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Drosophila, which Lacks Canonical Transcription-Coupled Repair Proteins, Performs Transcription-Coupled Repair

ABSTRACT: Previous work with the classic T4 Endonuclease V digestion of irradiated Drosophila DNA followed by Southern hybridization led to the conclusion that Drosophila lacked transcription-coupled repair (TCR). This conclusion was reinforced by the Drosophila Genome Project which revealed that Drosophila lacked CSA, CSB, or UVSSA homologs, whose orthologs are present in eukaryotes that carry out TCR ranging from Arabidopsis to humans. 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 strand-specific manner. Using these methods, we have discovered that Drosophila S2 cells carry out robust TCR comparable to that observed in mammalian cells. Our findings provide new insights into the mechanisms of TCR among various species.

ORGANISM(S): Homo sapiens Drosophila melanogaster

PROVIDER: GSE138846 | GEO | 2019/10/16

REPOSITORIES: GEO

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Genome-wide repair maps of nucleotide excision repair in Drosophila and S2 cells.

Project description:We report the application of single-molecule-based sequencing technology (XR-seq) for high-throughput profiling of nucleotide excision repair in Drosophila four developmental stages and S2 cells. By obtaining over six billion bases of sequence from UV and cisplatin damage antibodies immunoprecipitated excision DNA, we generated genome-wide nucleotide excision repair maps of Drosophila Embryo, Larva, Pupa , two gender of adults and S2 cells . We find that Drosophila performs transcription-coupled repair (TCR) at all its developmental stages. S2 cell carry out TCR response to both UV and Cisplatin damage. Finally, we show that XPC repair factor is required for both global and transcription-coupled repair in Drosophila. This study provides the mechanism of nucleotide excision repair of Drosophila in vivo and vitro response to UV and Cisplatin damage.

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Genome-wide Transcription-coupled Repair in E.coli is Mediated by the Mfd Protein

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STK19 accelerates the clearance of lesion-stalled RNAPII to facilitate transcription-coupled DNA repair [BrU-seq]

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eXcision Repair-sequencing (XR-seq) to map UV induced damage in U2OS cells and in U2OS cells in which CSA or UVSSA genes were knocked out

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