Coarsening dynamics can explain meiotic crossover patterning in both the presence and absence of the synaptonemal complex.

The shuffling of genetic material facilitated by meiotic crossovers is a critical driver of genetic variation. Therefore, the number and positions of crossover events must be carefully controlled. In an obligate crossover and repression of nearby crossovers on each chromosome pair are abolished in mutants that lack the synaptonemal complex (SC), a conserved protein scaffold. We use mathematical modelling and quantitative super-resolution microscopy to explore and mechanistically explain meiotic crossover pattering in lines with full, incomplete, or abolished synapsis. For mutants, which lack an SC, we develop a coarsening model in which crossover precursors globally compete for a limited pool of the pro-crossover factor HEI10, with dynamic HEI10 exchange mediated through the nucleoplasm. We demonstrate that this model is capable of quantitatively reproducing and predicting experimental crossover patterning and HEI10 foci intensity data. Additionally, we find that a model combining both SC- and nucleoplasm-mediated coarsening can explain crossover patterning in wild-type and in mutants, which display partial synapsis. Together, our results reveal that regulation of crossover patterning in wild-type and SC-defective mutants likely acts through the same underlying coarsening mechanism, differing only in the spatial compartments through which the pro-crossover factor diffuses.