DNA-dependent cohesin cleavage by separase

Kucej, Martin; Zou, Hui

doi:10.4161/nucl.1.1.10010

Cited by 4 publications

(4 citation statements)

References 48 publications

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“…Indeed, the Mcd1/Scc1 cleavage products were less abundant in clb5⌬ clb6⌬ cells compared to wild-type cells. Mcd1/Scc1 cleavage occurs preferentially on the chromatin-associated pool of cohesin complexes (22,27). The data are therefore consistent with our observation that Mcd1/ Scc1 is less abundant on chromatin during S phase in clb5⌬ clb6⌬ cells than in wild-type cells.…”

Section: Discussionsupporting

confidence: 91%

S-Phase Cyclin-Dependent Kinases Promote Sister Chromatid Cohesion in Budding Yeast

Hsu

Tsai

et al. 2011

Molecular and Cellular Biology

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Genome stability depends on faithful chromosome segregation, which relies on maintenance of chromatid cohesion during S phase. In eukaryotes, Pds1/securin is the only known inhibitor that can prevent loss of cohesion. However, pds1⌬ yeast cells and securin-null mice are viable. We sought to identify redundant mechanisms that promote cohesion within S phase in the absence of Pds1 and found that cells lacking the S-phase cyclins Clb5 and Clb6 have a cohesion defect under conditions of replication stress. Similar to the phenotype of pds1⌬ cells, loss of cohesion in cells lacking Clb5 and Clb6 is dependent on Esp1. However, Pds1 phosphorylation by Cdk-cyclin is not required for cohesion. Moreover, cells lacking Clb5, Clb6, and Pds1 are inviable and lose cohesion during an unperturbed S phase, indicating that Pds1 and specific B-type cyclins promote cohesion independently of one another. Consistent with this, we find that Mcd1/Scc1 is less abundant on chromosomes in cells lacking Clb5 and Clb6 during replication stress. However, clb5⌬ clb6⌬ cells do accumulate Mcd1/Scc1 at centromeres upon mitotic arrest, suggesting that the cyclin-dependent mechanism is S phase specific. These data indicate that Clb5 and Clb6 promote cohesion which is then protected by Pds1 and that both mechanisms are required during replication stress.

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Section: Discussionsupporting

confidence: 91%

S-Phase Cyclin-Dependent Kinases Promote Sister Chromatid Cohesion in Budding Yeast

Hsu

Tsai

et al. 2011

Molecular and Cellular Biology

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“…We suggest that a dynamic entrapment of chromatins is important for achieving the appropriate distribution of cohesin complexes along the genome; remodeling intrachromatid loops; removing what could be topological barriers under certain conditions during transcription, repair, or replication; and dissolving inappropriate connections between nonsister chromatids. This is in addition to the value of protecting a large fraction of the cohesin pool from separase as a consequence of its prior dissociation from chromosomes during prophase ( Kucej and Zou, 2010 ). Given that releasing activity destroys a state catalyzed by kollerin, it is possible that defects caused by haploinsufficiency of kollerin’s Scc2/Nipbl subunit ( Pehlivan et al., 2012 ) that are characteristic of Cornelia de Lange syndrome might be caused at least in part by releasing activity.…”

Section: Discussionmentioning

confidence: 99%

Cohesin’s DNA Exit Gate Is Distinct from Its Entrance Gate and Is Regulated by Acetylation

Chan

Roig

et al. 2012

Cell

248

334

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SummarySister chromatid cohesion is mediated by entrapment of sister DNAs by a tripartite ring composed of cohesin’s Smc1, Smc3, and α-kleisin subunits. Cohesion requires acetylation of Smc3 by Eco1, whose role is to counteract an inhibitory (antiestablishment) activity associated with cohesin’s Wapl subunit. We show that mutations abrogating antiestablishment activity also reduce turnover of cohesin on pericentric chromatin. Our results reveal a “releasing” activity inherent to cohesin complexes transiently associated with Wapl that catalyzes their dissociation from chromosomes. Fusion of Smc3’s nucleotide binding domain to α-kleisin’s N-terminal domain also reduces cohesin turnover within pericentric chromatin and permits establishment of Wapl-resistant cohesion in the absence of Eco1. We suggest that releasing activity opens the Smc3/α-kleisin interface, creating a DNA exit gate distinct from its proposed entry gate at the Smc1/3 interface. According to this notion, the function of Smc3 acetylation is to block its dissociation from α-kleisin. The functional implications of regulated ring opening are discussed.

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“… 35 We also observed upregulation of the separase Espl1 at the GVBD stage, which is responsible for cohesion degradation and chromosome segregation. 36 …”

Section: Resultsmentioning

confidence: 99%

“…35 We also observed upregulation of the separase Espl1 at the GVBD stage, which is responsible for cohesion degradation and chromosome segregation. 36 It has been reported that fully grown GV oocytes become transcriptionally silent during the period before meiosis resumption until aer fertilization. 37 Among the differential proteins during oocyte maturation, we found 59 ribosomal proteins, the majority (98%) of which were downregulated (Fig.…”

Section: Ocam For Single-cell Proteome Proling Of Mouse Oocyte Matur...mentioning

confidence: 99%

On-capillary alkylation micro-reactor: a facile strategy for proteo-metabolome profiling in the same single cells

He,

Yuan,

Liang

et al. 2023

Chem. Sci.

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DNA-dependent cohesin cleavage by separase

Cited by 4 publications

References 48 publications

S-Phase Cyclin-Dependent Kinases Promote Sister Chromatid Cohesion in Budding Yeast

S-Phase Cyclin-Dependent Kinases Promote Sister Chromatid Cohesion in Budding Yeast

Cohesin’s DNA Exit Gate Is Distinct from Its Entrance Gate and Is Regulated by Acetylation

On-capillary alkylation micro-reactor: a facile strategy for proteo-metabolome profiling in the same single cells

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