| Literature DB >> 31624146 |
Nazli Deger1, Yanyan Yang2, Laura A Lindsey-Boltz2, Aziz Sancar3, Christopher P Selby4.
Abstract
Previous work with the classic T4 endonuclease V digestion of DNA from irradiated Drosophila cells followed by Southern hybridization led to the conclusion that Drosophila lacks transcription-coupled repair (TCR). This conclusion was reinforced by the Drosophila Genome Project, which revealed that Drosophila lacks Cockayne syndrome WD repeat protein (CSA), CSB, or UV-stimulated scaffold protein A (UVSSA) homologs, whose orthologs are present in eukaryotes ranging from Arabidopsis to humans that carry out TCR. A recently developed in vivo excision assay and the excision repair-sequencing (XR-Seq) method have enabled genome-wide analysis of nucleotide excision repair in various organisms at single-nucleotide resolution and in a strand-specific manner. Using these methods, we have discovered that Drosophila S2 cells carry out robust TCR comparable with that observed in mammalian cells. Our findings provide critical new insights into the mechanisms of TCR among various different species.Entities:
Keywords: CSB; Cockayne syndrome WD repeat protein (CSA); DNA transcription; Drosophila; RNA polymerase II; Rad26; Rad28; UV DNA damage; cyclobutane pyrimidine dimers; excision repair sequencing (XR-Seq); nucleotide excision repair; transcription-coupled repair (TCR)
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Year: 2019 PMID: 31624146 PMCID: PMC6885609 DOI: 10.1074/jbc.AC119.011448
Source DB: PubMed Journal: J Biol Chem ISSN: 0021-9258 Impact factor: 5.157