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Mol Cell. 2001 Feb;7(2):293-300.

Regulation of Saccharomyces Rad53 checkpoint kinase during adaptation from DNA damage-induced G2/M arrest.

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1
Istituto F.I.R.C. di Oncologia Molecolare and, Dipartimento di Genetica e di Biologia dei, Microrganismi, Universita' degli Studi di Milano, 20133, Milan, Italy.

Abstract

Saccharomyces cells with one unrepaired double-strand break (DSB) adapt after checkpoint-mediated G2/M arrest. Adaptation is accompanied by loss of Rad53p checkpoint kinase activity and Chk1p phosphorylation. Rad53p kinase remains elevated in yku70delta and cdc5-ad cells that fail to adapt. Permanent G2/M arrest in cells with increased single-stranded DNA is suppressed by the rfa1-t11 mutation, but this RPA mutation does not suppress permanent arrest in cdc5-ad cells. Checkpoint kinase activation and inactivation can be followed in G2-arrested cells, but there is no kinase activation in G1-arrested cells. We conclude that activation of the checkpoint kinases in response to a single DNA break is cell cycle regulated and that adaptation is an active process by which these kinases are inactivated.

PMID:
11239458
DOI:
10.1016/s1097-2765(01)00177-0
[Indexed for MEDLINE]
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