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Variants of the human RAD52 gene confer defects in ionizing radiation resistance and homologous recombination repair in budding yeast

Alissa D. Clear, Glenn M. Manthey, Olivia Lewis, Isabelle Y. Lopez, Rossana Rico, Shannon Owens, M. Cristina Negritto, Elise W. Wolf, Jason Xu, Nikola Kenjić, J. Jefferson P. Perry, Aaron W. Adamson, Susan L. Neuhausen, Adam M. Bailis

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, HsRAD52 in rad52 mutant budding yeast cells can suppress both their ionizing radiation (IR) sensitivity and homologous recombination repair (HRR) defects. Intriguingly, we observed that HsRAD52 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 HsRAD52, one of which suppresses the pathogenicity of BRCA2 mutations, were unable to suppress the IR sensitivity and (…)

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