SGS1, the Saccharomyces cerevisiae homologue of BLM and WRN, suppresses genome instability and homeologous recombination

Nature Genetics

Volumn 27, Issue 1, 2001, Pages 113-116

  Myung, K ^a   Datta, A ^a   Chen, C ^a   Kolodner, R D ^a  

^a UNIVERSITY OF CALIFORNIA SAN DIEGO   (United States)

Author keywords

[No Author keywords available]

Indexed keywords

DNA; HELICASE;

ARTICLE; DNA SEQUENCE; FUNGUS GROWTH; GENETIC RECOMBINATION; GENOME; NONHUMAN; PHENOTYPE; PRIORITY JOURNAL; SACCHAROMYCES CEREVISIAE; YEAST;

ADENOSINE TRIPHOSPHATASES; BASE SEQUENCE; BLOOM SYNDROME; CHROMOSOME BREAKAGE; CHROMOSOME FRAGILITY; CHROMOSOMES, FUNGAL; DNA HELICASES; FUNGAL PROTEINS; GENES, FUNGAL; GENOME, FUNGAL; HUMANS; KINETICS; MOLECULAR SEQUENCE DATA; MUTATION; RECOMBINATION, GENETIC; RECQ HELICASES; SACCHAROMYCES CEREVISIAE; SACCHAROMYCES CEREVISIAE PROTEINS; SEQUENCE HOMOLOGY; WERNER SYNDROME;

ESCHERICHIA COLI; FUNGI; MYXOGASTRIA; SACCHAROMYCES CEREVISIAE;

EID: 0035158640     PISSN: 10614036     EISSN: None     Source Type: Journal    
DOI: 10.1038/83673     Document Type: Article

References (30)

1. Isolation and genetic characterization of a thymineless death-resistant mutant of Escherichia coli K12: Identification of a new mutation (recQ1) that blocks the RecF recombination pathway
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13. RecQ helicase, in concert with RecA and SSB proteins, initiates and disrupts DNA recombination
14. Homologous recombination is responsible for cell death in the absence of the Sgs1 and Srs2 helicases
15. The yeast Sgs1p helicase acts upstream of Rad53p in the DNA replication checkpoint and colocalizes with Rad53p in S-phase-specific foci
16. + regulates cell cycle checkpoint control and is homologous to the Bloom's syndrome disease gene
17. Replication focus-forming activity 1 and the Werner syndrome gene product
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27. Evidence for increased in vivo mutation and somatic recombination in Bloom's syndrome
28. RecQ DNA helicase is a suppressor of illegitimate recombination in Escherichia coli
29. The coding region of the Bloom syndrome BLM gene and of the CBL proto-oncogene is mutated in genetically unstable sporadic gastrointestinal tumors