Human Bub1 protects centromeric sister-chromatid cohesion through Shugoshin during mitosis

Tang, Zhanyun; Sun, Yuxiao; Harley, Sara E.; Zou, Hui; Yu, Hongtao

doi:10.1073/pnas.0408600102

Cited by 249 publications

(365 citation statements)

References 40 publications

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“…Cohesin binds densely to pericentric heterochromatin, and cohesin at centromeres is protected in both mitotic and meiotic cells by a member of the Shugoshin/Mei-S332 protein family (Kitajima et al 2004;McGuinness et al 2005;Salic et al 2004;Tang et al 1998Tang et al , 2004. Although Nipped-B completely colocalizes with Smc1 and Smc3 along meiotic chromosome cores, we did not see Nipped-B staining around the centromeres, where cohesin staining is the strongest.…”

Section: Does Nipped-b Regulate Cohesin Function At Centromeres?contrasting

confidence: 57%

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

et al. 2007

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Drosophila Nipped-B is an essential protein that has multiple functions. It facilitates expression of homeobox genes and is also required for sister chromatid cohesion. Nipped-B is conserved from yeast to man, and its orthologs also play roles in deoxyribonucleic acid repair and meiosis. Mutation of the human ortholog, Nipped-B-Like (NIPBL), causes Cornelia de Lange syndrome (CdLS), associated with multiple developmental defects. The Nipped-B protein family is required for the cohesin complex that mediates sister chromatid cohesion to bind to chromosomes. A key question, therefore, is whether the Nipped-B family regulates gene expression, meiosis, and development by controlling cohesin. To gain insights into Nipped-B's functions, we compared the effects of several Nipped-B mutations on gene expression, sister chromatid cohesion, and meiosis. We also examined association of Nipped-B and cohesin with somatic and meiotic chromosomes by immunostaining. Missense Nipped-B alleles affecting the same HEAT repeat motifs as CdLS-causing NIPBL mutations have intermediate effects on both gene expression and mitotic chromatid cohesion, linking these two functions and the role of NIPBL in human development. Nipped-B colocalizes extensively with cohesin on chromosomes in both somatic and meiotic cells and is present in soluble complexes

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Section: Does Nipped-b Regulate Cohesin Function At Centromeres?contrasting

confidence: 57%

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

et al. 2007

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“…This model may explain why we observed an increased distance between sister kinetochores in CENP-50 -deficient cells after long nocodazole treatment (Minoshima et al, 2005). There are reports in which the pathway of cohesin removal, which requires PLK1, is proteolysis independent (Tang et al, 2004;Kitajima et al, 2005;Resnick et al, 2006). Our findings related to CENP-O class proteins are distinct from the proteolysis-independent pathway of cohesin removal.…”

Section: Discussioncontrasting

confidence: 36%

CENP-O Class Proteins Form a Stable Complex and Are Required for Proper Kinetochore Function

Hori

Okada

Maenaka

et al. 2008

MBoC

126

183

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We previously identified a multisubunit complex (CENP-H/I complex) in kinetochores from human and chicken cells. We showed that the CENP-H/I complex is divided into three functional classes. In the present study, we investigated CENP-O class proteins, which include CENP-O, -P, -Q, -R, and -50 (U). We created chicken DT40 cell knockouts of each of these proteins, and we found that all knockout lines were viable, but that they showed slow proliferation and mitotic defects. Kinetochore localization of CENP-O, -P, -Q, and -50 was interdependent, but kinetochore localization of these proteins was observed in CENP-R-deficient cells. A coexpression assay in bacteria showed that CENP-O, -P, -Q, and -50 proteins form a stable complex that can associate with CENP-R. Phenotype analysis of knockout cells showed that all proteins except for CENP-R were required for recovery from spindle damage, and phosphorylation of CENP-50 was essential for recovery from spindle damage. We also found that treatment with the proteasome inhibitor MG132 partially rescued the severe mitotic phenotype observed in response to release from nocodazole block in CENP-50 -deficient cells. This suggests that CENP-O class proteins are involved in the prevention of premature sister chromatid separation during recovery from spindle damage.

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“…A similar conclusion can be drawn from the study of Bub1-null mouse embryonic fibroblasts (MEFs; Perera et al 2007). Bub1 is a component of the spindle assembly checkpoint, and it is also required for proper localization of Sgo at centromeres (Tang et al 2004;Kitajima et al 2005;Vaur et al 2005;Boyarchuk et al 2007). In Bub1-null MEFs treated with the APC/C inhibitor MG132 to prevent anaphase entry, there is no precocious separation of sister chromatids even though there is no Sgo1 at centromeres.…”

Section: Introductionmentioning

confidence: 99%

Shugoshin regulates cohesion by driving relocalization of PP2A in Xenopus extracts

Rivera

Losada

2008

Chromosoma

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Human Bub1 protects centromeric sister-chromatid cohesion through Shugoshin during mitosis

Cited by 249 publications

References 40 publications

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

Functional links between Drosophila Nipped-B and cohesin in somatic and meiotic cells

CENP-O Class Proteins Form a Stable Complex and Are Required for Proper Kinetochore Function

Shugoshin regulates cohesion by driving relocalization of PP2A in Xenopus extracts

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