Distinct intersecting pathways link homolog pairing to initiation of meiotic chromosome synapsis

Abstract

ABSTRACTFaithful meiotic segregation requires pairwise alignment of the homologous chromosomes and Synaptonemal Complex assembly (SC) at their interface. Here, we investigate on new factors that promote and coordinate these events duringC. elegansmeiosis. We identify BRA-2 (BMPReceptorAssociated family member2)as an interactor of HIM-17, previously shown to promote double-strand break formation. We found that loss ofbra-2specifically impairs synapsis licensing without affecting homologs recognition, SC maintenance or chromosome movement. Double mutant analysis revealed a previously unrecognized role for HIM-17 in promoting homolog pairing under dysfunctional SC assembly, without perturbing nuclear envelope recruitment of factors required for chromosome movement. We provide evidence thatbra-2andhim-17act in distinct pathways, exerting partially redundant functions in SC licensing, as well as separable roles in regulating homologs pairing. Altogether, our findings unveil novel mechanisms that ensure stabilization of homologous chromosome interaction via SC licensing upon homology assessment.