PRDX5 Life Styles In The Rich And / or Renowned

Remarkably, ?80% (20/26) of the hrq1�� GCR events were TAs ( Table 2; Figure?3B). Also surprising, the events leading to the GCRs were different in hrq1-KA (4.5% Autophagy inhibitor concentration TA, 1/22) and hrq1�� (77% TAs) cells, even though the GCR rates were the same in?these strains (p?= 0.264). Thus, unlike Pif1, which requires helicase activity to inhibit telomerase ( Myung et?al., 2001a?and?Zhou et?al., 2000), Hrq1 inhibited TA noncatalytically. In addition, HRQ1 and PIF1 did not act synergistically to suppress TAs, because the two helicases did not have additive effects on TA: the fraction of TAs in hrq1�� pif1-m2 cells was Tariquidar order shifting the recombination-TA equilibrium toward TAs. The ability of Hrq1 PRDX5 to suppress TAs to DSBs suggested that, like Pif1, it might also inhibit telomerase lengthening of existing telomeres. However, telomere length was indistinguishable from WT in hrq1�� and hrq1-KA cells ( Figure?4A). In contrast, telomeres in hrq1�� pif1-m2 cells were even longer than in pif1-m2. The hyperlengthening of telomeres in hrq1�� pif1-m2 cells could be due to recombination or telomerase. To distinguish between these possibilities, we analyzed telomere length in spore clones from a pif1-m2/WT hrq1��/WT rad52��/WT diploid (Rad52 is a protein required for virtually all homologous recombination [HR] [ Hiom, 1999]). Telomeres were even longer in hrq1�� pif1-m2 rad52�� cells than in recombination-proficient cells ( Figure?4A), demonstrating that the hyperlengthening was not recombination dependent. Telomeres are also longer in rad52 versions of other mutants with long telomeres (e.g., rif1 and rif2), suggesting that HR suppresses elongation in cells that already have long telomeres ( Teng et?al., 2000?and?Zhou et?al., 2000). Thus, Hrq1 limits telomerase, not recombination, at pif1-m2 telomeres. Hrq1 did not act catalytically to inhibit telomerase at DSBs (Table 2). To determine if it acts catalytically to affect telomere length in pif1-m2 cells, we analyzed telomeres in hrq1-KA pif1-m2 and hrq1-KA pif1-m2 rad52�� cells.