Putative antirecombinase Srs2 DNA helicase promotes noncrossover homologous recombination avoiding loss of heterozygosity

Human health is generally maintained even when important genes are mutated because the human genome is diploid, with two sets of genomic DNA. Thus, various genes are heterozygous, with one functional and one defective allele at their loci. Somatic cells often incur DNA double-strand breaks by the direct effects of DNA-damaging agents, including oxidative stress, and indirectly, such as through DNA replication-fork collapse at damaged sites. Double-strand breaks are repaired through recombination processes, including homologous recombination and nonhomologous end-joining. These processes include the risk of losing a functional allele, called loss of heterozygosity (LOH). This study revealed that a putative antirecombinase, Srs2 DNA helicase, is a key enzyme to promote LOH-less recombination repair of double-strand breaks.