PCH2, encoding a nucleolar-localized AAA-ATPase that was originally identified in an S. cerevisiae genetic screen for mutants that relieve pachytene arrest of asynaptic zip1 mutants [8], was recently determined to be an essential component of the pachytene synapsis (but not DSB repair) checkpoint in yeast and worms [2,12]. PCH2 orthologs are present in organisms that undergo synaptic meiosis, but not asynaptic meiosis, prompting the suggestion that a Pch2-dependent checkpoint evolved to monitor synaptonemal complex (SC) defects from yeast to humans [12]. Here, we generated mice deficient for the Trip13, the ortholog of PCH2, and evaluated whether it also plays a role in the pachytene checkpoint. Surprisingly, while we found no evidence for checkpoint function, we did uncover a potential role for this protein in noncrossover (NCO) repair of meiotic DSBs.