Nucleic Acids Research, Vol 26, Issue 17 3971-3976, Copyright © 1998 by Oxford University Press
CM Udell, SK Lee and S Davey
Eukaryotic cells arrest at the G2checkpoint in the presence of DNA damage
or incompletely replicated DNA. This cell cycle checkpoint prevents the
development and propagation of genomic instability. In the fission yeast,
this process requires the action of a number of genes, including rad1(+) .
We report here the identification of human and mouse cDNAs that exhibit
extensive sequence homology to rad1(+) . The human gene, called HRAD1 ,
encodes a 282 amino acid protein that is 27% identical and 53% similar to
yeast Rad1p. The human homologue maintains its sequence similarity over the
full length of the protein, including the three proposed 3'-->5'
exonuclease domains, and the leucine rich repeat region. The mouse gene,
called MRAD1 , encodes a 280 amino acid protein that is 90% identical and
96% similar to HRAD1 at the amino acid level. Expression of HRAD1 in yeast
rad1 mutants partially restores radiation resistance and G2checkpoint
proficiency to these mutants. Evolutionaryconservation of structure between
HRAD1 , MRAD1 , rad1(+), Saccharomyces cerevisiae RAD17 and the Ustilago
maydis REC1 checkpoint genes suggests that the function of the encoded
proteins is conserved as well. The ability of HRAD1 to partially complement
yeast rad1 mutants suggests that this gene is required for G2checkpoint
control in human cells.
ARTICLES
HRAD1 and MRAD1 encode mammalian homologues of the fission yeast rad1(+) cell cycle checkpoint control gene
Cancer Research Laboratories, Department of Oncology and Department of Pathology, Queen's University, Kingston K7L 3N6, Canada.
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