期刊
NATURE STRUCTURAL & MOLECULAR BIOLOGY
卷 20, 期 5, 页码 598-+出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/nsmb.2550
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资金
- Fondation Arc pour la Recherche sur le Cancer [SF1052]
- Centre National de la Recherche Scientifique (ATIP program)
- Agence Nationale de la Recherche of France [ANR-10-BLAN-1512-01]
- Agence Nationale de la Recherche [ANR-10-BLAN-1606-03]
- US National Institutes of Health [RO1 GM59447]
- Agence Nationale de la Recherche (ANR) [ANR-10-BLAN-1606, ANR-10-BLAN-1512] Funding Source: Agence Nationale de la Recherche (ANR)
Structure-specific DNA endonucleases have critical roles during DNA replication, repair and recombination, yet they also have the potential for causing genome instability. Controlling these enzymes may be essential to ensure efficient processing of ad hoc substrates and to prevent random, unscheduled processing of other DNA structures, but it is unknown whether structure-specific endonucleases are regulated in response to DNA damage. Here, we uncover DNA damage-induced activation of Mus81-Eme1 Holliday junction resolvase in fission yeast. This new regulation requires both Cdc2(CDK1)-and Rad3(ATR)-dependent phosphorylation of Eme1. Mus81-Eme1 activation prevents gross chromosomal rearrangements in cells lacking the BLM-related DNA helicase Rqh1. We propose that linking Mus81-Eme1 DNA damage-induced activation to cell-cycle progression ensures efficient resolution of Holliday junctions that escape dissolution by Rqh1-TopIII while preventing unnecessary DNA cleavages.
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