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dc.contributor.authorChan, Leon Y.
dc.contributor.authorAmon, Angelika B.
dc.date.accessioned2013-03-06T22:00:37Z
dc.date.available2013-03-06T22:00:37Z
dc.date.issued2009-07
dc.identifier.issn0890-9369
dc.identifier.issn1549-5477
dc.identifier.urihttp://hdl.handle.net/1721.1/77594
dc.description.abstractIn budding yeast, a surveillance mechanism known as the spindle position checkpoint (SPOC) ensures accurate genome partitioning. In the event of spindle misposition, the checkpoint delays exit from mitosis by restraining the activity of the mitotic exit network (MEN). To date, the only component of the checkpoint to be identified is the protein kinase Kin4. Furthermore, how the kinase is regulated by spindle position is not known. Here, we identify the protein phosphatase 2A (PP2A) in complex with the regulatory subunit Rts1 as a component of the SPOC. Loss of PP2A-Rts1 function abrogates the SPOC but not other mitotic checkpoints. We further show that the protein phosphatase functions upstream of Kin4, regulating the kinase's phosphorylation and localization during an unperturbed cell cycle and during SPOC activation, thus defining the phosphatase as a key regulator of SPOC function.en_US
dc.description.sponsorshipNational Science Foundation (U.S.) (Predoctoral Fellowship)en_US
dc.description.sponsorshipNational Institutes of Health (U.S.) (grant GM056800)en_US
dc.description.sponsorshipHoward Hughes Medical Institute (Investigator)en_US
dc.language.isoen_US
dc.publisherCold Spring Harbor Laboratory Pressen_US
dc.relation.isversionofhttp://dx.doi.org/10.1101/gad.1804609en_US
dc.rightsCreative Commons Attribution-Noncommercial-Share Alike 3.0en_US
dc.rights.urihttp://creativecommons.org/licenses/by-nc-sa/3.0/en_US
dc.sourceAmon via Jennifer Ciminoen_US
dc.titleThe protein phosphatase 2A functions in the spindle position checkpoint by regulating the checkpoint kinase Kin4en_US
dc.typeArticleen_US
dc.identifier.citationChan, L. Y., and A. Amon. “The Protein Phosphatase 2A Functions in the Spindle Position Checkpoint by Regulating the Checkpoint Kinase Kin4.” Genes & Development 23.14 (2009): 1639–1649. CrossRef. Web.en_US
dc.contributor.departmentDavid H. Koch Institute for Integrative Cancer Research at MITen_US
dc.contributor.approverAmon, Angelika B.
dc.contributor.mitauthorAmon, Angelika B.
dc.contributor.mitauthorChan, Leon Y.
dc.relation.journalGenes & Developmenten_US
dc.eprint.versionAuthor's final manuscripten_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsChan, L. Y.; Amon, A.en
dc.identifier.orcidhttps://orcid.org/0000-0001-9837-0314
mit.licenseOPEN_ACCESS_POLICYen_US


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