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.
Publication types
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
Ataxia Telangiectasia / genetics
-
Ataxia Telangiectasia Mutated Proteins
-
Cell Cycle / genetics*
-
Cell Cycle Proteins
-
DNA-Binding Proteins
-
Dose-Response Relationship, Radiation
-
Fungal Proteins / metabolism*
-
Genes, Fungal*
-
Humans
-
Intracellular Signaling Peptides and Proteins
-
Mating Factor
-
Nocodazole / pharmacology
-
Peptides / pharmacology
-
Protein Serine-Threonine Kinases*
-
Proteins / genetics
-
Saccharomyces cerevisiae / cytology
-
Saccharomyces cerevisiae / drug effects
-
Saccharomyces cerevisiae / genetics*
-
Saccharomyces cerevisiae / radiation effects*
-
Saccharomyces cerevisiae Proteins*
-
Sequence Homology
-
Tumor Suppressor Proteins
-
Ultraviolet Rays
Substances
-
Cell Cycle Proteins
-
DNA-Binding Proteins
-
Fungal Proteins
-
Intracellular Signaling Peptides and Proteins
-
Peptides
-
Proteins
-
Saccharomyces cerevisiae Proteins
-
Tumor Suppressor Proteins
-
Mating Factor
-
ATM protein, human
-
Ataxia Telangiectasia Mutated Proteins
-
MEC1 protein, S cerevisiae
-
Protein Serine-Threonine Kinases
-
Nocodazole