Cohesin acetylation speeds the replication fork

Marie-Emilie Terret, Rebecca Sherwood, Sadia Rahman, Jun Qin and Prasad V. Jallepalli ()
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Marie-Emilie Terret: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA
Rebecca Sherwood: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA
Sadia Rahman: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA
Jun Qin: Center for Molecular Discovery, Verna and Marrs McLean, Baylor College of Medicine, Houston, Texas 77030, USA
Prasad V. Jallepalli: Molecular Biology Program, Memorial Sloan-Kettering Cancer Center, 1275 York Avenue, New York, New York 10065, USA

Nature, 2009, vol. 462, issue 7270, 231-234

Abstract: Cohesin acetylation Cohesin rings encircle pairs of sister DNA molecules during cell division to allow their proper segregation. These rings inhibit progression of the transcriptional apparatus, but do not prevent the replication machinery from duplicating the genome in the S phase of the cell cycle. Single-molecule analysis now shows that a replication complex (called replication factor C–CTF18 clamp loader) acetylates cohesin, thereby alleviating cohesin's association with regulatory factors and facilitating replication fork progression. Loss of acetylation, as observed in cells from patients with Roberts syndrome, causes defects in fork progression and the accumulation of DNA damage.

Date: 2009
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DOI: 10.1038/nature08550

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