rec-1 loss of function increases recombination in the central gene clusters at the expense of autosomal pairing centers.

Meiotic control of crossover (CO) number and position is critical for homologous chromosome segregation and organismal fertility, recombination of parental genotypes, and the generation of novel genetic combinations. We here characterize the recombination rate landscape of a rec-1 loss of function modifier of CO position in Caenorhabditis elegans, one of the first ever modifiers discovered. By averaging CO position across hermaphrodite and male meioses and by genotyping 203 single-nucleotide variants covering about 95% of the genome, we find that the characteristic chromosomal arm-center recombination rate domain structure is lost in the loss of function rec-1 mutant.