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Mutations of the CDC28 gene and the radiation sensitivity of Saccharomyces cerevisiae
Author(s) -
Koltovaya Natalia A.,
Arman Inga P.,
Devin Alexander B.
Publication year - 1998
Publication title -
yeast
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.923
H-Index - 102
eISSN - 1097-0061
pISSN - 0749-503X
DOI - 10.1002/(sici)1097-0061(19980130)14:2<133::aid-yea206>3.0.co;2-0
Subject(s) - biology , mutation , saccharomyces cerevisiae , mutagenesis , mutant , radiation sensitivity , genetics , microbiology and biotechnology , gene , cyclin dependent kinase 1 , cell cycle , irradiation , physics , nuclear physics
CDC28‐srm , a non‐temperature‐sensitive (ts) mutation in the CDC28 gene of Saccharomyces cerevisiae that affects fidelity of mitotic transmission of both mitochondrial and nuclear genetic structures (Devin et al ., 1990), also affected cell growth and sensitivity to lethal effects of ionizing radiation. At 30°C CDC28‐13 , a ts mutation, was without appreciable effects on spontaneous mitochondrial rho − ‐mutagenesis, cell growth and radiation sensitivity, whereas all three cell characteristics mentioned were affected (although to a lesser degree than by CDC28‐srm ) by CDC28‐1 , another ts mutation. CDC28‐srm was without any significant effect on the rates of spontaneous nuclear gene mutations and γ‐ray‐induced mitotic recombination. An analysis of double mutants as regards their radiation sensitivity has revealed additive or even synergistic interactions between the CDC28‐srm mutation and every one of the rad6‐1 and rad52‐1 mutations. The rad9 Δ allele was found to be epistatic to CDC28‐srm. These data suggest that the p34 CDC28 protein is involved in the RAD9‐dependent feedback control of DNA integrity operating at the cell cycle checkpoints. © 1998 John Wiley & Sons, Ltd.