Mathematical modelling, together with super-resolution imaging in Arabidopsis, demonstrates that a recently proposed coarsening model for meiotic crossover interference can explain the dynamic patterning of crossovers in many contexts, including in zyp1 and pch2 chromosome structure mutants.

Coordination between crossover designation and synaptonemal complex disassembly is executed via a conserved MAP kinase pathway and is critical for accurate chromosome segregation during meiosis.

The meiotic DNA recombination landscape is locally influenced by the kinetochore to minimize potentially deleterious pericentromeric crossover recombination.

A regulatory circuit that localizes to the synaptonemal complex, a liquid crystalline compartment between chromosomes, ensures crossing-over while limiting the number of crossovers between homologous chromosomes during meiosis.

In humans, non-crossover gene conversion events transmit GC alleles in 68% of cases and exhibit a complex pattern of multiple disconnected tracts clustered within 20–30 kilobase intervals.

PLK-1/2-mediated SYP-4 phosphorylation is dependent on crossover precursor formation, triggering a switch in the dynamic state of the synaptonemal complex that reduces the formation of further double-strand breaks at late meiotic prophase.

The Zip3-like protein Vilya links the initiation of meiotic recombination with crossover formation.

A structural and biochemical study of human SYCP3 provides the first molecular model for the three-dimensional organisation that is imposed upon chromosomal DNA during meiosis and is essential for genetic exchange and fertility.

Genetic and cytological analyses reveal a regulatory circuit that controls a key cell cycle transition during meiosis and mediates feedback regulation in response to meiotic defects.

Developing eggs and sperm differentially regulate specific steps of meiotic DNA repair by altering the composition and dynamics of proteins within synaptonemal complex.