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Mol Gen Genet. 1998 Dec;260(5):426-33.

Cut5 is a component of the UV-responsive DNA damage checkpoint in fission yeast.

Author information

1
Trescowthick Research Laboratories, Peter MacCallum Cancer Institute, Melbourne VIC, Australia.

Abstract

A checkpoint responding to DNA damage in G2 results in a delay in the onset of mitosis through inhibition of p34cdc2 kinase activity via maintenance of inhibitory tyrosine phosphorylation. Genetic analyses of this checkpoint in fission yeast have identified single alleles of several genes, suggesting these screens are not yet saturating, and hence further genes await identification. To fully understand the complexity of this checkpoint it will be necessary to define all the genes involved. To this end we screened for new mutants defective in the ability to delay mitosis in the presence of DNA-damaging agents. Twenty-four mutants were isolated that were defective in UV-C and MMS-induced checkpoint delay. Amongst these mutants was an allele of cut5 that was also defective in the checkpoint responses. We show here, contrary to previous reports, that the UV-C induced checkpoint response is defective in cut5 mutants. Therefore, like all other checkpoint mutants, cut5 is required for G2 checkpoint arrest following DNA damage, regardless of the nature of the lesions involved.

PMID:
9894912
DOI:
10.1007/s004380050913
[Indexed for MEDLINE]

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