MRE11 promotes homologous pairing independently of its role in double-strand break repair in allotetraploid Brassica napus

Abstract

Meiotic recombination is initiated by the formation of DNA double-strand breaks (DSBs), whose subsequent resection is essential for their repair, thereby promoting homologous pairing, synapsis, and crossover formation. The conserved MRE11 protein, a core component of the MRE11-RAD50-NBS1 complex, has been established as a key factor in DSB resection during meiosis. However, whether MRE11 has other functions independently of its role in DSB repair remains unclear. Here, we investigate the role of MRE11 in the allotetraploid crop Brassica napus, which harbours two homologous MRE11 genes, enabling dosage-dependent functional analyses. We show that MRE11 localizes on meiotic chromosomes independently of both DSB formation and homologous pairing. Using CRISPR/Cas9-generated allelic mutant series, we demonstrate that while reduced MRE11 dosage is sufficient to support DSB repair as indicated by the absence of chromosome fragmentation, it leads to defects in homologous pairing and synapsis, resulting in the presence of univalents. In contrast, a hypomorphic homozygous mre11 mutant exhibits severe defects in DSB processing, causing severe chromosome fragmentation that is epistemically suppressed by eliminating SPO11–1-mediated DSB formation. Together, our results uncouple the roles of MRE11 in DSB repair and chromosome pairing, revealing a previously unrecognized, dosage-sensitive function of MRE11 in promoting homologous pairing and synapsis. These findings redefine the meiotic role of MRE11 and highlight a direct contribution of a conserved DNA repair factor to homologous pairing in plants.