p31<sup>comet</sup> acts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment

Hagan, Robert S; Manak, Michael S.; Buch, Håkon Kirkeby; Meier, Michelle G.; Meraldi, Patrick; Shah, Jagesh V.; Sorger, Peter K.

doi:10.1091/mbc.e11-03-0216

Cited by 52 publications

(63 citation statements)

References 41 publications

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“…The Mad2-binding protein p31 comet has important roles in checkpoint inactivation (11,12,14,(20)(21)(22) and MCC disassembly (10,21), and has been reported to bind to TRIP13 (16). We therefore examined whether the actions of TRIP13 described above require the participation of p31 comet .…”

Section: Resultsmentioning

confidence: 99%

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Eytan

Wang

Miniowitz-Shemtov

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

114

131

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Significance The mitotic checkpoint system has an important role to ensure accurate segregation of chromosomes in mitosis. This system regulates the activity of the ubiquitin ligase Anaphase-Promoting Complex/Cyclosome (APC/C) by the formation of a negatively acting Mitotic Checkpoint Complex (MCC). When the checkpoint is satisfied, MCC is disassembled, but the mechanisms of MCC disassembly are not well understood. We show here that the ATP-hydrolyzing enzyme Thyroid Receptor Interacting Protein 13 (TRIP13), along with the MCC-targeting protein p31 comet , promote the disassembly of the mitotic checkpoint complexes and the inactivation of the mitotic checkpoint. The results reveal an important molecular mechanism in the regulation of APC/C by the mitotic checkpoint.

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Section: Resultsmentioning

confidence: 99%

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Eytan

Wang

Miniowitz-Shemtov

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

114

131

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“…Still another, long-standing mystery is that though p31 comet binds to MCC already during active mitotic checkpoint (14,26,27), it acts only later to promote checkpoint silencing and exit from mitosis (14,15,(26)(27)(28). It is possible that p31 comet is converted to an active form when the checkpoint is turned off, or that an inhibitor of p31 comet action is eliminated at that time by some signal linked to the state of the mitotic checkpoint system.…”

Section: Discussionmentioning

confidence: 99%

Role of phosphorylation of Cdc20 in p31 ^comet -stimulated disassembly of the mitotic checkpoint complex

Miniowitz-Shemtov

Eytan

Ganoth

et al. 2012

Proc. Natl. Acad. Sci. U.S.A.

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The mitotic checkpoint system delays anaphase until all chromosomes are correctly attached to the mitotic spindle. When the checkpoint is turned on, it promotes the formation of the mitotic checkpoint complex (MCC), which inhibits the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C). MCC is composed of the checkpoint proteins BubR1, Bub3, and Mad2 bound to the APC/C activator Cdc20. When the checkpoint is satisfied, MCC is disassembled and APC/C becomes active. Previous studies have shown that the Mad2-binding protein p31 comet promotes the dissociation of Cdc20 from BubR1 in MCC in a process that requires ATP. We now show that a part of MCC dissociation is blocked by inhibitors of cyclin-dependent kinases (Cdks) and that purified Cdk1–cyclin B stimulates this process. The mutation of all eight potential Cdk phosphorylation sites of Cdc20 partially prevented its release from BubR1. Furthermore, p31 comet stimulated Cdk-catalyzed phosphorylation of Cdc20 in MCC. It is suggested that the binding of p31 comet to Mad2 in MCC may trigger a conformational change in Cdc20 that facilitates its phosphorylation by Cdk, and that the latter process may promote its dissociation from BubR1.

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“…[19][20][21][22][23][24][25][26][27][28] We queried the Oncomine database to examine the expression of p31…”

Section: P31mentioning

confidence: 99%

“…19 Overexpression of p31 Comet bypasses hyperactivation of the SAC caused by microtubule poisons. [20][21][22][23] Depletion of p31…”

Section: Introductionmentioning

confidence: 99%

Coordinated regulation of p31^Cometand Mad2 expression is required for cellular proliferation

Date¹,

Burrows²,

Venere³

et al. 2013

Cell Cycle

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p31^comet acts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment

Cited by 52 publications

References 41 publications

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Role of phosphorylation of Cdc20 in p31 ^comet -stimulated disassembly of the mitotic checkpoint complex

Coordinated regulation of p31^Cometand Mad2 expression is required for cellular proliferation

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p31comet acts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment

Cited by 52 publications

References 41 publications

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 comet

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 comet

Role of phosphorylation of Cdc20 in p31 comet -stimulated disassembly of the mitotic checkpoint complex

Coordinated regulation of p31Cometand Mad2 expression is required for cellular proliferation

Contact Info

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Resources

About

p31^comet acts to ensure timely spindle checkpoint silencing subsequent to kinetochore attachment

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Disassembly of mitotic checkpoint complexes by the joint action of the AAA-ATPase TRIP13 and p31 ^comet

Role of phosphorylation of Cdc20 in p31 ^comet -stimulated disassembly of the mitotic checkpoint complex

Coordinated regulation of p31^Cometand Mad2 expression is required for cellular proliferation