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 | |
| State | Published - 2001 |
| Externally published | Yes |
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ASJC Scopus subject areas
- Molecular Biology
Cite this
Regulation of Saccharomyces Rad53 checkpoint kinase during adaptation from DNA damage-induced G2/M arrest. / Pellicioli, Achille; Lee, Sang; Lucca, Chiara; Foiani, Marco; Haber, James E.
In: Molecular Cell, Vol. 7, No. 2, 2001, p. 293-300.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Regulation of Saccharomyces Rad53 checkpoint kinase during adaptation from DNA damage-induced G2/M arrest
AU - Pellicioli, Achille
AU - Lee, Sang
AU - Lucca, Chiara
AU - Foiani, Marco
AU - Haber, James E.
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.
UR - http://www.scopus.com/inward/record.url?scp=0035105240&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0035105240&partnerID=8YFLogxK
U2 - 10.1016/S1097-2765(01)00177-0
DO - 10.1016/S1097-2765(01)00177-0
M3 - Article
C2 - 11239458
AN - SCOPUS:0035105240
VL - 7
SP - 293
EP - 300
JO - Molecular Cell
JF - Molecular Cell
SN - 1097-2765
IS - 2
ER -