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Article: Id1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating Aurora A

TitleId1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating Aurora A
Authors
Issue Date2008
PublisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/
Citation
Molecular Biology Of The Cell, 2008, v. 19 n. 6, p. 2389-2401 How to Cite?
AbstractThe basic helix-loop-helix transcription factor, Id1, was shown to induce tetraploidy in telomerase-immortalized nasopharyngeal epithelial cells in this study. Using both transient and stable Id1-expressing cell models, multiple mitotic aberrations were detected, including centrosome amplification, binucleation, spindle defects, and microtubule perturbation. Many of these abnormal phenotypes have previously been reported in cells overexpressing Aurora A. Further experiments showed that Id1 could stabilize Aurora A, whereas knocking down Aurora A expression in Id1-expressing cells could rescue some of the mitotic defects. The mechanisms by which Aurora A could be modulated by Id1 were explored. DNA amplification of the Aurora A locus was not involved. Id1 could only weakly activate the transcriptional activity of the Aurora A promoter. We found that Id1 overexpression could affect Aurora A degradation, leading to its stabilization. Aurora A is normally degraded from mitosis exit by the APC/CCdh1-mediated proteasomal proteolysis pathway. Our results revealed that Id1 and Cdh1 are binding partners. The association of Id1 and Cdh1 was found to be dependent on the canonical destruction box motif of Id1, the increased binding of which may compete with the interaction between Cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells. © 2008 by The American Society for Cell Biology.
Persistent Identifierhttp://hdl.handle.net/10722/57291
ISSN
2015 Impact Factor: 4.037
2015 SCImago Journal Rankings: 3.665
PubMed Central ID
ISI Accession Number ID
Funding AgencyGrant Number
Research Grant Council, Hong KongHKU 7631/06M
HKU 7770/07M
Core Imaging Facility of the Faculty of Medicine, University of Hong
Funding Information:

We thank Prof. Akira Horii for providing the Aurora kinase A short hairpin constructs (pSR-shAURKA and pSR-shGL2) and Dr. J. Hasskarl for providing the flag-Id1 wild-type and mutant expression plasmids. We thank Prof. Yoshiaki Ishigatsubo for the Aurora A promoter luciferase constructs. This study was supported by Research Grant Council, Hong Kong grant HKU 7631/06M, HKU 7770/07M and the Core Imaging Facility of the Faculty of Medicine, University of Hong (for the live cell imaging study).

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DC FieldValueLanguage
dc.contributor.authorMan, Cen_HK
dc.contributor.authorRosa, Jen_HK
dc.contributor.authorYip, YLen_HK
dc.contributor.authorCheung, ALMen_HK
dc.contributor.authorKwong, YLen_HK
dc.contributor.authorDoxsey, SJen_HK
dc.contributor.authorTsao, SWen_HK
dc.date.accessioned2010-04-12T01:32:07Z-
dc.date.available2010-04-12T01:32:07Z-
dc.date.issued2008en_HK
dc.identifier.citationMolecular Biology Of The Cell, 2008, v. 19 n. 6, p. 2389-2401en_HK
dc.identifier.issn1059-1524en_HK
dc.identifier.urihttp://hdl.handle.net/10722/57291-
dc.description.abstractThe basic helix-loop-helix transcription factor, Id1, was shown to induce tetraploidy in telomerase-immortalized nasopharyngeal epithelial cells in this study. Using both transient and stable Id1-expressing cell models, multiple mitotic aberrations were detected, including centrosome amplification, binucleation, spindle defects, and microtubule perturbation. Many of these abnormal phenotypes have previously been reported in cells overexpressing Aurora A. Further experiments showed that Id1 could stabilize Aurora A, whereas knocking down Aurora A expression in Id1-expressing cells could rescue some of the mitotic defects. The mechanisms by which Aurora A could be modulated by Id1 were explored. DNA amplification of the Aurora A locus was not involved. Id1 could only weakly activate the transcriptional activity of the Aurora A promoter. We found that Id1 overexpression could affect Aurora A degradation, leading to its stabilization. Aurora A is normally degraded from mitosis exit by the APC/CCdh1-mediated proteasomal proteolysis pathway. Our results revealed that Id1 and Cdh1 are binding partners. The association of Id1 and Cdh1 was found to be dependent on the canonical destruction box motif of Id1, the increased binding of which may compete with the interaction between Cdh1 and Aurora A, leading to stabilization of Aurora A in Id1-overexpressing cells. © 2008 by The American Society for Cell Biology.en_HK
dc.languageengen_HK
dc.publisherAmerican Society for Cell Biology. The Journal's web site is located at http://www.molbiolcell.org/en_HK
dc.relation.ispartofMolecular Biology of the Cellen_HK
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.rightsMolecular Biology of the Cell. Copyright © American Society for Cell Biology.en_HK
dc.subject.meshInhibitor of Differentiation Protein 1 - chemistry - deficiency - metabolismen_HK
dc.subject.meshMitosisen_HK
dc.subject.meshPolyploidyen_HK
dc.subject.meshProtein-Serine-Threonine Kinases - genetics - metabolismen_HK
dc.subject.meshAmino Acid Motifsen_HK
dc.titleId1 overexpression induces tetraploidization and multiple abnormal mitotic phenotypes by modulating Aurora Aen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1059-1524&volume=19&issue=6&spage=2389&epage=2401&date=2008&atitle=Id1+overexpression+induces+tetraploidization+and+multiple+abnormal+mitotic+phenotypes+by+modulating+Aurora+Aen_HK
dc.identifier.emailCheung, ALM:lmcheung@hkucc.hku.hken_HK
dc.identifier.emailKwong, YL:ylkwong@hku.hken_HK
dc.identifier.emailTsao, SW:gswtsao@hkucc.hku.hken_HK
dc.identifier.authorityCheung, ALM=rp00332en_HK
dc.identifier.authorityKwong, YL=rp00358en_HK
dc.identifier.authorityTsao, SW=rp00399en_HK
dc.description.naturepublished_or_final_versionen_HK
dc.identifier.doi10.1091/mbc.E07-09-0875en_HK
dc.identifier.pmid18353975-
dc.identifier.pmcidPMC2397319en_HK
dc.identifier.scopuseid_2-s2.0-48749085488en_HK
dc.identifier.hkuros147169-
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-48749085488&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume19en_HK
dc.identifier.issue6en_HK
dc.identifier.spage2389en_HK
dc.identifier.epage2401en_HK
dc.identifier.eissn1939-4586-
dc.identifier.isiWOS:000259155200005-
dc.publisher.placeUnited Statesen_HK
dc.relation.projectMechanisms involved in Id1 induced centrosome abnormalities-
dc.identifier.scopusauthoridMan, C=7005722377en_HK
dc.identifier.scopusauthoridRosa, J=8758103700en_HK
dc.identifier.scopusauthoridYip, YL=7005596403en_HK
dc.identifier.scopusauthoridCheung, ALM=7401806497en_HK
dc.identifier.scopusauthoridKwong, YL=7102818954en_HK
dc.identifier.scopusauthoridDoxsey, SJ=7004246781en_HK
dc.identifier.scopusauthoridTsao, SW=7102813116en_HK

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