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

Achille Pellicioli; Sang Eun Lee; Chiara Lucca; Marco Foiani; James E. Haber

doi:10.1016/S1097-2765(01)00177-0

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

Achille Pellicioli, Sang Eun Lee, Chiara Lucca, Marco Foiani, James E. Haber

Research output: Contribution to journal › Article › peer-review

224 Scopus citations

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 yku70Δ 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.

Original language	English (US)
Pages (from-to)	293-300
Number of pages	8
Journal	Molecular Cell
Volume	7
Issue number	2
DOIs	https://doi.org/10.1016/S1097-2765(01)00177-0
State	Published - 2001
Externally published	Yes

ASJC Scopus subject areas

Molecular Biology
Cell Biology

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title = "Regulation of Saccharomyces Rad53 checkpoint kinase during adaptation from DNA damage-induced G2/M arrest",

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 yku70Δ 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.",

author = "Achille Pellicioli and Lee, {Sang Eun} and Chiara Lucca and Marco Foiani and Haber, {James E.}",

note = "Funding Information: We wish to thank all members of J. E. H. and M. F.'s laboratory for enthusiastic discussions. We are grateful to T. Weinert, K. Labib, and J. Diffley for the gift of plasmids and S. Prinz and A. Amon for providing the cdc23-1 strain. M. F. is supported by grants from Associazione Italiana per la Ricerca sul Cancro and from Telethon-Italy (Grant No. E.1108). S. E. L. is a Hildegarde D. Becher Foundation fellow of The Leukemia and Lymphoma Society. J. E. H. is supported by a grant from DOE 99ER62729 and NIH GM20056 and by a John Simon Guggenheim Foundation Fellowship.",

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doi = "10.1016/S1097-2765(01)00177-0",

language = "English (US)",

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AU - Pellicioli, Achille

AU - Lee, Sang Eun

AU - Lucca, Chiara

AU - Foiani, Marco

AU - Haber, James E.

N1 - Funding Information: We wish to thank all members of J. E. H. and M. F.'s laboratory for enthusiastic discussions. We are grateful to T. Weinert, K. Labib, and J. Diffley for the gift of plasmids and S. Prinz and A. Amon for providing the cdc23-1 strain. M. F. is supported by grants from Associazione Italiana per la Ricerca sul Cancro and from Telethon-Italy (Grant No. E.1108). S. E. L. is a Hildegarde D. Becher Foundation fellow of The Leukemia and Lymphoma Society. J. E. H. is supported by a grant from DOE 99ER62729 and NIH GM20056 and by a John Simon Guggenheim Foundation Fellowship.

PY - 2001

Y1 - 2001

N2 - 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 yku70Δ 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.

AB - 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 yku70Δ 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.

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

Abstract

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