HRR25, a putative protein kinase from budding yeast

Association with repair of damaged DNA

Merl F. Hoekstra, Robert (Mike) Liskay, Alan C. Ou, Anthony J. Demaggio, David G. Burbee, Fred Heffron

    Research output: Contribution to journalArticle

    138 Citations (Scopus)

    Abstract

    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.

    Original languageEnglish (US)
    Pages (from-to)1031-1034
    Number of pages4
    JournalScience
    Volume253
    Issue number5023
    StatePublished - Aug 30 1991

    Fingerprint

    Saccharomycetales
    DNA Repair
    Protein Kinases
    Mutation
    Methyl Methanesulfonate
    Phenotype
    Endonucleases
    Pheromones
    Homozygote
    Eukaryota
    Glutamine
    Proline
    Cell Division
    Genes
    Sequence Analysis
    Saccharomyces cerevisiae
    Cell Cycle
    Proteins
    Peptides
    DNA

    ASJC Scopus subject areas

    • General

    Cite this

    Hoekstra, M. F., Liskay, R. M., Ou, A. C., Demaggio, A. J., Burbee, D. G., & Heffron, F. (1991). HRR25, a putative protein kinase from budding yeast: Association with repair of damaged DNA. Science, 253(5023), 1031-1034.

    HRR25, a putative protein kinase from budding yeast : Association with repair of damaged DNA. / Hoekstra, Merl F.; Liskay, Robert (Mike); Ou, Alan C.; Demaggio, Anthony J.; Burbee, David G.; Heffron, Fred.

    In: Science, Vol. 253, No. 5023, 30.08.1991, p. 1031-1034.

    Research output: Contribution to journalArticle

    Hoekstra, MF, Liskay, RM, Ou, AC, Demaggio, AJ, Burbee, DG & Heffron, F 1991, 'HRR25, a putative protein kinase from budding yeast: Association with repair of damaged DNA', Science, vol. 253, no. 5023, pp. 1031-1034.
    Hoekstra MF, Liskay RM, Ou AC, Demaggio AJ, Burbee DG, Heffron F. HRR25, a putative protein kinase from budding yeast: Association with repair of damaged DNA. Science. 1991 Aug 30;253(5023):1031-1034.
    Hoekstra, Merl F. ; Liskay, Robert (Mike) ; Ou, Alan C. ; Demaggio, Anthony J. ; Burbee, David G. ; Heffron, Fred. / HRR25, a putative protein kinase from budding yeast : Association with repair of damaged DNA. In: Science. 1991 ; Vol. 253, No. 5023. pp. 1031-1034.
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    abstract = "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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    AU - Ou, Alan C.

    AU - Demaggio, Anthony J.

    AU - Burbee, David G.

    AU - Heffron, Fred

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    N2 - 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.

    AB - 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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