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

Ted A. Weinert, Leland Hartwell

Research output: Contribution to journalArticle

897 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)317-322
Number of pages6
JournalScience
Volume241
Issue number4863
StatePublished - 1988
Externally publishedYes

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cdc Genes
Cell Cycle Checkpoints
Cell Division
DNA Damage
Saccharomyces cerevisiae
Haploidy
G2 Phase
Poisons
G1 Phase
Microtubules
DNA Repair
Cell Cycle
Yeasts
X-Rays
Genes

ASJC Scopus subject areas

  • General

Cite this

The RAD9 gene controls the cell cycle response to DNA damage in saccharomyces cerevisiae. / Weinert, Ted A.; Hartwell, Leland.

In: Science, Vol. 241, No. 4863, 1988, p. 317-322.

Research output: Contribution to journalArticle

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abstract = "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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