Collective
    Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding.”
    American Chemical Society , 2019. <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s001">https://doi.org/10.1021/acs.nanolett.9b04445.s001</a>.
  ieee: M. C. Ucar and R. Lipowsky, “Supplementary information - Collective force
    generation by molecular motors is determined by strain-induced unbinding.” American
    Chemical Society , 2019.
  ista: Ucar MC, Lipowsky R. 2019. Supplementary information - Collective force generation
    by molecular motors is determined by strain-induced unbinding, American Chemical
    Society , <a href="https://doi.org/10.1021/acs.nanolett.9b04445.s001">10.1021/acs.nanolett.9b04445.s001</a>.
  mla: Ucar, Mehmet C., and Reinhard Lipowsky. <i>Supplementary Information - Collective
    Force Generation by Molecular Motors Is Determined by Strain-Induced Unbinding</i>.
    American Chemical Society , 2019, doi:<a href="https://doi.org/10.1021/acs.nanolett.9b04445.s001">10.1021/acs.nanolett.9b04445.s001</a>.
  short: M.C. Ucar, R. Lipowsky, (2019).
date_created: 2021-07-27T09:51:46Z
date_published: 2019-12-19T00:00:00Z
date_updated: 2023-08-17T14:07:52Z
day: '19'
department:
- _id: EdHa
doi: 10.1021/acs.nanolett.9b04445.s001
month: '12'
oa_version: Published Version
publisher: 'American Chemical Society '
related_material:
  record:
  - id: '7166'
    relation: used_in_publication
    status: public
status: public
title: Supplementary information - Collective force generation by molecular motors
  is determined by strain-induced unbinding
type: research_data_reference
user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf
year: '2019'
...
---
_id: '288'
abstract:
- lang: eng
  text: Recent lineage tracing studies have revealed that mammary gland homeostasis
    relies on unipotent stem cells. However, whether and when lineage restriction
    occurs during embryonic mammary development, and which signals orchestrate cell
    fate specification, remain unknown. Using a combination of in vivo clonal analysis
    with whole mount immunofluorescence and mathematical modelling of clonal dynamics,
    we found that embryonic multipotent mammary cells become lineage-restricted surprisingly
    early in development, with evidence for unipotency as early as E12.5 and no statistically
    discernable bipotency after E15.5. To gain insights into the mechanisms governing
    the switch from multipotency to unipotency, we used gain-of-function Notch1 mice
    and demonstrated that Notch activation cell autonomously dictates luminal cell
    fate specification to both embryonic and basally committed mammary cells. These
    functional studies have important implications for understanding the signals underlying
    cell plasticity and serve to clarify how reactivation of embryonic programs in
    adult cells can lead to cancer.
article_processing_charge: No
article_type: original
author:
- first_name: Anna
  full_name: Lilja, Anna
  last_name: Lilja
- first_name: Veronica
  full_name: Rodilla, Veronica
  last_name: Rodilla
- first_name: Mathilde
  full_name: Huyghe, Mathilde
  last_name: Huyghe
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Camille
  full_name: Landragin, Camille
  last_name: Landragin
- first_name: Olivier
  full_name: Renaud, Olivier
  last_name: Renaud
- first_name: Olivier
  full_name: Leroy, Olivier
  last_name: Leroy
- first_name: Steffen
  full_name: Rulands, Steffen
  last_name: Rulands
- first_name: Benjamin
  full_name: Simons, Benjamin
  last_name: Simons
- first_name: Silvia
  full_name: Fré, Silvia
  last_name: Fré
citation:
  ama: Lilja A, Rodilla V, Huyghe M, et al. Clonal analysis of Notch1-expressing cells
    reveals the existence of unipotent stem cells that retain long-term plasticity
    in the embryonic mammary gland. <i>Nature Cell Biology</i>. 2018;20(6):677-687.
