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Science 15 July 1988:
Vol. 241. no. 4863, pp. 317 - 322
DOI: 10.1126/science.3291120
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Articles

Science, Vol 241, Issue 4863, 317-322
Copyright © 1988 by American Association for the Advancement of Science

articles

The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae

TA Weinert and LH Hartwell

Department of Genetics, University of Washington, Seattle 98195.

Cell division is arrested in many organisms in response to DNA damage. Examinations of the genetic basis for this response in the yeast Saccharomyces cerevisiae indicate that the RAD9 gene product is essential for arrest of cell division induced by DNA damage. Wild-type haploid cells irradiated with x-rays either arrest or delay cell division in the G2 phase of the cell cycle. Irradiated G1 and M phase haploid cells arrest irreversibly in G2 and die, whereas irradiated G2 phase haploid cells delay in G2 for a time proportional to the extent of damage before resuming cell division. In contrast, irradiated rad9 cells in any phase of the cycle do not delay cell division in G2, but continue to divide for several generations and die. However, efficient DNA repair can occur in irradiated rad9 cells if irradiated cells are blocked for several hours in G2 by treatment with a microtubule poison. The RAD9-dependent response detects potentially lethal DNA damage and causes arrest of cells in G2 until such damage is repaired.


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mus304 encodes a novel DNA damage checkpoint protein required during Drosophila development.
M. H. Brodsky, J. J. Sekelsky, G. Tsang, R. S. Hawley, and G. M. Rubin (2000)
Genes & Dev. 14, 666-678
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Mik1 levels accumulate in S phase and may mediate an intrinsic link between S phase and mitosis.
P. U. Christensen, N. J. Bentley, R. G. Martinho, O. Nielsen, and A. M. Carr (2000)
PNAS 97, 2579-2584
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DNA Damage-Inducible and RAD52-Independent Repair of DNA Double-Strand Breaks in Saccharomyces cerevisiae.
C. W. Mo