File Download
  Links for fulltext
     (May Require Subscription)
Supplementary

Article: Mitotic slippage is determined by p31comet and the weakening of the spindle-assembly checkpoint

TitleMitotic slippage is determined by p31<sup>comet</sup> and the weakening of the spindle-assembly checkpoint
Authors
Issue Date2020
Citation
Oncogene, 2020, v. 39, n. 13, p. 2819-2834 How to Cite?
AbstractMitotic slippage involves cells exiting mitosis without proper chromosome segregation. Although degradation of cyclin B1 during prolonged mitotic arrest is believed to trigger mitotic slippage, its upstream regulation remains obscure. Whether mitotic slippage is caused by APC/CCDC20 activity that is able to escape spindle-assembly checkpoint (SAC)-mediated inhibition, or is actively promoted by a change in SAC activity remains an outstanding issue. We found that a major culprit for mitotic slippage involves reduction of MAD2 at the kinetochores, resulting in a progressive weakening of SAC during mitotic arrest. A further level of control of the timing of mitotic slippage is through p31comet-mediated suppression of MAD2 activation. The loss of kinetochore MAD2 was dependent on APC/CCDC20, indicating a feedback control of APC/C to SAC during prolonged mitotic arrest. The gradual weakening of SAC during mitotic arrest enables APC/CCDC20 to degrade cyclin B1, cumulating in the cell exiting mitosis by mitotic slippage.
Persistent Identifierhttp://hdl.handle.net/10722/307288
ISSN
2023 Impact Factor: 6.9
2023 SCImago Journal Rankings: 2.334
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorLok, Tsun Ming-
dc.contributor.authorWang, Yang-
dc.contributor.authorXu, Wendy Kaichun-
dc.contributor.authorXie, Siwei-
dc.contributor.authorMa, Hoi Tang-
dc.contributor.authorPoon, Randy Y.C.-
dc.date.accessioned2021-11-03T06:22:18Z-
dc.date.available2021-11-03T06:22:18Z-
dc.date.issued2020-
dc.identifier.citationOncogene, 2020, v. 39, n. 13, p. 2819-2834-
dc.identifier.issn0950-9232-
dc.identifier.urihttp://hdl.handle.net/10722/307288-
dc.description.abstractMitotic slippage involves cells exiting mitosis without proper chromosome segregation. Although degradation of cyclin B1 during prolonged mitotic arrest is believed to trigger mitotic slippage, its upstream regulation remains obscure. Whether mitotic slippage is caused by APC/CCDC20 activity that is able to escape spindle-assembly checkpoint (SAC)-mediated inhibition, or is actively promoted by a change in SAC activity remains an outstanding issue. We found that a major culprit for mitotic slippage involves reduction of MAD2 at the kinetochores, resulting in a progressive weakening of SAC during mitotic arrest. A further level of control of the timing of mitotic slippage is through p31comet-mediated suppression of MAD2 activation. The loss of kinetochore MAD2 was dependent on APC/CCDC20, indicating a feedback control of APC/C to SAC during prolonged mitotic arrest. The gradual weakening of SAC during mitotic arrest enables APC/CCDC20 to degrade cyclin B1, cumulating in the cell exiting mitosis by mitotic slippage.-
dc.languageeng-
dc.relation.ispartofOncogene-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleMitotic slippage is determined by p31<sup>comet</sup> and the weakening of the spindle-assembly checkpoint-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1038/s41388-020-1187-6-
dc.identifier.pmid32029899-
dc.identifier.pmcidPMC7098889-
dc.identifier.scopuseid_2-s2.0-85079706552-
dc.identifier.volume39-
dc.identifier.issue13-
dc.identifier.spage2819-
dc.identifier.epage2834-
dc.identifier.eissn1476-5594-
dc.identifier.isiWOS:000511540800001-

Export via OAI-PMH Interface in XML Formats


OR


Export to Other Non-XML Formats