Data from budding yeast also indicate that Pch2p functions in recombination. Deletion of PCH2 delays meiotic progression by ∼2 h in SK1 yeast, and causes a minor decrease in ascus formation [50]. DSBs persist >2 h longer in pch2Δ yeast than in wild type, and hyperresection of DSBs in dmc1Δ pch2Δ double mutants is lower than in dmc1Δ cells [10]. Additionally, it was reported that pch2Δ yeast had a meiosis I delay dependent on the RAD17–SAE2 checkpoint that monitors recombination intermediates [12]. However, the exact role of TRIP13 (or Pch2) in recombination is unclear. Because synapsis occurs in TRIP13-deficient spermatocytes and is dependent on DSB formation (activity of SPO11 and MEI1), we suggest that TRIP13 functions after homology recognition and strand exchange, and that recombination events entering the CO repair pathway are either completed or nearly so (because OA treated resulted in bivalent chromosomes). One possibility for TRIP13′s role in recombination is that it is directly involved in a step specific to resolution of NCO recombination intermediates. Another possibility is that TRIP13 is required for disassembly of NCO recombinational repair complexes [51] containing those proteins that persist abnormally on Trip13Gt/Gt pachytene chromosomes. Notably, TRIP13 has two putative ATPase domains, a signature of AAA-ATPase ClpA/B chaperones that perform protein or protein/DNA complex disassembly [52]. These potential recombination roles might not be limited to meiosis, since Trip13 is widely transcribed and the mutant animals exhibited developmental defects. Finally, TRIP13 might play an indirect role, such as providing a “licensing” signal for the resolution of NCO intermediates and completion of meiosis.