The Saccharomyces cerevisiae MEC1 gene, which encodes a homolog of the human ATM gene product, is required for G1 arrest following radiation treatment

Author:

Siede W1,Allen J B1,Elledge S J1,Friedberg E C1

Affiliation:

1. Division of Cancer Biology, Department of Radiation Oncology and Winship Cancer Center, Emory University School of Medicine, Atlanta, Georgia 30322, USA.

Abstract

The Saccharomyces cerevisiae gene MEC1 represents a structural homolog of the human gene ATM mutated in ataxia telangiectasia patients. Like human ataxia telangiectasia cell lines, mec1 mutants are defective in G2 and S-phase cell cycle checkpoints in response to radiation treatment. Here we show an additional defect in G1 arrest following treatment with UV light or gamma rays and map a defective arrest stage at or upstream of START in the yeast cell cycle.

Publisher

American Society for Microbiology

Subject

Molecular Biology,Microbiology

Reference23 articles.

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2. The role of the ataxia telangiectasia gene in the p53, WAF1/CIP1(p21)- and GADD45-mediated response to DNA damage produced by ionising radiation;Artuso M.;Oncogene,1995

3. The p53-dependent G1 cell cycle checkpoint pathway and ataxiatelangiectasia;Canman C. E.;Cancer Res.,1994

4. p53-dependent inhibition of cyclindependent kinase activities in human fibroblasts during radiation-induced G1 arrest;Dulic V.;Cell,1994

5. TEL1, a gene involved in controlling telomere length in S. cerevisiae, is homologous to the human ataxia telangiectasia gene;Greenwell P. W.;Cell,1995

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