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Article: Orderly inactivation of the key checkpoint protein mitotic arrest deficient 2 (MAD2) during mitotic progression

TitleOrderly inactivation of the key checkpoint protein mitotic arrest deficient 2 (MAD2) during mitotic progression
Authors
Issue Date2011
Citation
Journal of Biological Chemistry, 2011, v. 286, n. 15, p. 13052-13059 How to Cite?
AbstractAnaphase is promoted by the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) only when all the chromosomes have achieved bipolar attachment to the mitotic spindles. Unattached kinetochores or the absence of tension between the paired kinetochores activates a surveillance mechanism termed the spindle-assembly checkpoint. A fundamental principle of the checkpoint is the activation of mitotic arrest deficient 2 (MAD2). MAD2 then forms a diffusible complex called mitotic checkpoint complex (designated as MAD2(MCC)) before it is recruited to APC/C (designated as MAD2 (APC/C)). Large gaps in our knowledge remain on how MAD2 is inactivated after the checkpoint is satisfied. In this study, we have investigated the regulation of MAD2-containing complexes during mitotic progression. Using selective immunoprecipitation of checkpoint components and gel filtration chromatography, we found that MAD2(MCC) and MAD2 (APC/C) were regulated very differently during mitotic exit. Temporally, MAD2(MCC) was broken down ahead of MAD2 (APC/C). The inactivation of the two complexes also displayed different requirements of proteolysis; although APC/C and proteasome activities were dispensable for MAD2(MCC) inactivation, they are required for MAD2(APC/C) inactivation. In fact, the degradation of CDC20 is inextricably linked to the breakdown of MAD2(APC/C). These data extended our understanding of the checkpoint complexes during checkpoint silencing. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/307110
ISSN
2020 Impact Factor: 5.157
2023 SCImago Journal Rankings: 1.766
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorMa, Hoi Tang-
dc.contributor.authorPoon, Randy Y.C.-
dc.date.accessioned2021-11-03T06:21:57Z-
dc.date.available2021-11-03T06:21:57Z-
dc.date.issued2011-
dc.identifier.citationJournal of Biological Chemistry, 2011, v. 286, n. 15, p. 13052-13059-
dc.identifier.issn0021-9258-
dc.identifier.urihttp://hdl.handle.net/10722/307110-
dc.description.abstractAnaphase is promoted by the ubiquitin ligase anaphase-promoting complex/cyclosome (APC/C) only when all the chromosomes have achieved bipolar attachment to the mitotic spindles. Unattached kinetochores or the absence of tension between the paired kinetochores activates a surveillance mechanism termed the spindle-assembly checkpoint. A fundamental principle of the checkpoint is the activation of mitotic arrest deficient 2 (MAD2). MAD2 then forms a diffusible complex called mitotic checkpoint complex (designated as MAD2(MCC)) before it is recruited to APC/C (designated as MAD2 (APC/C)). Large gaps in our knowledge remain on how MAD2 is inactivated after the checkpoint is satisfied. In this study, we have investigated the regulation of MAD2-containing complexes during mitotic progression. Using selective immunoprecipitation of checkpoint components and gel filtration chromatography, we found that MAD2(MCC) and MAD2 (APC/C) were regulated very differently during mitotic exit. Temporally, MAD2(MCC) was broken down ahead of MAD2 (APC/C). The inactivation of the two complexes also displayed different requirements of proteolysis; although APC/C and proteasome activities were dispensable for MAD2(MCC) inactivation, they are required for MAD2(APC/C) inactivation. In fact, the degradation of CDC20 is inextricably linked to the breakdown of MAD2(APC/C). These data extended our understanding of the checkpoint complexes during checkpoint silencing. © 2011 by The American Society for Biochemistry and Molecular Biology, Inc.-
dc.languageeng-
dc.relation.ispartofJournal of Biological Chemistry-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.titleOrderly inactivation of the key checkpoint protein mitotic arrest deficient 2 (MAD2) during mitotic progression-
dc.typeArticle-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.1074/jbc.M110.201897-
dc.identifier.pmid21335556-
dc.identifier.pmcidPMC3075651-
dc.identifier.scopuseid_2-s2.0-79953851782-
dc.identifier.volume286-
dc.identifier.issue15-
dc.identifier.spage13052-
dc.identifier.epage13059-
dc.identifier.eissn1083-351X-
dc.identifier.isiWOS:000289282200025-

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