Orderly segregation of chromosomes during meiosis requires that crossovers form between homologous chromosomes by recombination. Programmed DNA double-strand breaks (DSBs) initiate meiotic recombination. We identify ANKRD31 as a key component of complexes of DSB-promoting proteins that assemble on meiotic chromosome axes. Genome-wide, ANKRD31 deficiency causes delayed recombination initiation. In addition, loss of ANKRD31 alters DSB distribution because of reduced selectivity for sites that normally attract DSBs. Strikingly, ANKRD31 deficiency also abolishes uniquely high rates of recombination that normally characterize pseudoautosomal regions (PARs) of X and Y chromosomes. Consequently, sex chromosomes do not form crossovers, leading to chromosome segregation failure in ANKRD31-deficient spermatocytes. These defects co-occur with a genome-wide delay in assembling DSB-promoting proteins on autosome axes and loss of a specialized PAR-axis domain that is highly enriched for DSB-promoting proteins in wild type. Thus, we propose a model for spatiotemporal patterning of recombination by ANKRD31-dependent control of axis-associated DSB-promoting proteins. • Wild-type spatial positioning and timely initiation of recombination require ANKRD31 • Selective use of PRDM9 binding sites as DSB sites requires ANKRD31 • Enrichment of pro-DSB factors in the PAR requires ANKRD31 but not IHO1 • Recombination in the PAR depends on ANKRD31 Papanikos et al. identify ANKRD31 as a component of the DNA double-strand break-generating machinery, which initiates meiotic recombination. ANKRD31 is needed for timely recombination initiation. It prevents recombination initiation at promoters and ensures elevated recombination in the pseudoautosomal region, which permits correct sex chromosome segregation during male meiosis. [ABSTRACT FROM AUTHOR]