Cohesin association to replication sites depends on rad50 and promotes fork restart.
Cohesin association to replication sites depends on rad50 and promotes fork restart.
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DOI:
10.1016/j.molcel.2012.07.004
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发表时间:
2012-10-12
期刊:
影响因子:
16
通讯作者:
Cobb, Jennifer A.
中科院分区:
文献类型:
--
作者:
Tittel-Elmer, Mireille;Lengronne, Armelle;Davidson, Marta B.;Bacal, Julien;Francois, Philippe;Hohl, Marcel;Petrini, John H. J.;Pasero, Philippe;Cobb, Jennifer A.
The cohesin complex holds together newly-replicated chromatids and is involved in diverse pathways that preserve genome integrity. We show that in budding yeast, cohesin is transiently recruited to active replication origins and it spreads along DNA as forks progress. When DNA synthesis is impeded, cohesin accumulates at replication sites and is critical for the recovery of stalled forks. Cohesin enrichment at replication forks does not depend on γH2A(X) formation, which differs from its loading requirements at DNA double-strand breaks (DSBs). However, cohesin localization is largely reduced in rad50Δ mutants and cells lacking both Mec1 and Tel1 checkpoint kinases. Interestingly, cohesin loading at replication sites depends on the structural features of Rad50 that are important for bridging sister chromatids, including the CXXC hook domain and the length of the coiled-coil extensions. Together, these data reveal a function for cohesin in the maintenance of genome integrity during S phase.
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影响因子:
16.8
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影响因子:
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作者:
Bernard, Pascal;Drogat, Julie;Javerzat, Jean-Paul
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DOI:
10.1083/jcb.200111002
发表时间:
2002-02-04
期刊:
The Journal of cell biology
影响因子:
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作者:
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影响因子:
64.5
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