Heteromorphic sex chromosomes, such as the X/Y pair in mammals, differ in size and DNA sequence yet function as homologs during meiosis; this bivalent asymmetry presents special challenges for meiotic completion. In Caenorhabditis elegans males carrying mnT12, an X;IV fusion chromosome, mnT12 and IV form an asymmetric bivalent: chromosome IV sequences are capable of pairing and synapsis, while the contiguous X portion of mnT12 lacks a homologous pairing partner. Here, we investigate the meiotic behavior of this asymmetric neo-X/Y chromosome pair in C. elegans. Through immunolocalization of the axis component HIM-3, we demonstrate that the unpaired X axis has a distinct, coiled morphology while synapsed axes are linear and extended. By showing that loci at the fusion-proximal end of IV become unpaired while remaining synapsed as pachytene progresses, we directly demonstrate the occurrence of synaptic adjustment in this organism. We further demonstrate that meiotic crossover distribution is markedly altered in males with the asymmetric mnT12/1 bivalent relative to controls, resulting in greatly reduced crossover formation near the X;IV fusion point and elevated crossovers at the distal end of the bivalent. In effect, the distal end of the bivalent acts as a neo-pseudoautosomal region in these males. We discuss implications of these findings for mechanisms that ensure crossover formation during meiosis. Furthermore, we propose that redistribution of crossovers triggered by bivalent asymmetry may be an important driving force in sex chromosome evolution.

Meiosis is a specialized cell division that leads to a reduction of ploidy in sexually reproducing organisms through segregation of homologous chromosomes at the first meiotic division. Improper segregation of chromosomes during meiosis results in anueploidy, which is usually fatal during embryonic development. The meiotic process is therefore tightly regulated. Typically, proper segregation of homologs at meiosis I requires pairing of homologous chromosomes, followed by crossover recombination between homologs. Crossovers enable proper chromosomal segregation during the first meiotic division in part by establishing tension in the meiotic spindle. However, in the absence of crossovers, some cells maintain the ability to direct homologous chromosomes to opposite spindle poles, through a poorly understood mechanism known as distributive segregation.We are using the common brewers yeast Saccharomyces cerevisiae to determine possible roles of two genes in distributive segregation. The genes of interest, Ndj1 and Tid1, have been previously demonstrated to play a role in crossover interference, but their roles in distributive segregation are not well understood. Ndj1 has been shown to function in the tethering of telomeres to the nuclear envelope and may aid in the homology search chromosomes undergo. Tid1 has been characterized as a recombination accessory factor and may stimulate crossovers by directing recombinases to double strand break sites early in meiosis. To assay distributive segregation, we use yeast in which crossing over between one chromosome pair is prevented (due to sequence divergence). Using this system, we can assay the ability of yeast to carry out distributive segregation. Our results indicate that mutations in Ndj1 impair the ability of yeast to carry out distributive segregation, while mutations in Tid1 do not affect distributive segregation. These results, in turn, suggest that Ndj1 may play a role in distributive segregation. This experiment is part of a larger question to determine whether crossover assurance and crossover interference are independent mechanisms.