Inductive asymmetric cell division: The WRM leads the way
dc.contributor.author | Ishidate, Takao | |
dc.contributor.author | Kim, Soyoung | |
dc.contributor.author | Mello, Craig C. | |
dc.contributor.author | Shirayama, Masaki | |
dc.date | 2022-08-11T08:10:18.000 | |
dc.date.accessioned | 2022-08-23T17:03:24Z | |
dc.date.available | 2022-08-23T17:03:24Z | |
dc.date.issued | 2013-10-01 | |
dc.date.submitted | 2014-10-01 | |
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.issn | 2162-4046 | |
dc.identifier.doi | 10.4161/worm.26276 | |
dc.identifier.pmid | 24524013 | |
dc.identifier.uri | http://hdl.handle.net/20.500.14038/44416 | |
dc.description.abstract | 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. | |
dc.language.iso | en_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.subject | Asymmetric Cell Division | |
dc.subject | Biochemistry | |
dc.subject | Cell Biology | |
dc.subject | Cellular and Molecular Physiology | |
dc.subject | Genetic Processes | |
dc.subject | Molecular Biology | |
dc.subject | Molecular Genetics | |
dc.title | Inductive asymmetric cell division: The WRM leads the way | |
dc.type | Journal Article | |
dc.source.journaltitle | Worm | |
dc.source.volume | 2 | |
dc.source.issue | 4 | |
dc.identifier.legacyfulltext | https://escholarship.umassmed.edu/cgi/viewcontent.cgi?article=1014&context=pmm_pp&unstamped=1 | |
dc.identifier.legacycoverpage | https://escholarship.umassmed.edu/pmm_pp/15 | |
dc.identifier.contextkey | 6191396 | |
refterms.dateFOA | 2022-08-23T17:03:24Z | |
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.submissionpath | pmm_pp/15 | |
dc.contributor.department | Program in Molecular Medicine | |
dc.contributor.department | RNA Therapeutics Institute | |
dc.source.pages | e26276 |