Fig. 7

Decreased homologous synapsis but similar crossover rate in SHR males with Prdm9 deletions compared to wild-type. a, b Percentage of normal pachytene spermatocytes (with all autosomes synapsed). Each dot represents a single animal (over 50 cells). Antibodies used for the staining of chromosomal spreads are given in the headings of each graph. Nuclear spreads used for the analysis of autosomal synapsis in both a and b were used for the analysis of XY synapsis in c and d. c Percentage of nuclei with full autosomal synapsis out of nuclei with XY asynapsis in Prdm9-deficient and control rat testes. d percentage of nuclei with both autosomal and XY asynapsis in Prdm9-deficient and control rat testes. e, f, Examples of normal pachytene cells. Immunocytochemistry with antibodies against: e Synaptonemal complex (SYCP1, SYCP3) and chromatin surrounding DSB sites (γH2AX); f SYCP3, γH2AX, and unsynapsed chromosomal axes (HORMAD2). See Additional file 1: Fig. S6 for the images of representative nuclei from Prdm9-deficient males. Differences between Prdm9 genotypes were analyzed using LRM with subsequent Tukey test and Holm adjustment for multiple testing. g Representative image of chromosomal spread from a Prdm9-deficient rat immunostained for cyclin-dependent kinase 2 (CDK2) and synaptonemal complex (SYCP1), confirming that CDK2 localizes both to crossover nodules and telomeres as in the mouse. h Counts of autosomal crossover nodules per cell (N = 2 animals for both Prdm9^KO/wt and Prdm9^KO/KO, N = 1 for wild-type)