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.

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.

Formation of a phase-separated interface between homologous chromosomes during meiosis enables regulatory signals to spread in cis over long distances, illuminating the longstanding mystery of crossover interference.

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.

The scaffolding that holds chromosome pairs together plays a key role in limiting the levels of double-strand breaks.

Prdm9-generated meiotic asynapsis of homologous chromosomes in mouse subspecific hybrids causes hybrid sterility and can be reversed by introducing random stretches of consubspecific sequence (≥ 27Mb) on four chromosomes most sensitive to asynapsis.

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

Building on previous work (Syrjänen, Pellegrini, & Davies, 2014), it is shown that SYCP3 contributes to the architecture of meiotic chromosomes through local bridging interactions that result in large-scale compaction of the chromosome axis.

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.

Cell division by meiosis during sperm production depends on expression of an RNA-binding protein that prevents abnormal RNA-processing pathways.