ArticleNucleic acids research2013
Active transcriptomic and proteomic reprogramming in the C. elegans nucleotide excision repair mutant xpa-1.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
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- The Influence of 2'-Deoxyguanosine Lesions on the Electronic Properties ofMolecules (Basel, Switzerland) · 2024Review
- Biochemical and structural characterization of Fapy•dG replication by Human DNA polymerase β.Nucleic acids research · 2024Article
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- DNA repair, recombination, and damage signaling.Genetics · 2022Review
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- DNA damage and regulation of protein homeostasis.DNA repair · 2021Review
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- Xeroderma pigmentosum: overview of pharmacology and novel therapeutic strategies for neurological symptoms.British journal of pharmacology · 2019Review
- Measurement of Oxidatively Induced DNA Damage inAnalytical chemistry · 2019Article
- 5',8-Cyclopurine Lesions in DNA Damage: Chemical, Analytical, Biological, and Diagnostic Significance.Cells · 2019Review
- Article
- BRCA1 and BARD1 mediate apoptotic resistance but not longevity upon mitochondrial stress inEMBO reports · 2018Article
- Transcriptional consequences of XPA disruption in human cell lines.DNA repair · 2017Article
- Formation and repair of oxidatively generated damage in cellular DNA.Free radical biology & medicine · 2017Review
- The C. elegans model in toxicity testing.Journal of applied toxicology : JAT · 2017Review
- Nematode signaling molecules derived from multimodular assembly of primary metabolic building blocks.Organic letters · 2015Article
- Oxidative and energy metabolism as potential clues for clinical heterogeneity in nucleotide excision repair disorders.The Journal of investigative dermatology · 2015Review
Corrections and comments
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Authors and funding
17 authors at 4 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Transcription-blocking oxidative DNA damage is believed to contribute to aging and to underlie activation of oxidative stress responses and down-regulation of insulin-like signaling (ILS) in Nucleotide Excision Repair (NER) deficient mice. Here, we present the first quantitative proteomic description of the Caenorhabditis elegans NER-defective xpa-1 mutant and compare the proteome and transcriptome signatures. Both methods indicated activation of oxidative stress responses, which was substantiated biochemically by a bioenergetic shift involving increased steady-state reactive oxygen species (ROS) and Adenosine triphosphate (ATP) levels. We identify the lesion-detection enzymes of Base Excision Repair (NTH-1) and global genome NER (XPC-1 and DDB-1) as upstream requirements for transcriptomic reprogramming as RNA-interference mediated depletion of these enzymes prevented up-regulation of genes over-expressed in the xpa-1 mutant. The transcription factors SKN-1 and SLR-2, but not DAF-16, were identified as effectors of reprogramming. As shown in human XPA cells, the levels of transcription-blocking 8,5'-cyclo-2'-deoxyadenosine lesions were reduced in the xpa-1 mutant compared to the wild type. Hence, accumulation of cyclopurines is unlikely to be sufficient for reprogramming. Instead, our data support a model where the lesion-detection enzymes NTH-1, XPC-1 and DDB-1 play active roles to generate a genomic stress signal sufficiently strong to result in transcriptomic reprogramming in the xpa-1 mutant.
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