ArticleNature communications2026
GNL3 SUMOylation is essential for DNA double-strand break repair by homologous recombination.
Article in Nature communications, 2026. 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
DNA double-strand break repair via homologous recombination is critical for maintaining genomic integrity and requires proper DNA end resection. Here, we identify GNL3, a nucleolar GTP-binding protein, as a key regulator of homologous recombination in human cells via SUMOylation-dependent control of DNA end resection. Expression of wild-type GNL3, but not the SUMO-defective K196R mutant, abolished DNA damage induced by knockdown of endogenous GNL3. GNL3 interacts with the BLM-DNA2 helicase-nuclease complex, promoting DNA end resection and subsequent RPA and RAD51 loading. This interaction requires SUMOylation and SUMO-interacting motifs in both proteins. We further show that USP36 acts as a SUMO ligase for GNL3, while SENP3 deSUMOylates GNL3. Breast cancer-derived GNL3 variants disrupting its SUMOylation or SUMO-interacting motif fail to interact with the BLM-DNA2 complex. GNL3 depletion sensitizes homologous recombination-proficient breast cancer cells to etoposide and Olaparib treatment, highlighting GNL3 and its SUMOylation as potential therapeutic targets in cancer.
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