BioProject

In meiosis, an excess number of DNA double-strand breaks (DSBs), the initiating DNA lesion, is formed compared to the number of crossovers, one of their repair products that creates the physical links between homologs and allows their correct segregation. More...

In meiosis, an excess number of DNA double-strand breaks (DSBs), the initiating DNA lesion, is formed compared to the number of crossovers, one of their repair products that creates the physical links between homologs and allows their correct segregation. It is not known if all DSB hotspots are also crossover hotspots, or if the ratio between DSB and crossovers varies with the chromosomal location. Here, to systematically investigate variation in the DSB/crossover ratio, we have established the genome-wide map of the Zip3 protein binding sites in budding yeast meiosis. We show that Zip3 associates with DSB sites when these are engaged into repair by crossing over, and that Zip3 binding frequency at DSB reflects its tendency to be repaired as a crossover. We further show that the relative amount of Zip3 per DSB varies with the chromosomal location and identify chromosomal features associated with high or low Zip3 per DSB ratio. Among these is the negative regulation by proximity to a centromere and positive by the proximity to axis-associated sequences. This work opens interesting perspectives to understand the role of these extra DSB that are not frequently used for crossover and our findings may extend to mammals that have a large excess of DSB compared to crossovers. Overall design: ChIP-chip experiment in meiotic diploid SK1 yeast cells - two biological replicates Less...