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dc.contributor.authorIshidate, Takao
dc.contributor.authorKim, Soyoung
dc.contributor.authorMello, Craig C.
dc.contributor.authorShirayama, Masaki
dc.date2022-08-11T08:10:18.000
dc.date.accessioned2022-08-23T17:03:24Z
dc.date.available2022-08-23T17:03:24Z
dc.date.issued2013-10-01
dc.date.submitted2014-10-01
dc.identifier.citation<p>Ishidate T, Kim S, Mello CC, Shirayama M. Inductive asymmetric cell division: The WRM leads the way. Worm 2013; 2:e26276; http://dx.doi.org/10.4161/worm.26276</p>
dc.identifier.issn2162-4046
dc.identifier.doi10.4161/worm.26276
dc.identifier.pmid24524013
dc.identifier.urihttp://hdl.handle.net/20.500.14038/44416
dc.description.abstractC. elegans, with its invariant cell lineage, provides a powerful model system in which to study signaling-dependent asymmetric cell division. The C. elegans β-catenin-related protein, WRM-1, specifies endoderm at the 4-cell stage during the first cell signaling-induced asymmetric cell division of embryogenesis. During this interaction, Wnt signaling and the cell cycle regulator CDK-1 act together to induce the asymmetric cortical release of WRM-1 at prophase of the EMS cell cycle. Genetic studies suggest that release of WRM-1 unmasks a cortical site that drives EMS spindle rotation onto the polarized axis of the cell, simultaneously making WRM-1 available for nuclear translocation, and downstream signaling to specify endoderm. These studies suggest a general paradigm for how cortical factors like WRM-1 can function at the cell cortex to mask potentially confounding polarity cues, and when released with appropriate cell cycle timing, can also function downstream to define cell fate.
dc.language.isoen_US
dc.relation<a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=24524013&dopt=Abstract">Link to article in PubMed</a>
dc.rights<p>This is an open-access article licensed under a <a href="http://creativecommons.org/licenses/by-nc/3.0/" target="_BLANK">Creative Commons Attribution-NonCommercial 3.0 Unported License</a>. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.</p>
dc.subjectAsymmetric Cell Division
dc.subjectBiochemistry
dc.subjectCell Biology
dc.subjectCellular and Molecular Physiology
dc.subjectGenetic Processes
dc.subjectMolecular Biology
dc.subjectMolecular Genetics
dc.titleInductive asymmetric cell division: The WRM leads the way
dc.typeJournal Article
dc.source.journaltitleWorm
dc.source.volume2
dc.source.issue4
dc.identifier.legacyfulltexthttps://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1014&amp;context=pmm_pp&amp;unstamped=1
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/pmm_pp/15
dc.identifier.contextkey6191396
refterms.dateFOA2022-08-23T17:03:24Z
html.description.abstract<p>C. elegans, with its invariant cell lineage, provides a powerful model system in which to study signaling-dependent asymmetric cell division. The C. elegans β-catenin-related protein, WRM-1, specifies endoderm at the 4-cell stage during the first cell signaling-induced asymmetric cell division of embryogenesis. During this interaction, Wnt signaling and the cell cycle regulator CDK-1 act together to induce the asymmetric cortical release of WRM-1 at prophase of the EMS cell cycle. Genetic studies suggest that release of WRM-1 unmasks a cortical site that drives EMS spindle rotation onto the polarized axis of the cell, simultaneously making WRM-1 available for nuclear translocation, and downstream signaling to specify endoderm. These studies suggest a general paradigm for how cortical factors like WRM-1 can function at the cell cortex to mask potentially confounding polarity cues, and when released with appropriate cell cycle timing, can also function downstream to define cell fate.</p>
dc.identifier.submissionpathpmm_pp/15
dc.contributor.departmentProgram in Molecular Medicine
dc.contributor.departmentRNA Therapeutics Institute
dc.source.pagese26276


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