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Article: TAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity

TitleTAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity
Authors
KeywordsSpindle checkpoint
Bub1
Meiosis
p73
Mitotic arrest
Issue Date2009
Citation
Proceedings of the National Academy of Sciences of the United States of America, 2009, v. 106, n. 3, p. 797-802 How to Cite?
AbstractThe role of various p73 isoforms in tumorigenesis has been controversial. However, as we have recently shown, the generation of TAp73-deficient (TAp73-/-) mice reveals that TAp73 isoforms exert tumor-suppressive functions, indicating an emerging role for Trp-73 in the maintenance of genomic stability. Unlike mice lacking all p73 isoforms, TAp73-/- mice show a high incidence of spontaneous tumors. Moreover, TAp73-/- mice are infertile and produce oocytes exhibiting spindle abnormalities. These data suggest a link between TAp73 activities and the common molecular machinery underlying meiosis and mitosis. Previous studies have indicated that the spindle assembly checkpoint (SAC) complex, whose activation leads to mitotic arrest, also regulates meiosis. In this study, we demonstrate in murine and human cells that TAp73 is able to interact directly with several partners of the SAC complex (Bub1, Bub3, and BubR1). We also show that TAp73 is involved in SAC protein localization and activities. Moreover, we show that decreased TAp73 expression correlates with increases of SAC protein expression in patients with lung cancer. Our results establish TAp73 as a regulator of SAC responses and indicate that TAp73 loss can lead to mitotic arrest defects. Our data suggest that SAC impairment in the absence of functional TAp73 could explain the genomic instability and increased aneuploidy observed in TAp73-deficient cells. © 2009 by The National Academy of Sciences of the USA.
Persistent Identifierhttp://hdl.handle.net/10722/291874
ISSN
2023 Impact Factor: 9.4
2023 SCImago Journal Rankings: 3.737
PubMed Central ID
ISI Accession Number ID
Errata

 

DC FieldValueLanguage
dc.contributor.authorTomasini, Richard-
dc.contributor.authorTsuchihara, Katsuya-
dc.contributor.authorTsuda, Chiharu-
dc.contributor.authorLau, Suzanne K.-
dc.contributor.authorWilhelm, Margareta-
dc.contributor.authorRuffini, Alessandro-
dc.contributor.authorTsao, Ming Sound-
dc.contributor.authorIovanna, Juan L.-
dc.contributor.authorJurisicova, Andrea-
dc.contributor.authorMelino, Gerry-
dc.contributor.authorMak, Tak W.-
dc.date.accessioned2020-11-17T14:55:17Z-
dc.date.available2020-11-17T14:55:17Z-
dc.date.issued2009-
dc.identifier.citationProceedings of the National Academy of Sciences of the United States of America, 2009, v. 106, n. 3, p. 797-802-
dc.identifier.issn0027-8424-
dc.identifier.urihttp://hdl.handle.net/10722/291874-
dc.description.abstractThe role of various p73 isoforms in tumorigenesis has been controversial. However, as we have recently shown, the generation of TAp73-deficient (TAp73-/-) mice reveals that TAp73 isoforms exert tumor-suppressive functions, indicating an emerging role for Trp-73 in the maintenance of genomic stability. Unlike mice lacking all p73 isoforms, TAp73-/- mice show a high incidence of spontaneous tumors. Moreover, TAp73-/- mice are infertile and produce oocytes exhibiting spindle abnormalities. These data suggest a link between TAp73 activities and the common molecular machinery underlying meiosis and mitosis. Previous studies have indicated that the spindle assembly checkpoint (SAC) complex, whose activation leads to mitotic arrest, also regulates meiosis. In this study, we demonstrate in murine and human cells that TAp73 is able to interact directly with several partners of the SAC complex (Bub1, Bub3, and BubR1). We also show that TAp73 is involved in SAC protein localization and activities. Moreover, we show that decreased TAp73 expression correlates with increases of SAC protein expression in patients with lung cancer. Our results establish TAp73 as a regulator of SAC responses and indicate that TAp73 loss can lead to mitotic arrest defects. Our data suggest that SAC impairment in the absence of functional TAp73 could explain the genomic instability and increased aneuploidy observed in TAp73-deficient cells. © 2009 by The National Academy of Sciences of the USA.-
dc.languageeng-
dc.relation.ispartofProceedings of the National Academy of Sciences of the United States of America-
dc.subjectSpindle checkpoint-
dc.subjectBub1-
dc.subjectMeiosis-
dc.subjectp73-
dc.subjectMitotic arrest-
dc.titleTAp73 regulates the spindle assembly checkpoint by modulating BubR1 activity-
dc.typeArticle-
dc.description.naturelink_to_OA_fulltext-
dc.identifier.doi10.1073/pnas.0812096106-
dc.identifier.pmid19139399-
dc.identifier.pmcidPMC2621249-
dc.identifier.scopuseid_2-s2.0-58849134327-
dc.identifier.volume106-
dc.identifier.issue3-
dc.identifier.spage797-
dc.identifier.epage802-
dc.identifier.eissn1091-6490-
dc.identifier.isiWOS:000262809700024-
dc.relation.erratumdoi:10.1073/pnas.1814112115-
dc.relation.erratumeid:eid_2-s2.0-85053055113-
dc.identifier.issnl0027-8424-

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