ArticleMolecular biology of the cell2002
DNA repair and transcriptional effects of mutations in TFIIH in Drosophila development.
Article in Molecular biology of the cell, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 31 citations in OpenAlex.
- Review
- Nucleotide excision repair genes shaping embryonic development.Open biology · 2019Review
- Controlling the Master: Chromatin Dynamics at the MYC Promoter Integrate Developmental Signaling.Genes · 2017Review
- Analysis of Drosophila p8 and p52 mutants reveals distinct roles for the maintenance of TFIIH stability and male germ cell differentiation.Open biology · 2016Article
- Defective Hfp-dependent transcriptional repression of dMYC is fundamental to tissue overgrowth in Drosophila XPB models.Nature communications · 2015Article
- A Drosophila XPD model links cell cycle coordination with neuro-development and suggests links to cancer.Disease models & mechanisms · 2015Article
- The basal transcription machinery as a target for cancer therapy.Cancer cell international · 2014Article
- Physical and functional interactions between Drosophila homologue of Swc6/p18Hamlet subunit of the SWR1/SRCAP chromatin-remodeling complex with the DNA repair/transcription factor TFIIH.The Journal of biological chemistry · 2012Article
- Penetrance of biallelic SMARCAL1 mutations is associated with environmental and genetic disturbances of gene expression.Human molecular genetics · 2012Article
- Drosophila p53 is required to increase the levels of the dKDM4B demethylase after UV-induced DNA damage to demethylate histone H3 lysine 9.The Journal of biological chemistry · 2010Article
- p8/TTDA overexpression enhances UV-irradiation resistance and suppresses TFIIH mutations in a Drosophila trichothiodystrophy model.PLoS genetics · 2008Article
- DNA repair and transcriptional deficiencies caused by mutations in the Drosophila p52 subunit of TFIIH generate developmental defects and chromosome fragility.Molecular and cellular biology · 2007Article
- Cdk7 is required for full activation of Drosophila heat shock genes and RNA polymerase II phosphorylation in vivo.Molecular and cellular biology · 2003Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mutations in XPB and XPD TFIIH helicases have been related with three hereditary human disorders: xeroderma pigmentosum, Cockayne syndrome, and trichothiodystrophy. The dual role of TFIIH in DNA repair and transcription makes it difficult to discern which of the mutant TFIIH phenotypes is due to defects in any of these different processes. We used haywire (hay), the Drosophila XPB homolog, to dissect this problem. Our results show that when hay dosage is affected, the fly shows defects in structures that require high levels of transcription. We found a genetic interaction between hay and cdk7, and we propose that some of these phenotypes are due to transcriptional deficiencies. We also found more apoptotic cells in imaginal discs and in the CNS of hay mutant flies than in wild-type flies. Because this abnormal level of apoptosis was not detected in cdk7 flies, this phenotype could be related to defects in DNA repair. In addition the apoptosis induced by p53 Drosophila homolog (Dmp53) is suppressed in heterozygous hay flies.
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