ArticleCurrent genetics1995
RAD58 (XRS4)--a new gene in the RAD52 epistasis group.
Article in Current genetics, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
8 citing papers in PubMed.
- Multiple pathways of recombination induced by double-strand breaks in Saccharomyces cerevisiae.Microbiology and molecular biology reviews : MMBR · 1999Review
- The nuclease activity of Mre11 is required for meiosis but not for mating type switching, end joining, or telomere maintenance.Molecular and cellular biology · 1999Article
- Targeted inactivation of mouse RAD52 reduces homologous recombination but not resistance to ionizing radiation.Molecular and cellular biology · 1998Article
- A novel mre11 mutation impairs processing of double-strand breaks of DNA during both mitosis and meiosis.Molecular and cellular biology · 1998Article
- The Drosophila melanogaster RAD54 homolog, DmRAD54, is involved in the repair of radiation damage and recombination.Molecular and cellular biology · 1997Article
- Article
- Isolation of COM1, a new gene required to complete meiotic double-strand break-induced recombination in Saccharomyces cerevisiae.Genetics · 1997Article
- Mutations in two Ku homologs define a DNA end-joining repair pathway in Saccharomyces cerevisiae.Molecular and cellular biology · 1996Article
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The RAD58 (XRS4) gene of Saccharomyces cerevisiae has been previously identified as a DNA repair gene. In this communication, we show that RAD58 also encodes an essential meiotic function. The spore inviability of rad58 strains is not rescued by a spo13 mutation. The rad50 mutation suppresses spore inviability of a spo13 rad58 strain suggesting that RAD58 acts after RAD50 in meiotic recombination. The rad58-4 mutation does not prevent mitotic recombination events. Haploid rad58 cells fail to carry out G2-repair of gamma-induced lesions, whereas rad58/rad58 diploids are able to perform some diploid-specific repair of these lesions.
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Registered trials
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