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dc.contributor.authorGuertin, David A.
dc.contributor.authorVenkatram, Srinivas
dc.contributor.authorGould, K. Lance
dc.contributor.authorMcCollum, Dannel
dc.date2022-08-11T08:08:58.000
dc.date.accessioned2022-08-23T16:14:08Z
dc.date.available2022-08-23T16:14:08Z
dc.date.issued2002-12-14
dc.date.submitted2008-09-23
dc.identifier.citation<p>Dev Cell. 2002 Dec;3(6):779-90.</p>
dc.identifier.issn1534-5807 (Print)
dc.identifier.doi10.1016/S1534-5807(02)00367-2
dc.identifier.pmid12479804
dc.identifier.urihttp://hdl.handle.net/20.500.14038/33790
dc.description.abstractIn the fission yeast Schizosaccharomyces pombe, the septation initiation network (SIN) triggers cytokinesis after mitosis. We investigated the relationship between Dma1p, a spindle checkpoint protein and cytokinesis inhibitor, and the SIN. Deletion of dma1 inactivates the spindle checkpoint and allows precocious SIN activation, while overexpressing Dma1p reduces SIN signaling. Dma1p seems to function by inhibiting the SIN activator, Plo1p kinase, since dma1 overexpression and deletion phenotypes suggest that Dma1p antagonizes Plo1p localization. Furthermore, failure to maintain high cyclin-dependent kinase (CDK) activity during spindle checkpoint activation in dma1 deletion cells requires Plo1p. Dma1p itself localizes to spindle pole bodies through interaction with Sid4p. Our observations suggest that Dma1p functions to prevent mitotic exit and cytokinesis during spindle checkpoint arrest by inhibiting SIN signaling.
dc.language.isoen_US
dc.relation<p><a href="http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=12479804&dopt=Abstract">Link to article in PubMed</a></p>
dc.relation.urlhttps://doi.org/10.1016/S1534-5807(02)00367-2
dc.subjectCell Cycle Proteins; Cell Division; *Drosophila Proteins; Genes, cdc; Microtubule-Associated Proteins; Microtubules; Mitosis; Mitotic Spindle Apparatus; Models, Biological; Mutation; Protein Structure, Tertiary; Protein-Serine-Threonine Kinases; Schizosaccharomyces; *Schizosaccharomyces pombe Proteins; Signal Transduction
dc.subjectLife Sciences
dc.subjectMedicine and Health Sciences
dc.titleDma1 prevents mitotic exit and cytokinesis by inhibiting the septation initiation network (SIN)
dc.typeJournal Article
dc.source.journaltitleDevelopmental cell
dc.source.volume3
dc.source.issue6
dc.identifier.legacycoverpagehttps://escholarship.umassmed.edu/gsbs_sp/451
dc.identifier.contextkey635946
html.description.abstract<p>In the fission yeast Schizosaccharomyces pombe, the septation initiation network (SIN) triggers cytokinesis after mitosis. We investigated the relationship between Dma1p, a spindle checkpoint protein and cytokinesis inhibitor, and the SIN. Deletion of dma1 inactivates the spindle checkpoint and allows precocious SIN activation, while overexpressing Dma1p reduces SIN signaling. Dma1p seems to function by inhibiting the SIN activator, Plo1p kinase, since dma1 overexpression and deletion phenotypes suggest that Dma1p antagonizes Plo1p localization. Furthermore, failure to maintain high cyclin-dependent kinase (CDK) activity during spindle checkpoint activation in dma1 deletion cells requires Plo1p. Dma1p itself localizes to spindle pole bodies through interaction with Sid4p. Our observations suggest that Dma1p functions to prevent mitotic exit and cytokinesis during spindle checkpoint arrest by inhibiting SIN signaling.</p>
dc.identifier.submissionpathgsbs_sp/451
dc.contributor.departmentDepartment of Molecular Genetics and Microbiology
dc.contributor.departmentGraduate School of Biomedical Sciences
dc.source.pages779-90


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