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dc.contributor.authorChan, Leon Y.
dc.contributor.authorFalk, Jill
dc.contributor.authorAmon, Angelika B
dc.date.accessioned2012-04-25T21:06:02Z
dc.date.available2012-04-25T21:06:02Z
dc.date.issued2011-08
dc.date.submitted2011-04
dc.identifier.issn0027-8424
dc.identifier.issn1091-6490
dc.identifier.urihttp://hdl.handle.net/1721.1/70141
dc.description.abstractFor a daughter cell to receive a complete genomic complement, it is essential that the mitotic spindle be positioned accurately within the cell. In budding yeast, a signaling system known as the spindle position checkpoint (SPOC) monitors spindle position and regulates the activity of the mitotic exit network (MEN), a GTPase signaling pathway that promotes exit from mitosis. The protein kinase Kin4 is a central component of the spindle position checkpoint. Kin4 primarily localizes to the mother cell and associates with spindle pole bodies (SPBs) located in the mother cell to inhibit MEN signaling. In contrast, the kinase does not associate with the SPB in the bud. Thus, only when a MEN bearing SPB leaves the mother cell and the spindle is accurately positioned along the mother–bud axis can MEN signaling occur and cell division proceed. Here, we describe a mechanism ensuring that Kin4 only associates with mother cell-located SPBs. The bud-localized MEN regulator Lte1, whose molecular function has long been unclear, prevents Kin4 that escapes into the bud from associating with SPBs in the daughter cell.en_US
dc.description.sponsorshipHoward Hughes Medical Instituteen_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.language.isoen_US
dc.publisherNational Academy of Sciences (U.S.)en_US
dc.relation.isversionofhttp://dx.doi.org/10.1073/pnas.1107784108en_US
dc.rightsArticle is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.en_US
dc.sourcePNASen_US
dc.titleLte1 promotes mitotic exit by controlling the localization of the spindle position checkpoint kinase Kin4en_US
dc.typeArticleen_US
dc.identifier.citationFalk, J. E., L. Y. Chan, and A. Amon. “Lte1 Promotes Mitotic Exit by Controlling the Localization of the Spindle Position Checkpoint Kinase Kin4.” Proceedings of the National Academy of Sciences 108.31 (2011): 12584–12590. Web.en_US
dc.contributor.departmentMassachusetts Institute of Technology. Department of Biological Engineeringen_US
dc.contributor.departmentKoch Institute for Integrative Cancer Research at MITen_US
dc.contributor.approverAmon, Angelika B.
dc.contributor.mitauthorAmon, Angelika B.
dc.contributor.mitauthorFalk, Jill E.
dc.contributor.mitauthorChan, Leon Y.
dc.relation.journalProceedings of the National Academy of Sciences of the United States of Americaen_US
dc.eprint.versionFinal published versionen_US
dc.type.urihttp://purl.org/eprint/type/JournalArticleen_US
eprint.statushttp://purl.org/eprint/status/PeerRevieweden_US
dspace.orderedauthorsFalk, J. E.; Chan, L. Y.; Amon, A.en
dc.identifier.orcidhttps://orcid.org/0000-0003-2910-9803
dc.identifier.orcidhttps://orcid.org/0000-0001-9837-0314
mit.licensePUBLISHER_POLICYen_US
mit.metadata.statusComplete


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