    doi:<a href="https://doi.org/10.1038/s41556-018-0108-1">10.1038/s41556-018-0108-1</a>
  apa: Lilja, A., Rodilla, V., Huyghe, M., Hannezo, E. B., Landragin, C., Renaud,
    O., … Fré, S. (2018). Clonal analysis of Notch1-expressing cells reveals the existence
    of unipotent stem cells that retain long-term plasticity in the embryonic mammary
    gland. <i>Nature Cell Biology</i>. Nature Publishing Group. <a href="https://doi.org/10.1038/s41556-018-0108-1">https://doi.org/10.1038/s41556-018-0108-1</a>
  chicago: Lilja, Anna, Veronica Rodilla, Mathilde Huyghe, Edouard B Hannezo, Camille
    Landragin, Olivier Renaud, Olivier Leroy, Steffen Rulands, Benjamin Simons, and
    Silvia Fré. “Clonal Analysis of Notch1-Expressing Cells Reveals the Existence
    of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic Mammary
    Gland.” <i>Nature Cell Biology</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41556-018-0108-1">https://doi.org/10.1038/s41556-018-0108-1</a>.
  ieee: A. Lilja <i>et al.</i>, “Clonal analysis of Notch1-expressing cells reveals
    the existence of unipotent stem cells that retain long-term plasticity in the
    embryonic mammary gland,” <i>Nature Cell Biology</i>, vol. 20, no. 6. Nature Publishing
    Group, pp. 677–687, 2018.
  ista: Lilja A, Rodilla V, Huyghe M, Hannezo EB, Landragin C, Renaud O, Leroy O,
    Rulands S, Simons B, Fré S. 2018. Clonal analysis of Notch1-expressing cells reveals
    the existence of unipotent stem cells that retain long-term plasticity in the
    embryonic mammary gland. Nature Cell Biology. 20(6), 677–687.
  mla: Lilja, Anna, et al. “Clonal Analysis of Notch1-Expressing Cells Reveals the
    Existence of Unipotent Stem Cells That Retain Long-Term Plasticity in the Embryonic
    Mammary Gland.” <i>Nature Cell Biology</i>, vol. 20, no. 6, Nature Publishing
    Group, 2018, pp. 677–87, doi:<a href="https://doi.org/10.1038/s41556-018-0108-1">10.1038/s41556-018-0108-1</a>.
  short: A. Lilja, V. Rodilla, M. Huyghe, E.B. Hannezo, C. Landragin, O. Renaud, O.
    Leroy, S. Rulands, B. Simons, S. Fré, Nature Cell Biology 20 (2018) 677–687.
date_created: 2018-12-11T11:45:38Z
date_published: 2018-05-21T00:00:00Z
date_updated: 2023-09-11T12:44:08Z
day: '21'
department:
- _id: EdHa
doi: 10.1038/s41556-018-0108-1
external_id:
  isi:
  - '000433237300003'
  pmid:
  - '29784917'
intvolume: '        20'
isi: 1
issue: '6'
language:
- iso: eng
main_file_link:
- open_access: '1'
  url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6984964
month: '05'
oa: 1
oa_version: Submitted Version
page: 677 - 687
pmid: 1
publication: Nature Cell Biology
publication_status: published
publisher: Nature Publishing Group
publist_id: '7594'
quality_controlled: '1'
scopus_import: '1'
status: public
title: Clonal analysis of Notch1-expressing cells reveals the existence of unipotent
  stem cells that retain long-term plasticity in the embryonic mammary gland
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 20
year: '2018'
...
---
_id: '3'
abstract:
- lang: eng
  text: SETD5 gene mutations have been identified as a frequent cause of idiopathic
    intellectual disability. Here we show that Setd5-haploinsufficient mice present
    developmental defects such as abnormal brain-to-body weight ratios and neural
    crest defect-associated phenotypes. Furthermore, Setd5-mutant mice show impairments
    in cognitive tasks, enhanced long-term potentiation, delayed ontogenetic profile
    of ultrasonic vocalization, and behavioral inflexibility. Behavioral issues are
    accompanied by abnormal expression of postsynaptic density proteins previously
    associated with cognition. Our data additionally indicate that Setd5 regulates
    RNA polymerase II dynamics and gene transcription via its interaction with the
    Hdac3 and Paf1 complexes, findings potentially explaining the gene expression
    defects observed in Setd5-haploinsufficient mice. Our results emphasize the decisive
    role of Setd5 in a biological pathway found to be disrupted in humans with intellectual
    disability and autism spectrum disorder.
