ArticleTransactions of the American Clinical and Climatological Association2025
THE GID COMPLEX REGULATES DNA END PROCESSING DURING DNA DOUBLE-STRAND BREAK REPAIR BY NONHOMOLOGOUS END JOINING.
Article in Transactions of the American Clinical and Climatological Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Genome instability is a hallmark of cancer, allowing for clonal evolution and improved tumor fitness. The mis-repair of DNA double-strand breaks (DSBs) is a major source of genome instability. DNA DSBs are normally repaired by homologous recombination (HR) and nonhomologous end joining (NHEJ). The nucleolytic resection of broken DNA ends generates single-stranded DNA (ssDNA) overhangs that are required for HR, but inhibitory to NHEJ. DNA end resection must be prevented in nondividing cells where NHEJ is the only active DSB repair pathway. Using a novel whole genome gRNA CRISPR/Cas9 screen, we identified the GID complex as functioning to protect DNA ends from nucleolytic resection. The GID complex contains multiple E3 ubiquitin ligase subunits and regulates the expression and function of pro-resection machinery. Thus, by antagonizing DNA end resection GID may prevent homology-mediated joining leading to aberrant DSB repair and genome instability in normal and cancerous nondividing cells.
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