The pachytene checkpoint is known to monitor two aspects of meiotic chromosome metabolism in S. cerevisiae and C. elegans: (1) DSB repair and (2) chromosome synapsis [2,12]. In mice, both spermatocytes and oocytes harboring mutations that disrupt DSB repair (such as Dmc1, Msh5, and Atm) are efficiently eliminated in pachynema, but spermatocytes are much more sensitive to DSB repair–independent synapsis defects than oocytes [13–15]. However, because recombination is required for synapsis in mice (mutations in recombination genes such as Dmc1 cause extensive asynapsis [16]), it has remained formally uncertain whether there is a distinct pachytene checkpoint that responds to defects in meiotic recombination, and if so, whether it would be identical to that used in somatic cells. The mechanisms of putative pachytene checkpoint control remain unknown in mammals, since no mutations have been identified that abolish it.