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Morphogenetic degeneracies in the actomyosin cortex.

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cam.issuedOnline2018-10-22
dc.contributor.authorNaganathan, Sundar Ram
dc.contributor.authorFürthauer, Sebastian
dc.contributor.authorRodriguez, Josana
dc.contributor.authorFievet, Bruno Thomas
dc.contributor.authorJülicher, Frank
dc.contributor.authorAhringer, Julie
dc.contributor.authorCannistraci, Carlo Vittorio
dc.contributor.authorGrill, Stephan W
dc.contributor.orcidNaganathan, Sundar Ram [0000-0001-5106-8687]
dc.contributor.orcidFürthauer, Sebastian [0000-0001-9581-5963]
dc.contributor.orcidRodriguez, Josana [0000-0001-8800-1283]
dc.contributor.orcidJülicher, Frank [0000-0003-4731-9185]
dc.contributor.orcidAhringer, Julie [0000-0002-7074-4051]
dc.contributor.orcidCannistraci, Carlo Vittorio [0000-0003-0100-8410]
dc.date.accessioned2018-12-08T00:30:56Z
dc.date.available2018-12-08T00:30:56Z
dc.date.issued2018-10-22
dc.description.abstractOne of the great challenges in biology is to understand the mechanisms by which morphogenetic processes arise from molecular activities. We investigated this problem in the context of actomyosin-based cortical flow in C. elegans zygotes, where large-scale flows emerge from the collective action of actomyosin filaments and actin binding proteins (ABPs). Large-scale flow dynamics can be captured by active gel theory by considering force balances and conservation laws in the actomyosin cortex. However, which molecular activities contribute to flow dynamics and large-scale physical properties such as viscosity and active torque is largely unknown. By performing a candidate RNAi screen of ABPs and actomyosin regulators we demonstrate that perturbing distinct molecular processes can lead to similar flow phenotypes. This is indicative for a 'morphogenetic degeneracy' where multiple molecular processes contribute to the same large-scale physical property. We speculate that morphogenetic degeneracies contribute to the robustness of bulk biological matter in development.
dc.format.mediumElectronic
dc.identifier.doi10.17863/CAM.33836
dc.identifier.eissn2050-084X
dc.identifier.issn2050-084X
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/286526
dc.languageeng
dc.language.isoeng
dc.publishereLife Sciences Publications, Ltd
dc.publisher.urlhttp://dx.doi.org/10.7554/elife.37677
dc.rightsAttribution 4.0 International
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/
dc.subjectC. elegans
dc.subjectRNAi screen
dc.subjectactomyosin
dc.subjectcell biology
dc.subjectcortical flow
dc.subjectdegeneracy
dc.subjecthydrodynamics
dc.subjectphysics of living systems
dc.subjectActins
dc.subjectActomyosin
dc.subjectAnimals
dc.subjectCaenorhabditis elegans
dc.subjectCaenorhabditis elegans Proteins
dc.subjectEmbryo, Nonmammalian
dc.subjectFluorescence
dc.subjectHydrodynamics
dc.subjectMicrofilament Proteins
dc.subjectModels, Biological
dc.subjectMorphogenesis
dc.subjectMyosins
dc.subjectRNA Interference
dc.subjectRheology
dc.titleMorphogenetic degeneracies in the actomyosin cortex.
dc.typeArticle
dcterms.dateAccepted2018-10-16
prism.publicationDate2018
prism.publicationNameElife
prism.volume7
pubs.funder-project-idWellcome Trust (084598/Z/07/Z)
pubs.funder-project-idWellcome Trust (101863/Z/13/Z)
pubs.funder-project-idEuropean Commission Horizon 2020 (H2020) Marie Sk?odowska-Curie actions (641639)
rioxxterms.licenseref.startdate2018-10-22
rioxxterms.licenseref.urihttp://www.rioxx.net/licenses/all-rights-reserved
rioxxterms.typeJournal Article/Review
rioxxterms.versionVoR
rioxxterms.versionofrecord10.7554/eLife.37677

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