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

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

PROVIDER: PRJNA577587 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10277907.fastq.gz	Fastqsanger.gz
	SRR10277908.fastq.gz	Fastqsanger.gz
	SRR10277909.fastq.gz	Fastqsanger.gz
	SRR10277910.fastq.gz	Fastqsanger.gz
	SRR10277911.fastq.gz	Fastqsanger.gz

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

Project description: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.

2019-10-16 | GSE138846 | GEO

<i>Drosophila</i>, which lacks canonical transcription-coupled repair proteins, performs transcription-coupled repair.

Project description: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.

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Project description:We have adapted the eXcision Repair-sequencing (XR-seq) method to generate single-nucleotide resolution dynamic repair maps of UV-induced cyclobutane pyrimidine dimers (CPD) photoproducts in the Caenorhabditis elegans (C. elegans) genome. We focus on the C. elegans ortholog of the human XPC-deficient strain (xpc-1) and its exclusive use of transcription-coupled repair. We provide evidence demonstrating the utility of xpc-1 XR-seq as a remarkable tool for detecting nascent transcription and identifying new transcripts. The integration of epigenetic markers, chromatin states, and non-coding RNA annotations supports the robust detection of intergenic nascent transcription by XR-seq. Overall, our results provide a comprehensive view of the transcription-coupled repair landscape in C. elegans, highlighting their potential contributions to our understanding of DNA repair mechanisms and non-coding RNA biology.

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Project description:PxP-MS (Purification of x-linked Proteins coupled to Mass Spectrometry) was used to assess the role of CSB in DNA-protein crosslink repair. The CSB protein is a sensor that can detect stalled RNA polymerases at sites of DNA damage, thereby triggering transcription-coupled repair mechanisms. DPCs were induced in WT and CSB knock-out RPE1 cells using a pulse of formaldehyde. To identify crosslinked proteins that specifically require CSB for repair, DNA-protein crosslinks were isolated from cells using PxP either directly after formaldehyde exposure or following a chase in drug-free media and identified by mass spectrometry.

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