ArticleCommunications biology2021
C. elegans TFIIH subunit GTF-2H5/TTDA is a non-essential transcription factor indispensable for DNA repair.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 13 citations in OpenAlex.
- L-citrulline protects testicular Sertoli cell function by mitigating DNA damage via the gut-testis axis of sheep fed a high-concentrate diet.NPJ biofilms and microbiomes · 2025Article
- Article
- Identification of candidate proteins influencing spermatogenesis in Shandong black cattle via integrated multiomics analysis.BMC genomics · 2025Article
- Xeroderma pigmentosum protein XPD controls caspase-mediated stress responses.Nature communications · 2024Article
- Persistent TFIIH binding to non-excised DNA damage causes cell and developmental failure.Nature communications · 2024Article
- Ribosomal Dysfunction Is a Common Pathomechanism in Different Forms of Trichothiodystrophy.Cells · 2023Article
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
The 10-subunit TFIIH complex is vital to transcription and nucleotide excision repair. Hereditary mutations in its smallest subunit, TTDA/GTF2H5, cause a photosensitive form of the rare developmental disorder trichothiodystrophy. Some trichothiodystrophy features are thought to be caused by subtle transcription or gene expression defects. TTDA/GTF2H5 knockout mice are not viable, making it difficult to investigate TTDA/GTF2H5 in vivo function. Here we show that deficiency of C. elegans TTDA ortholog GTF-2H5 is, however, compatible with life, in contrast to depletion of other TFIIH subunits. GTF-2H5 promotes TFIIH stability in multiple tissues and is indispensable for nucleotide excision repair, in which it facilitates recruitment of TFIIH to DNA damage. Strikingly, when transcription is challenged, gtf-2H5 embryos die due to the intrinsic TFIIH fragility in absence of GTF-2H5. These results support the idea that TTDA/GTF2H5 mutations cause transcription impairment underlying trichothiodystrophy and establish C. elegans as model for studying pathogenesis of this disease.
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