acknowledged_ssus:
- _id: M-Shop
- _id: PreCl
acknowledgement: This work was supported by the Simons Foundation Autism Research
  Initiative (grant 401299) to G.N. and the DFG (SPP1738 grant NO 1249) to K.-M.N.
article_processing_charge: No
article_type: original
author:
- first_name: Elena
  full_name: Deliu, Elena
  id: 37A40D7E-F248-11E8-B48F-1D18A9856A87
  last_name: Deliu
  orcid: 0000-0002-7370-5293
- first_name: Niccoló
  full_name: Arecco, Niccoló
  last_name: Arecco
- first_name: Jasmin
  full_name: Morandell, Jasmin
  id: 4739D480-F248-11E8-B48F-1D18A9856A87
  last_name: Morandell
- first_name: Christoph
  full_name: Dotter, Christoph
  id: 4C66542E-F248-11E8-B48F-1D18A9856A87
  last_name: Dotter
  orcid: 0000-0002-9033-9096
- first_name: Ximena
  full_name: Contreras, Ximena
  id: 475990FE-F248-11E8-B48F-1D18A9856A87
  last_name: Contreras
- first_name: Charles
  full_name: Girardot, Charles
  last_name: Girardot
- first_name: Eva
  full_name: Käsper, Eva
  last_name: Käsper
- first_name: Alena
  full_name: Kozlova, Alena
  id: C50A9596-02D0-11E9-976E-E38CFE5CBC1D
  last_name: Kozlova
- first_name: Kasumi
  full_name: Kishi, Kasumi
  id: 3065DFC4-F248-11E8-B48F-1D18A9856A87
  last_name: Kishi
- first_name: Ilaria
  full_name: Chiaradia, Ilaria
  id: B6467F20-02D0-11E9-BDA5-E960C241894A
  last_name: Chiaradia
  orcid: 0000-0002-9529-4464
- first_name: Kyung
  full_name: Noh, Kyung
  last_name: Noh
- first_name: Gaia
  full_name: Novarino, Gaia
  id: 3E57A680-F248-11E8-B48F-1D18A9856A87
  last_name: Novarino
  orcid: 0000-0002-7673-7178
citation:
  ama: Deliu E, Arecco N, Morandell J, et al. Haploinsufficiency of the intellectual
    disability gene SETD5 disturbs developmental gene expression and cognition. <i>Nature
    Neuroscience</i>. 2018;21(12):1717-1727. doi:<a href="https://doi.org/10.1038/s41593-018-0266-2">10.1038/s41593-018-0266-2</a>
  apa: Deliu, E., Arecco, N., Morandell, J., Dotter, C., Contreras, X., Girardot,
    C., … Novarino, G. (2018). Haploinsufficiency of the intellectual disability gene
    SETD5 disturbs developmental gene expression and cognition. <i>Nature Neuroscience</i>.
    Nature Publishing Group. <a href="https://doi.org/10.1038/s41593-018-0266-2">https://doi.org/10.1038/s41593-018-0266-2</a>
  chicago: Deliu, Elena, Niccoló Arecco, Jasmin Morandell, Christoph Dotter, Ximena
    Contreras, Charles Girardot, Eva Käsper, et al. “Haploinsufficiency of the Intellectual
    Disability Gene SETD5 Disturbs Developmental Gene Expression and Cognition.” <i>Nature
    Neuroscience</i>. Nature Publishing Group, 2018. <a href="https://doi.org/10.1038/s41593-018-0266-2">https://doi.org/10.1038/s41593-018-0266-2</a>.
  ieee: E. Deliu <i>et al.</i>, “Haploinsufficiency of the intellectual disability
    gene SETD5 disturbs developmental gene expression and cognition,” <i>Nature Neuroscience</i>,
    vol. 21, no. 12. Nature Publishing Group, pp. 1717–1727, 2018.
  ista: Deliu E, Arecco N, Morandell J, Dotter C, Contreras X, Girardot C, Käsper
    E, Kozlova A, Kishi K, Chiaradia I, Noh K, Novarino G. 2018. Haploinsufficiency
    of the intellectual disability gene SETD5 disturbs developmental gene expression
    and cognition. Nature Neuroscience. 21(12), 1717–1727.
