Novel pof1 mutation suppresses the sensitivity to DNA replication inhibitor in fission yeast RecQ helicase mutant

Homologous recombination is vital for DNA double-strand break repair. Dysfunction in homologous recombination can lead to cell death, mutations, and cancer. In fission yeast (Schizosaccharomyces pombe), RecQ helicase Rqh1 resolves recombination intermediates. We found that rqh1-hd strain impaired growth in media containing hydroxyurea and thiabendazole. Using this condition, we identified a novel pof1 mutation (pof1-A81T) that suppress the poor growth of the rqh1-hd strain on the plate containing hydroxyurea and thiabendazole. Compared to rqh1-hd, rqh1-hd pof1-A81T cells displayed reduced Replication Protein A foci on chromosome bridges after hydroxyurea treatment. This suggests that pof1-A81T mutation suppresses the accumulation of recombination intermediates in hydroxyurea-treated rqh1-hd cells. Additionally, pof1-A81T mutation rescued the segregation defect of nucleolar protein Gar2 observed in hydroxyurea-treated rqh1-hd cells, potentially by mitigating recombination intermediate accumulation in rDNA. These results suggest that the pof1-A81T mutation suppresses the accumulation of recombination intermediates, particularly in rDNA, and alleviates the rqh1 deficiency phenotype in S. pombe. [Display omitted] •pof1 mutation suppresses the sensitivity to DNA replication inhibitor in rqh1 mutant.•pof1 mutation suppresses the accumulation of recombination intermediates in rqh1 mutant.•pof1 mutation may lead to the accumulation of the protein that suppresses the accumulation of recombination intermediates.