Several sources of DNA damage compromise the integrity and stability of the genome of every organism. Specifically, DNA double-strand breaks (DSBs) can have lethal consequences for the cell. To repair this type of DNA damage, the cells employ homology-directed repair pathways or non-homologous
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Several sources of DNA damage compromise the integrity and stability of the genome of every organism. Specifically, DNA double-strand breaks (DSBs) can have lethal consequences for the cell. To repair this type of DNA damage, the cells employ homology-directed repair pathways or non-homologous end joining. Homology-directed repair requires the activity of the
RAD52 epistasis group of genes. Rad52 is the main recombination protein in the budding yeast
Saccharomyces cerevisiae, and
rad52Δ mutants have been characterized to show severe defects in DSB repair and other recombination events. Here, we identified the
RAD52 gene in the budding yeast
Naumovozyma castellii. Our analysis showed that the primary amino acid sequence of
N. castellii Rad52 shared 70% similarity with
S. cerevisiae Rad52. To characterize the gene function, we developed
rad52Δ mutant strains by targeted gene replacement transformation. We found that
N. castellii rad52Δ mutants showed lowered growth capacity, a moderately altered cell morphology and increased sensitivity to genotoxic agents. The decreased viability of the
N. castellii rad52Δ mutants in the presence of genotoxic agents indicates that the role of the Rad52 protein in the repair of DNA damage is conserved in this species.
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