HCR2 limits interfering crossovers in Arabidopsis thaliana

During meiosis the programmed DSBs (DNA double strand break sites) are induced by DNA topoisomerase II-like complexes. DSBs are processed to single strand DNAs that invade homologous chromosomes, producing intermediate joint molecules. The repair of joint molecules leads to a reciprocal crossover or a gene conversion event via different DNA repair pathways. The number of crossovers is limited to ~1–3 along chromosomes and crossover interference leads to more even distribution of crossovers. Approximately 80–85% crossovers are interfering and require ZMM proteins (ZIP4, MSH4, MSH5, MER3, HEI10, SHOC1, PTD, MLH1, MLH3), while 10–15% of crossovers are non-interfering and formed by MUS81 resolvase. Genetic disruption of FANCM, RECQ4 and FIGL1 increases non-interfering crossovers. However, how the number of interfering crossovers is limited remains largely unexplored. Here we isolated hcr2 (higher crossover rate 2) mutant via a genetic screening using fluorescent seed-based crossover measurement system. The hcr2 mutant shows increased crossover frequency in chromosome arms and similar crossover rates around centromeres, compared to wild type plant. HCR2 gene encodes a heat shock factor binding protein that is known as a negative transcriptional regulator in heat shock response. We found that the hcr2 mutation leads to increased transcript level of an E3 ligase gene HEI10, which promotes interfering-crossovers in a dosage dependent manner. Together, our data demonstrate that HCR2 is a novel transcriptional regulator limiting interfering crossovers.2