  mla: Deliu, Elena, et al. “Haploinsufficiency of the Intellectual Disability Gene
    SETD5 Disturbs Developmental Gene Expression and Cognition.” <i>Nature Neuroscience</i>,
    vol. 21, no. 12, Nature Publishing Group, 2018, pp. 1717–27, doi:<a href="https://doi.org/10.1038/s41593-018-0266-2">10.1038/s41593-018-0266-2</a>.
  short: E. Deliu, N. Arecco, J. Morandell, C. Dotter, X. Contreras, C. Girardot,
    E. Käsper, A. Kozlova, K. Kishi, I. Chiaradia, K. Noh, G. Novarino, Nature Neuroscience
    21 (2018) 1717–1727.
date_created: 2018-12-11T11:44:05Z
date_published: 2018-11-19T00:00:00Z
date_updated: 2024-03-25T23:30:25Z
day: '19'
ddc:
- '570'
department:
- _id: GaNo
- _id: EdHa
doi: 10.1038/s41593-018-0266-2
external_id:
  isi:
  - '000451324700010'
file:
- access_level: open_access
  checksum: 60abd0f05b7cdc08a6b0ec460884084f
  content_type: application/pdf
  creator: dernst
  date_created: 2019-04-09T07:41:57Z
  date_updated: 2020-07-14T12:45:58Z
  file_id: '6255'
  file_name: 2017_NatureNeuroscience_Deliu.pdf
  file_size: 8167169
  relation: main_file
file_date_updated: 2020-07-14T12:45:58Z
has_accepted_license: '1'
intvolume: '        21'
isi: 1
issue: '12'
language:
- iso: eng
month: '11'
oa: 1
oa_version: Submitted Version
page: 1717 - 1727
project:
- _id: 254BA948-B435-11E9-9278-68D0E5697425
  grant_number: '401299'
  name: Probing development and reversibility of autism spectrum disorders
publication: Nature Neuroscience
publication_status: published
publisher: Nature Publishing Group
publist_id: '8054'
pubrep_id: '1071'
quality_controlled: '1'
related_material:
  link:
  - description: News on IST Homepage
    relation: press_release
    url: https://ist.ac.at/en/news/mutation-that-causes-autism-and-intellectual-disability-makes-brain-less-flexible/
  record:
  - id: '6074'
    relation: popular_science
    status: public
  - id: '12364'
    relation: dissertation_contains
    status: public
scopus_import: '1'
status: public
title: Haploinsufficiency of the intellectual disability gene SETD5 disturbs developmental
  gene expression and cognition
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 21
year: '2018'
...
---
_id: '5787'
abstract:
- lang: eng
  text: "Branching  morphogenesis  remains  a  subject  of  abiding  interest.  Although
    \ much  is  \r\nknown about the gene regulatory programs and signaling pathways
    that operate at \r\nthe cellular scale, it has remained unclear how the macroscopic
    features of branched \r\norgans,  including  their  size,  network  topology  and
    \ spatial  patterning,  are  encoded.  \r\nLately, it has been proposed that,
    these features can be explained quantitatively in \r\nseveral organs within a
    single unifying framework. Based on large-\r\nscale organ recon\r\n-\r\nstructions
    \ and  cell  lineage  tracing,  it  has  been  argued  that  morphogenesis  follows
    \ \r\nfrom the collective dynamics of sublineage- \r\nrestricted self- \r\nrenewing
    progenitor cells, \r\nlocalized at ductal tips, that act cooperatively to drive
    a serial process of ductal elon\r\n-\r\ngation and stochastic tip bifurcation.
