ArticleDNA repair2016
A C. elegans homolog for the UV-hypersensitivity syndrome disease gene UVSSA.
Article in DNA repair, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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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.
- Chromatin context shapes DNA damage formation and nucleotide excision repair dynamics in Caenorhabditis elegans.Nucleic acids research · 2025Article
- Review
- Review
- C. elegans TFIIH subunit GTF-2H5/TTDA is a non-essential transcription factor indispensable for DNA repair.Communications biology · 2021Article
- Article
- A C. elegans model for neurodegeneration in Cockayne syndrome.Nucleic acids research · 2020Article
- UVSSA, UBP12, and RDO2/TFIIS Contribute to Arabidopsis UV Tolerance.Frontiers in plant science · 2019Article
- A simple answer to complex questions: Caenorhabditis elegans as an experimental model for examining the DNA damage response and disease genes.Journal of cellular physiology · 2018Review
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
The transcription-coupled repair pathway (TC-NER) plays a vital role in removing transcription-blocking DNA lesions, particularly UV-induced damage. Clinical symptoms of the two TC-NER-deficiency syndromes, Cockayne syndrome (CS) and UV-hypersensitivity syndrome (UVSS) are dissimilar and the underlying molecular mechanism causing this difference in disease pathology is not yet clearly understood. UV-stimulated scaffold protein A (UVSSA) has been identified recently as a new causal gene for UVSS. Here we describe a functional homolog of the human UVSSA gene in the nematode Caenorhabditis elegans, uvs-1 (UVSSA-like-1). Mutations in uvs-1 render the animals hypersensitive to UV-B irradiation and transcription-blocking lesion-inducing illudin-M, similar to mutations in TC-NER deficient mutants. Moreover, we demonstrate that TC-NER factors including UVS-1 are required for the survival of the adult animals after UV-treatment.
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Registered trials
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