TY - JOUR
T1 - CDC5 and CKII control adaptation to the yeast DNA damage checkpoint
AU - Toczyski, David P.
AU - Galgoczy, David J.
AU - Hartwell, Leland H.
N1 - Funding Information:
We would like to thank members of the Hartwell laboratory for many useful discussions and comments on the manuscript, especially A. Paulovich and E. Foss. In addition, we would like to thank the following individuals for reagents, discussions during various stages of this work, and/or comments on the manuscript: in order of appearance, L. Sandell, V. Zakian, L. Breeden, S. Friend, B. Thornton, C. Nugent, J. Bachant, A. Murray, A. Emili, C. Glover, and many members of the Seattle area cell cycle community. Finally, we thank J. Charles, K. Hardwick, D. Morgan, A. Murray, and A. Rudner for communicating results prior to publication. This work was supported by the Jane Coffin Childs foundation (D. P. T.), the molecular training program in cancer research, grant CAO9437 (D. P. T.), a grant from the National Institutes of Health, General Medical Sciences (GM-17709), and a research professorship (L. H. H.) from the American Cancer Society.
PY - 1997/9/19
Y1 - 1997/9/19
N2 - A single double-stranded DNA (dsDNA) break will cause yeast cells to arrest in G2/M at the DNA damage checkpoint. If the dsDNA break cannot be repaired, cells will eventually override (that is, adapt to) this checkpoint, even though the damage that elicited the arrest is still present. Here, we report the identification of two adaptation-defective mutants that remain permanently arrested as large-budded cells when faced with an irreparable dsDNA break in a nonessential chromosome. This adaptation-defective phenotype was entirely relieved by deletion of RADg, a gene required for the G2/M DNA damage checkpoint arrest. We show that one mutation resides in CDCS, which encodes a polo-like kinase, whereas a second, less penetrant, adaptation- defective mutant is affected at the CKB2 locus, which encodes a nonessential specificity subunit of casein kinase II.
AB - A single double-stranded DNA (dsDNA) break will cause yeast cells to arrest in G2/M at the DNA damage checkpoint. If the dsDNA break cannot be repaired, cells will eventually override (that is, adapt to) this checkpoint, even though the damage that elicited the arrest is still present. Here, we report the identification of two adaptation-defective mutants that remain permanently arrested as large-budded cells when faced with an irreparable dsDNA break in a nonessential chromosome. This adaptation-defective phenotype was entirely relieved by deletion of RADg, a gene required for the G2/M DNA damage checkpoint arrest. We show that one mutation resides in CDCS, which encodes a polo-like kinase, whereas a second, less penetrant, adaptation- defective mutant is affected at the CKB2 locus, which encodes a nonessential specificity subunit of casein kinase II.
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U2 - 10.1016/S0092-8674(00)80375-X
DO - 10.1016/S0092-8674(00)80375-X
M3 - Article
C2 - 9323137
AN - SCOPUS:0030885666
SN - 0092-8674
VL - 90
SP - 1097
EP - 1106
JO - Cell
JF - Cell
IS - 6
ER -