    By correlating differentiation or cell cycle exit \r\nwith proximity to maturing
    ducts, this dynamic results in the specification of a com-\r\nplex  network  of
    \ defined  density  and  statistical  organization.  These  results  suggest  \r\nthat,
    for several mammalian tissues, branched epithelial structures develop as a self-
    \r\norganized  process,  reliant  upon  a  strikingly  simple,  but  generic,
    \ set  of  local  rules,  \r\nwithout  recourse  to  a  rigid  and  deterministic
    \ sequence  of  genetically  programmed  \r\nevents. Here, we review the basis
    of these findings and discuss their implications."
article_processing_charge: No
author:
- first_name: Edouard B
  full_name: Hannezo, Edouard B
  id: 3A9DB764-F248-11E8-B48F-1D18A9856A87
  last_name: Hannezo
  orcid: 0000-0001-6005-1561
- first_name: Benjamin D.
  full_name: Simons, Benjamin D.
  last_name: Simons
citation:
  ama: Hannezo EB, Simons BD. Statistical theory of branching morphogenesis. <i>Development
    Growth and Differentiation</i>. 2018;60(9):512-521. doi:<a href="https://doi.org/10.1111/dgd.12570">10.1111/dgd.12570</a>
  apa: Hannezo, E. B., &#38; Simons, B. D. (2018). Statistical theory of branching
    morphogenesis. <i>Development Growth and Differentiation</i>. Wiley. <a href="https://doi.org/10.1111/dgd.12570">https://doi.org/10.1111/dgd.12570</a>
  chicago: Hannezo, Edouard B, and Benjamin D. Simons. “Statistical Theory of Branching
    Morphogenesis.” <i>Development Growth and Differentiation</i>. Wiley, 2018. <a
    href="https://doi.org/10.1111/dgd.12570">https://doi.org/10.1111/dgd.12570</a>.
  ieee: E. B. Hannezo and B. D. Simons, “Statistical theory of branching morphogenesis,”
    <i>Development Growth and Differentiation</i>, vol. 60, no. 9. Wiley, pp. 512–521,
    2018.
  ista: Hannezo EB, Simons BD. 2018. Statistical theory of branching morphogenesis.
    Development Growth and Differentiation. 60(9), 512–521.
  mla: Hannezo, Edouard B., and Benjamin D. Simons. “Statistical Theory of Branching
    Morphogenesis.” <i>Development Growth and Differentiation</i>, vol. 60, no. 9,
    Wiley, 2018, pp. 512–21, doi:<a href="https://doi.org/10.1111/dgd.12570">10.1111/dgd.12570</a>.
  short: E.B. Hannezo, B.D. Simons, Development Growth and Differentiation 60 (2018)
    512–521.
date_created: 2018-12-30T22:59:14Z
date_published: 2018-12-09T00:00:00Z
date_updated: 2023-09-19T09:32:49Z
day: '09'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1111/dgd.12570
external_id:
  isi:
  - '000453555100002'
file:
- access_level: open_access
  checksum: a6d30b0785db902c734a84fecb2eadd9
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  creator: dernst
  date_created: 2019-02-06T10:40:46Z
  date_updated: 2020-07-14T12:47:11Z
  file_id: '5933'
  file_name: 2018_DevGrowh_Hannezo.pdf
  file_size: 1313606
  relation: main_file
file_date_updated: 2020-07-14T12:47:11Z
has_accepted_license: '1'
intvolume: '        60'
isi: 1
issue: '9'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
page: 512-521
publication: Development Growth and Differentiation
publication_identifier:
  issn:
  - '00121592'
publisher: Wiley
quality_controlled: '1'
scopus_import: '1'
status: public
title: Statistical theory of branching morphogenesis
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1
volume: 60
year: '2018'
...
---
_id: '5859'
abstract:
- lang: eng
  text: The emergence of syntax during childhood is a remarkable example of how complex
    correlations unfold in nonlinear ways through development. In particular, rapid
    transitions seem to occur as children reach the age of two, which seems to separate
    a two-word, tree-like network of syntactic relations among words from the scale-free
    graphs associated with the adult, complex grammar. Here, we explore the evolution
    of syntax networks through language acquisition using the chromatic number, which
    captures the transition and provides a natural link to standard theories on syntactic
    structures. The data analysis is compared to a null model of network growth dynamics
    which is shown to display non-trivial and sensible differences. At a more general
    level, we observe that the chromatic classes define independent regions of the
    graph, and thus, can be interpreted as the footprints of incompatibility relations,
    somewhat as opposed to modularity considerations.
