Homologous recombination during meiosis generates genetic diversity while ensuring chromosome segregation. The repair of DNA double-strand breaks into crossovers (COs) is tightly regulated, and in many species the synaptonemal complex (SC) coordinates both homologue synapsis and CO distribution. In Arabidopsis thaliana, however, COs can form without a fully assembled SC, raising questions about its precise function.
A new study identifies SCEP3 as a central element (CE) protein of the Arabidopsis SC. SCEP3 colocalizes with ZYP1, interacts directly with its N terminus, and loads independently of other CE proteins. Intriguingly, SCEP3 is sufficient to recruit ZYP1, suggesting a role as a synapsis initiation factor. Structural similarity to nematode SYP-4 and mammalian SIX6OS1 indicates deep evolutionary conservation of CE architecture.
Loss-of-function scep3 mutants reveal the protein’s dual role. Like other CE mutants, they lack CO interference, assurance, and heterochiasmy, but uniquely, they also show a stronger reduction in CO numbers. Most remaining COs are ZMM-dependent, although a minority are class II. SCEP3 also associates with the CO factor HEI10, even in SC-deficient cells, and is required for the extra HEI10-dependent COs that arise in zyp1 mutants. This suggests that SCEP3 couples recombination intermediates to SC assembly, possibly stabilizing them or modulating HEI10 dynamics.
Together, these findings position SCEP3 as both a structural CE component and a recombination regulator. Arabidopsis may organize its SC into at least two modules, SCEP3-ZYP1 and SCEP1-SCEP2, whose interplay remains unresolved. Conserved motifs in SCEP3’s disordered N terminus hint at further regulatory potential, reminiscent of worm SYP-4.
By filling a missing piece of the plant SC, this work underscores how chromosome architecture and recombination are interlinked, and highlights both conserved and plant-specific strategies for shaping CO patterns.