biostudies-literatureClear ADNCI NIH HHS270-285https://www.ebi.ac.uk/biostudies/studies/S-EPMC7517009biostudies-literatureUnknown7(10)RAD52 is a structurally and functionally conserved component of the DNA double-strand break (DSB) repair apparatus from budding yeast to humans. We recently showed that expressing the human gene, <i>HsRAD52</i> in <i>rad52</i> mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that <i>HsRAD52</i> supports DSB repair by a mechanism of HRR that conserves genome structure and is independent of the canonical HR machinery. In this study we report that naturally occurring variants of <i>HsRAD52</i>, one of which suppresses the pathogenicity of <i>BRCA2</i> mutations, were unable to suppress the IR sensitivity and HRR defects of <i>rad52</i> mutant yeast cells, but fully suppressed a dMicrobial cell (Graz, Austria)Variants of the human <i>RAD52</i> gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast.PMC7517009R01 CA184585R50 CA211280Clear ADNegritto MCLewis OWolf EWOwens SBailis AMXu JManthey GMPerry JJPAdamson AWRico RKenjic NNeuhausen SLLopez IYfalseVariants of the human <i>RAD52</i> gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast.RAD52 is a structurally and functionally conserved component of the DNA double-strand break (DSB) repair apparatus from budding yeast to humans. We recently showed that expressing the human gene, <i>HsRAD52</i> in <i>rad52</i> mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that <i>HsRAD52</i> supports DSB repair by a mechanism of HRR that conserves genome structure and is independent of the canonical HR machinery. In this study we report that naturally occurring variants of <i>HsRAD52</i>, one of which suppresses the pathogenicity of <i>BRCA2</i> mutations, were unable to suppress the IR sensitivity and HRR defects of <i>rad52</i> mutant yeast cells, but fully suppressed a d2020-01-01T00:00:00Z2020 Jul2025-04-05T12:57:33.315Z2025-04-05T12:57:33.315ZS-EPMC75170093301514110.15698/mic2020.10.732