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The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism

Journal Article:

Abstract

Damage-inducible mutagenesis in prokaryotes is largely dependent upon the activity of the UmuD'C-like proteins. Since many DNA repair processes are structurally and/or functionally conserved between prokaryotes and eukaryotes, we investigated the role of RAD30, a previously uncharacterized Saccharomyces cerevisiae DNA repair gene related to the Escherichia coli dinB, umuC and S. cerevisiae REV1 genes, in UV resistance and UV-induced mutagenesis. Similar to its prokaryotic homologues, RAD30 was found to be damage inducible. Like many S. cerevisiae genes involved in error-prone DNA repair, epistasis analysis clearly places RAD30 in the RAD6 group and rad30 mutants display moderate UV sensitivity reminiscent of rev mutants. However, unlike rev mutants, no defect in UV-induced reversion was seen in rad30 strains. While rad6 and rad18 are both epistatic to rad30, no epistasis was observed with rev1, rev3, rev7 or rad5, all of which are members of the RAD6 epistasis group. These findings suggest that RD30 participates in a novel error-free repair pathway dependent on RAD6 and RAD18, but independent of REV1, REV3, REV7 and RAD5. (author)
Authors:
McDonald, J. P.; [1]  Levine, A. S.; Woodgate, R.
  1. NIH, Bethesda, MD. (United States)
Publication Date:
Dec 15, 1997
Product Type:
Journal Article
Resource Relation:
Journal Name: Genetics; Journal Volume: 147; Journal Issue: 4; Other Information: FAO/AGRIS record; ARN: US1997082044; Country of input: International Atomic Energy Agency (IAEA)
Subject:
60 APPLIED LIFE SCIENCES; AMINO ACID SEQUENCE; DNA; DNA DAMAGES; DNA REPAIR; ERRORS; ESCHERICHIA COLI; FUNCTIONS; GENES; MESSENGER-RNA; MUTAGENESIS; MUTANTS; SACCHAROMYCES CEREVISIAE
OSTI ID:
22420934
Country of Origin:
FAO
Language:
English
Other Identifying Numbers:
Journal ID: ISSN 0016-6731; TRN: XF15A1321126830
Submitting Site:
INIS
Size:
page(s) 1557-1568
Announcement Date:
Jan 06, 2016

Journal Article:

Citation Formats

McDonald, J. P., Levine, A. S., and Woodgate, R. The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism. FAO: N. p., 1997. Web.
McDonald, J. P., Levine, A. S., & Woodgate, R. The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism. FAO.
McDonald, J. P., Levine, A. S., and Woodgate, R. 1997. "The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism." FAO.
@misc{etde_22420934,
title = {The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism}
author = {McDonald, J. P., Levine, A. S., and Woodgate, R.}
abstractNote = {Damage-inducible mutagenesis in prokaryotes is largely dependent upon the activity of the UmuD'C-like proteins. Since many DNA repair processes are structurally and/or functionally conserved between prokaryotes and eukaryotes, we investigated the role of RAD30, a previously uncharacterized Saccharomyces cerevisiae DNA repair gene related to the Escherichia coli dinB, umuC and S. cerevisiae REV1 genes, in UV resistance and UV-induced mutagenesis. Similar to its prokaryotic homologues, RAD30 was found to be damage inducible. Like many S. cerevisiae genes involved in error-prone DNA repair, epistasis analysis clearly places RAD30 in the RAD6 group and rad30 mutants display moderate UV sensitivity reminiscent of rev mutants. However, unlike rev mutants, no defect in UV-induced reversion was seen in rad30 strains. While rad6 and rad18 are both epistatic to rad30, no epistasis was observed with rev1, rev3, rev7 or rad5, all of which are members of the RAD6 epistasis group. These findings suggest that RD30 participates in a novel error-free repair pathway dependent on RAD6 and RAD18, but independent of REV1, REV3, REV7 and RAD5. (author)}
journal = {Genetics}
issue = {4}
volume = {147}
journal type = {AC}
place = {FAO}
year = {1997}
month = {Dec}
}