ArticleProceedings of the National Academy of Sciences of the United States of America2013
Roles of different pools of the mitotic checkpoint complex and the mechanisms of their disassembly.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 22 citations in OpenAlex.
- Role of phosphorylation of Cdc20 in the regulation of the action of APC/C in mitosis.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- Role of ubiquitin-protein ligase UBR5 in the disassembly of mitotic checkpoint complexes.Proceedings of the National Academy of Sciences of the United States of America · 2022Article
- TRIP13, identified as a hub gene of tumor progression, is the target of microRNA-4693-5p and a potential therapeutic target for colorectal cancer.Cell death discovery · 2022Article
- Role of Polo-like kinase 1 in the regulation of the action of p31Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Insights into a Crucial Role of TRIP13 in Human Cancer.Computational and structural biotechnology journal · 2019Review
- APC/C: current understanding and future perspectives.F1000Research · 2019Review
- Mechanism for remodelling of the cell cycle checkpoint protein MAD2 by the ATPase TRIP13.Nature · 2018Article
- USP9X Limits Mitotic Checkpoint Complex Turnover to Strengthen the Spindle Assembly Checkpoint and Guard against Chromosomal Instability.Cell reports · 2018Article
- TRIP13 promotes tumor growth and is associated with poor prognosis in colorectal cancer.Cell death & disease · 2018Article
- Role of ubiquitylation of components of mitotic checkpoint complex in their dissociation from anaphase-promoting complex/cyclosome.Proceedings of the National Academy of Sciences of the United States of America · 2018Article
- Visualizing the complex functions and mechanisms of the anaphase promoting complex/cyclosome (APC/C).Open biology · 2017Review
- Fission Yeast Apc15 Stabilizes MCC-Cdc20-APC/C Complexes, Ensuring Efficient Cdc20 Ubiquitination and Checkpoint Arrest.Current biology : CB · 2017Article
- TRIP13 impairs mitotic checkpoint surveillance and is associated with poor prognosis in multiple myeloma.Oncotarget · 2017Article
- Role of CCT chaperonin in the disassembly of mitotic checkpoint complexes.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Cryo-EM of Mitotic Checkpoint Complex-Bound APC/C Reveals Reciprocal and Conformational Regulation of Ubiquitin Ligation.Molecular cell · 2016Article
- Connecting the microtubule attachment status of each kinetochore to cell cycle arrest through the spindle assembly checkpoint.Chromosoma · 2015Review
- Spatiotemporal regulation of the anaphase-promoting complex in mitosis.Nature reviews. Molecular cell biology · 2015Review
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mitotic (or spindle assembly) checkpoint system prevents premature separation of sister chromatids in mitosis. When the checkpoint is turned on, the mitotic checkpoint complex (MCC) inhibits the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C). MCC is composed of the checkpoint proteins BubR1, Bub3, and Mad2 associated with the APC/C activator Cdc20. The mechanisms of the assembly of MCC when the checkpoint is turned on, and of its disassembly when the checkpoint is inactivated, are not sufficiently understood. Previous reports indicated that APC/C-mediated polyubiquitylation of Cdc20 in MCC is required for the dissociation of APC/C-associated MCC, but not of free MCC. The pool of free MCC is disassembled by an ATP-dependent process stimulated by the Mad2-binding protein p31(comet). It remained unknown whether free MCC is the precursor or the dissociation product of APC/C-bound MCC. By characterizing the mechanisms of the disassembly of APC/C-bound MCC in a purified system, we find that it cannot be the source of free MCC, because it is bound at high affinity and is released only in ubiquitylated or partially disassembled forms. By the use of a cell-free system from Xenopus eggs that reproduces the mitotic checkpoint, we show that MCC can be assembled in the absence of APC/C in a checkpoint-dependent manner. We propose that when the checkpoint is turned on, free MCC is the precursor of APC/C-bound MCC. When the mitotic checkpoint is extinguished, both APC/C-bound and free MCC pools have to be disassembled to release APC/C from inhibition.
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