Cited by 292DNA Repair MechanismsFungal and yeast genetics researchBacterial Genetics and Biotechnology

Characterization of postreplication repair in Saccharomyces cerevisiae and effects of rad6, rad18, rev3 and rad52 mutations

Prakash, Louise·1981·Molecular and General Genetics MGG

Abstract

Postreplication repair of nuclear DNA was examined in an excision defective haploid strain of yeast lacking mitochondrial DNA (rad1 rho 0). The size of the DNA synthesized in cells exposed to various fluences of ultraviolet light (UV) corresponds approximately to the average interdimer distance in the parental DNA. Upon further incubation of cells following exposure to 2.5 J/m2, the DNA increases in size; by 4 h, it corresponds to DNA from uniformly labeled cells. The alkaline sucrose sedimentation pattern of DNA pulse labeled at various times after UV irradiation, for up to 4 h, does not change substantially, indicating that dimers continue to block DNA replication. A significant amount of postreplication repair requires de novo protein synthesis, as determined by its inhibition by cycloheximide. The rad6 mutant does not carry out postreplication repair, the rad18 and rad52 mutants show great inhibition while the rev3 mutation does not affect postreplication repair. Both recombinational and nonrecombinational repair mechanisms may function in postreplication repair and most of postreplication repair is error free.

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Crossref · 10.1007/bf00352525

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  • Blocked polymerases can leave the lesion and PCNA behind and re-initiate downstream via re-priming, generating numerous ssDNA gaps behind forks that likely cause strong Mec1 activation during S phase in UV-irradiated cells.

    “Blocked polymerase can leave the lesion and PCNA behind and re-initiate downstream of the lesion via a re-priming mechanism, generating numerous ssDNA gaps behind the forks, which are likely responsible for the strong activation of Mec1 during S phase in UV-irradiated cells [51,82–85].”

    From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [85]

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Authors
Prakash, L.
Affiliations
University of Rochester Medicine (US)
Corresponding author
Prakash, Louise
Venue
Molecular and General Genetics MGG
Published
1981-12
Volume
184
Issue
3
Pages
471-478
ISSN
  • 0026-8925 (ISSN-L)
  • 1432-1874
OpenAlex
W2045887257
Cited by
291
References
57
Citations by year
2026: 1 · 2025: 1 · 2024: 3 · 2022: 2 · 2021: 8 · 2020: 10 · 2019: 3 · 2018: 4 · 2017: 4 · 2016: 8 · 2015: 7 · 2014: 8 · 2013: 9 · 2012: 3
FWCI
2.06
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular and General Genetics MGG (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords
postreplication repair, Saccharomyces cerevisiae, UV-induced DNA damage, thymine dimers, DNA replication block, Rad6, RAD18, REV3, RAD52, mitochondrial DNA deletions, cycloheximide, recombinational repair, error-free repair
MeSH terms
Cycloheximide, DNA Repair, DNA Replication, DNA, Fungal, Kinetics, Molecular Weight, Mutation, Saccharomyces cerevisiae, Spheroplasts, Ultraviolet Rays

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