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Science 30 August 1991:
Vol. 253. no. 5023, pp. 1031 - 1034
DOI: 10.1126/science.1887218
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Articles

Science, Vol 253, Issue 5023, 1031-1034
Copyright © 1991 by American Association for the Advancement of Science

articles

HRR25, a putative protein kinase from budding yeast: association with repair of damaged DNA

MF Hoekstra, RM Liskay, AC Ou, AJ DeMaggio, DG Burbee, and F Heffron

Molecular Biology and Virology Laboratory, Salk Institute for Biological Studies, La Jolla, CA 92186.

In simple eukaryotes, protein kinases regulate mitotic and meiotic cell cycles, the response to polypeptide pheromones, and the initiation of nuclear DNA synthesis. The protein HRR25 from the budding yeast Saccharomyces cerevisiae was defined by the mutation hrr25-1. This mutation resulted in sensitivity to continuous expression of the HO double-strand endonuclease, to methyl methanesulfonate, and to x-irradiation. Homozygotes of hrr25-1 were unable to sporulate and disruption and deletion of HRR25 interfered with mitotic and meiotic cell division. Sequence analysis revealed two distinctive regions in the protein. The NH2-terminus of HRR25 contains the hallmark features of protein kinases, whereas the COOH-terminus is rich in proline and glutamine. Mutations in HRR25 at conserved residues found in all protein kinases inactivated the gene, and these mutants exhibited the hrr25 null phenotypes. Taken together, the hrr25 mutant phenotypes and the features of the gene product indicate that HRR25 is a distinctive member of the protein kinase superfamily.


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