Cited by 48DNA Repair MechanismsCell death mechanisms and regulationGenetics, Aging, and Longevity in Model Organisms

NER and HR pathways act sequentially to promote UV-C-induced germ cell apoptosis in Caenorhabditis elegans

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Stergiou, L, Eberhard, R, Doukoumetzidis, K, Hengartner, M O·2011·Cell Death & Differentiation

Abstract

Ultraviolet (UV) radiation-induced DNA damage evokes a complex network of molecular responses, which culminate in DNA repair, cell cycle arrest and apoptosis. Here, we provide an in-depth characterization of the molecular pathway that mediates UV-C-induced apoptosis of meiotic germ cells in the nematode Caenorhabditis elegans. We show that UV-C-induced DNA lesions are not directly pro-apoptotic. Rather, they must first be recognized and processed by the nucleotide excision repair (NER) pathway. Our data suggest that NER pathway activity transforms some of these lesions into other types of DNA damage, which in turn are recognized and acted upon by the homologous recombination (HR) pathway. HR pathway activity is in turn required for the recruitment of the C. elegans homolog of the yeast Rad9-Hus1-Rad1 (9-1-1) complex and activation of downstream checkpoint kinases. Blocking either the NER or HR pathway abrogates checkpoint pathway activation and UV-C-induced apoptosis. Our results show that, following UV-C, multiple DNA repair pathways can cooperate to signal to the apoptotic machinery to eliminate potentially hazardous cells.

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  • In these conditions, repair may not be completed and ssDNA extension may both activate the checkpoint and channel the problematic lesion to another repair pathway such as recombination.

    “In these conditions, repair may not be completed and the extension of the ssDNA region may meet two purposes: activating the checkpoint response and channeling the problematic lesion to a different repair pathway (e.g., recombination) [66–68].”

    From Mind the gap: keeping UV lesions in check (2011) · cites this paper as [68]

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Authors
Stergiou, L., Eberhard, R., Doukoumetzidis, K., & Hengartner, M. O.
Affiliations
University of Zurich (CH)
Corresponding author
Hengartner, M O
Venue
Cell Death & Differentiation
Published
2010-12-10
Volume
18
Issue
5
Pages
897-906
ISSN
  • 1350-9047 (ISSN-L)
  • 1476-5403
OpenAlex
W2057510083
Cited by
48
References
40
Citations by year
2026: 1 · 2025: 1 · 2024: 3 · 2023: 1 · 2022: 2 · 2021: 5 · 2019: 2 · 2018: 4 · 2017: 3 · 2016: 3 · 2015: 3 · 2014: 7 · 2013: 5 · 2012: 3
FWCI
1.56
Type
journal article
Language
en
Open access
Locations
  • Cell Death and Differentiation (publishedVersion)
  • PubMed Central (publishedVersion)
  • PubMed (publishedVersion)
  • Zurich Open Repository and Archive (University of Zurich) (acceptedVersion, other-oa)
  • Zurich Open Repository and Archive (University of Zurich) (submittedVersion, other-oa)
  • Zurich Open Repository and Archive (University of Zurich)
Funders
  • National Science Foundation
  • Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung
  • National Institutes of Health
  • National Center for Research Resources
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Cell death mechanisms and regulation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Aging › Genetics, Aging, and Longevity in Model Organisms
Keywords
germ cells, nucleotide excision repair, homologous recombination, DNA damage response, meiotic cells, checkpoint kinase, Caenorhabditis elegans
MeSH terms
Animals, Cell Survival, DNA Repair, DNA-Binding Proteins, Endonucleases, Germ Cells, Pyrimidine Dimers, Recombination, Genetic, Ultraviolet Rays, Signal Transduction, Caenorhabditis elegans, Apoptosis, Cell Cycle Proteins, Caenorhabditis elegans Proteins, Animals, Genetically Modified, RNA Interference, Apoptosis Regulatory Proteins

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