Abstract

Homologous chromosomes must pair and recombine to ensure faithful chromosome segregation during meiosis, a specialised type of cell division that occurs in sexually reproducing eukaryotes. Meiotic recombination initiates by programmed induction of DNA double-strand breaks (DSBs) by the conserved type II topoisomerase-like enzyme SPO11 . A subset of meiotic DSBs are resolved as crossovers, whereby reciprocal exchange of DNA occurs between homologous chromosomes. Importantly, DSBs are non-randomly distributed along eukaryotic chromosomes, forming preferentially in permissive regions known as hotspots. REC8 -cohesin organises an axis between the recombining chromosomes and is required to prevent fragmentation. Defective axis assembly occurs in Arabidopsis rec8 mutants, leading to catastrophic non-homologous recombination. In wild type, REC8 ChIP-seq shows strong enrichment in centromeric heterochromatin, where recombination is suppressed despite loading of the DSB machinery in these regions. Loss of the heterochromatic marks H3K9me2 and non-CG DNA methylation in kryptonite/suvh4 suvh5 suvh6 mutants causes remodelling of REC8 and gain of meiotic recombination in pericentromeric regions, although centromeric cohesion is maintained. In the chromosome arms, REC8 is enriched within gene bodies, exons and GC-rich sequences, and anti-correlates with transcription. Our findings therefore indicate that as REC8 organises meiotic chromosome architecture and interhomologue recombination, it is shaped by multiple chromatin states and transcription.