acknowledgement: This work was supported by the James McDonnell Foundation (B.C-M.,
  S.V. and R.S.)
article_number: '181286'
article_processing_charge: No
article_type: original
author:
- first_name: Bernat
  full_name: Corominas-Murtra, Bernat
  id: 43BE2298-F248-11E8-B48F-1D18A9856A87
  last_name: Corominas-Murtra
  orcid: 0000-0001-9806-5643
- first_name: Martí Sànchez
  full_name: Fibla, Martí Sànchez
  last_name: Fibla
- first_name: Sergi
  full_name: Valverde, Sergi
  last_name: Valverde
- first_name: Ricard
  full_name: Solé, Ricard
  last_name: Solé
citation:
  ama: Corominas-Murtra B, Fibla MS, Valverde S, Solé R. Chromatic transitions in
    the emergence of syntax networks. <i>Royal Society Open Science</i>. 2018;5(12).
    doi:<a href="https://doi.org/10.1098/rsos.181286">10.1098/rsos.181286</a>
  apa: Corominas-Murtra, B., Fibla, M. S., Valverde, S., &#38; Solé, R. (2018). Chromatic
    transitions in the emergence of syntax networks. <i>Royal Society Open Science</i>.
    The Royal Society. <a href="https://doi.org/10.1098/rsos.181286">https://doi.org/10.1098/rsos.181286</a>
  chicago: Corominas-Murtra, Bernat, Martí Sànchez Fibla, Sergi Valverde, and Ricard
    Solé. “Chromatic Transitions in the Emergence of Syntax Networks.” <i>Royal Society
    Open Science</i>. The Royal Society, 2018. <a href="https://doi.org/10.1098/rsos.181286">https://doi.org/10.1098/rsos.181286</a>.
  ieee: B. Corominas-Murtra, M. S. Fibla, S. Valverde, and R. Solé, “Chromatic transitions
    in the emergence of syntax networks,” <i>Royal Society Open Science</i>, vol.
    5, no. 12. The Royal Society, 2018.
  ista: Corominas-Murtra B, Fibla MS, Valverde S, Solé R. 2018. Chromatic transitions
    in the emergence of syntax networks. Royal Society Open Science. 5(12), 181286.
  mla: Corominas-Murtra, Bernat, et al. “Chromatic Transitions in the Emergence of
    Syntax Networks.” <i>Royal Society Open Science</i>, vol. 5, no. 12, 181286, The
    Royal Society, 2018, doi:<a href="https://doi.org/10.1098/rsos.181286">10.1098/rsos.181286</a>.
  short: B. Corominas-Murtra, M.S. Fibla, S. Valverde, R. Solé, Royal Society Open
    Science 5 (2018).
date_created: 2019-01-20T22:59:18Z
date_published: 2018-12-12T00:00:00Z
date_updated: 2023-10-18T06:41:12Z
day: '12'
ddc:
- '570'
department:
- _id: EdHa
doi: 10.1098/rsos.181286
external_id:
  isi:
  - '000456566500027'
  pmid:
  - '30662738'
file:
- access_level: open_access
  checksum: 9664d4417f6b792242e31eea77ce9501
  content_type: application/pdf
  creator: dernst
  date_created: 2019-02-05T14:38:09Z
  date_updated: 2020-07-14T12:47:13Z
  file_id: '5924'
  file_name: 2018_RoyalSocOS_Corominas.pdf
  file_size: 646732
  relation: main_file
file_date_updated: 2020-07-14T12:47:13Z
has_accepted_license: '1'
intvolume: '         5'
isi: 1
issue: '12'
language:
- iso: eng
month: '12'
oa: 1
oa_version: Published Version
pmid: 1
publication: Royal Society Open Science
publication_identifier:
  issn:
  - 2054-5703
publication_status: published
publisher: The Royal Society
quality_controlled: '1'
scopus_import: '1'
status: public
title: Chromatic transitions in the emergence of syntax networks
tmp:
  image: /images/cc_by.png
  legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode
  name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)
  short: CC BY (4.0)
type: journal_article
user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87
volume: 5
year: '2018'
...
