Abstract
In eukaryotic cells, S phase can be reversibly arrested by drugs that inhibit DNA synthesis or DNA damage. Here we show that recovery from such treatments is under genetic control and is defective in fission yeast rqh1 mutants. rqh1+, previously known as hus2+, encodes a putative DNA helicase related to the Escherichia coli RecQ helicase, with particular homology to the gene products of the human BLM and WRN genes and the Saccharomyces cerevisiae SGS1 gene. BLM and WRN are mutated in patients with Bloom's syndrome and Werner's syndrome respectively. Both syndromes are associated with genomic instability and cancer susceptibility. We show that, like BLM and SGS1, rqh1+ is required to prevent recombination and that in fission yeast suppression of inappropriate recombination is essential for reversible S phase arrest.
Publication types
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Comparative Study
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Adenosine Triphosphatases / genetics
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Amino Acid Sequence
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Bloom Syndrome / genetics
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DNA Helicases / genetics*
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DNA Replication
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Exodeoxyribonucleases
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Gene Deletion
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Genes, Fungal*
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Hydroxyurea / pharmacology
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Mitosis / drug effects
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Mitosis / genetics*
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Mitosis / radiation effects
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Molecular Sequence Data
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Multigene Family
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RecQ Helicases
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Recombination, Genetic
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S Phase / genetics*
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Schizosaccharomyces / genetics*
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Schizosaccharomyces pombe Proteins*
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Sequence Homology, Amino Acid
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Ultraviolet Rays
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Werner Syndrome / genetics
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Werner Syndrome Helicase
Substances
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Schizosaccharomyces pombe Proteins
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Exodeoxyribonucleases
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Adenosine Triphosphatases
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Bloom syndrome protein
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RECQL protein, human
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RecQ protein, E coli
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DNA Helicases
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RecQ Helicases
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WRN protein, human
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Werner Syndrome Helicase
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Rqh1 protein, S pombe
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Hydroxyurea