Regarding the cause of cell death in Trip13 mutants, our data indicate that this is triggered by defective DSB repair rather than asynapsis. We base this conclusion on two observations: (1) oocyte elimination is dependent upon DSB formation and (2) synapsis is normal in spermatocytes of adult testes. Indeed, this mutant is unique in that recombination defects occur in the absence of asynapsis (e.g., as in Dmc1 knockouts). Thus, the Trip13 mutant provides the first evidence that unrepaired DNA damage alone can trigger the mammalian pachytene checkpoint response. Furthermore, our results allow us to conclude that oocytes and spermatocytes share a similar, if not identical, DNA damage pachytene checkpoint that is decoupled from a synapsis checkpoint.