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Article: PRC1 cooperates with CLASP1 to organize central spindle plasticity in mitosis

TitlePRC1 cooperates with CLASP1 to organize central spindle plasticity in mitosis
Authors
Issue Date2009
PublisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/
Citation
Journal Of Biological Chemistry, 2009, v. 284 n. 34, p. 23059-23071 How to Cite?
AbstractDuring cell division, chromosome segregation is governed by the interaction of spindle microtubules with the kinetochore. A dramatic remodeling of interpolar microtubules into an organized central spindle between the separating chromatids is required for the initiation and execution of cytokinesis. Central spindle organization requires mitotic kinesins, microtubule-bundling protein PRC1, and Aurora B kinase complex. However, the precise role of PRC1 in central spindle organization has remained elusive. Here we show that PRC1 recruits CLASP1 to the central spindle at early anaphase onset. CLASP1 belongs to a conserved microtubule-binding protein family that mediates the stabilization of overlapping microtubules of the central spindle. PRC1 physically interacts with CLASP1 and specifies its localization to the central spindle. Repression of CLASP1 leads to sister-chromatid bridges and depolymerization of spindle midzone microtubules. Disruption of PRC1-CLASP1 interaction by a membrane-permeable peptide abrogates accurate chromosome segregation, resulting in sister chromatid bridges. These findings reveal a key role for the PRC1-CLASP1 interaction in achieving a stable anti-parallel microtubule organization essential for faithful chromosome segregation. We propose that PRC1 forms a link between stabilization of CLASP1 association with central spindle microtubules and anti-parallel microtubule elongation. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.
Persistent Identifierhttp://hdl.handle.net/10722/136774
ISSN
2015 Impact Factor: 4.258
2015 SCImago Journal Rankings: 3.151
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
National Institutes of HealthDK-56292
CA89019
CA92080
Chinese 973 Projects2002CB713700
2010CB912103
2007CB914503
2009CB861703
Chinese Academy of ScienceKSCX1-YW-R65
KSCX2-YW-H-10
Chinese Natural Science Foundation39925018
90508002
30870990
China National Key Projects for Infectious Disease2008ZX10002-021
Anhui Province Chemical Biology08040102005
Atlanta Clinical ant Translation Science Institute
Funding Information:

This work was supported, in whole or in part, by National Institutes of Health Grants DK-56292, CA89019, and CA92080 (to X. Y.). This work was also supported by Chinese 973 Projects 2002CB713700, 2010CB912103, 2007CB914503, and 2009CB861703, Chinese Academy of Science Grants KSCX1-YW-R65 and KSCX2-YW-H-10, Chinese Natural Science Foundation Grants 39925018 and 90508002 (to X. Y.) and 30870990 (to X. D.), China National Key Projects for Infectious Disease Grant 2008ZX10002-021, a Georgia Cancer Coalition Breast Cancer research grant, Anhui Province Chemical Biology Key Project Grant 08040102005, and an Atlanta Clinical ant Translation Science Institute research grant.

References

 

DC FieldValueLanguage
dc.contributor.authorLiu, Jen_HK
dc.contributor.authorWang, Zen_HK
dc.contributor.authorJiang, Ken_HK
dc.contributor.authorZhang, Len_HK
dc.contributor.authorZhao, Len_HK
dc.contributor.authorHua, Sen_HK
dc.contributor.authorYan, Fen_HK
dc.contributor.authorYang, Yen_HK
dc.contributor.authorWang, Den_HK
dc.contributor.authorFu, Cen_HK
dc.contributor.authorDing, Xen_HK
dc.contributor.authorGuo, Zen_HK
dc.contributor.authorYao, Xen_HK
dc.date.accessioned2011-07-29T02:11:58Z-
dc.date.available2011-07-29T02:11:58Z-
dc.date.issued2009en_HK
dc.identifier.citationJournal Of Biological Chemistry, 2009, v. 284 n. 34, p. 23059-23071en_HK
dc.identifier.issn0021-9258en_HK
dc.identifier.urihttp://hdl.handle.net/10722/136774-
dc.description.abstractDuring cell division, chromosome segregation is governed by the interaction of spindle microtubules with the kinetochore. A dramatic remodeling of interpolar microtubules into an organized central spindle between the separating chromatids is required for the initiation and execution of cytokinesis. Central spindle organization requires mitotic kinesins, microtubule-bundling protein PRC1, and Aurora B kinase complex. However, the precise role of PRC1 in central spindle organization has remained elusive. Here we show that PRC1 recruits CLASP1 to the central spindle at early anaphase onset. CLASP1 belongs to a conserved microtubule-binding protein family that mediates the stabilization of overlapping microtubules of the central spindle. PRC1 physically interacts with CLASP1 and specifies its localization to the central spindle. Repression of CLASP1 leads to sister-chromatid bridges and depolymerization of spindle midzone microtubules. Disruption of PRC1-CLASP1 interaction by a membrane-permeable peptide abrogates accurate chromosome segregation, resulting in sister chromatid bridges. These findings reveal a key role for the PRC1-CLASP1 interaction in achieving a stable anti-parallel microtubule organization essential for faithful chromosome segregation. We propose that PRC1 forms a link between stabilization of CLASP1 association with central spindle microtubules and anti-parallel microtubule elongation. © 2009 by The American Society for Biochemistry and Molecular Biology, Inc.en_HK
dc.languageengen_US
dc.publisherAmerican Society for Biochemistry and Molecular Biology, Inc. The Journal's web site is located at http://www.jbc.org/en_HK
dc.relation.ispartofJournal of Biological Chemistryen_HK
dc.titlePRC1 cooperates with CLASP1 to organize central spindle plasticity in mitosisen_HK
dc.typeArticleen_HK
dc.identifier.emailFu, C:chuanhai@hku.hken_HK
dc.identifier.authorityFu, C=rp01515en_HK
dc.description.naturelink_to_subscribed_fulltexten_US
dc.identifier.doi10.1074/jbc.M109.009670en_HK
dc.identifier.pmid19561070-
dc.identifier.pmcidPMC2755712-
dc.identifier.scopuseid_2-s2.0-69249127889en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-69249127889&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume284en_HK
dc.identifier.issue34en_HK
dc.identifier.spage23059en_HK
dc.identifier.epage23071en_HK
dc.identifier.eissn1083-351X-
dc.identifier.isiWOS:000268963100058-
dc.publisher.placeUnited Statesen_HK
dc.identifier.scopusauthoridLiu, J=36066808300en_HK
dc.identifier.scopusauthoridWang, Z=35103769100en_HK
dc.identifier.scopusauthoridJiang, K=26643372700en_HK
dc.identifier.scopusauthoridZhang, L=35104143400en_HK
dc.identifier.scopusauthoridZhao, L=16243104200en_HK
dc.identifier.scopusauthoridHua, S=35074095200en_HK
dc.identifier.scopusauthoridYan, F=35745269200en_HK
dc.identifier.scopusauthoridYang, Y=7409382210en_HK
dc.identifier.scopusauthoridWang, D=7407071911en_HK
dc.identifier.scopusauthoridFu, C=8583808400en_HK
dc.identifier.scopusauthoridDing, X=12140021800en_HK
dc.identifier.scopusauthoridGuo, Z=7404658143en_HK
dc.identifier.scopusauthoridYao, X=7402530401en_HK

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