To better characterize the degree of meiotic progression in Trip13Gt/Gt spermatocytes, we immunostained chromosome spreads for SYCP3 and SYCP1, components of the axial/lateral elements and transverse filaments, respectively, of the synaptonemal complex (SC). Pachytene spermatocyte nuclei from postpubertal mutant testes could assemble normal SC cores and exhibited full synapsis of chromosomes as judged by colabeling of SYCP1 and SYCP3 along the full lengths of all autosomes (Figure 4A). Additionally, the X and Y chromosomes were normally synapsed at their pseudoautosomal region. More prepubertal (17.5 d postpartum) mutant spermatocytes contained asynaptic or terminally asynapsed chromosomes than age-matched controls (62.5% versus 25%, respectively; Figure 4B). We attribute this to a delay in the first wave of postnatal spermatogenesis (Figure 2D and 2E), likely related to systemic developmental retardation (Figure 2A and 2B). Nevertheless, since Trip13Gt/Gt spermatocytes progress to pachynema with no gross SC abnormalities, and oocytes were eliminated soon after birth (a characteristic of DNA repair mutants [13]), this suggested that unrepaired DSBs are responsible for eventual meiotic arrest and elimination.