In humans, specific sequence features can predict whether meiotic recombination occurs at sites bound by the protein PRDM9, whose DNA-binding zinc-finger domain can unexpectedly bind to gene promoters and to other copies of PRDM9.
ZCWPW1 has co-evolved with PRDM9, in particular the PRDM9-SET domain, and although not involved in PRDM9's role in positioning recombination events, it is required for PRDM9's role in pairing chromosomes.
ZCWPW1 is a histone modification reader that localizes to DMC1-labelled double-strand break hotspots in a largely PRDM9-dependent manner, where it facilitates completion of synapsis by mediating DSB repair process.
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 exogenous DNA DSBs improve meiotic chromosome pairing in mouse inter-subspecific hybrids, thus providing an evidence for a DSB-dependent mechanism of the PRDM9-controlled synapsis failure and infertility.
The meiotic recombination landscape in vertebrates was re-engineered via the co-evolution of a dual histone H3K4/H3K36 methylation 'writer' PRDM9 and its 'reader' ZCWPW1 that facilitates efficient double strand break repair.
Variation in codon usage among functional categories of human genes is not due to selection for translation efficiency, but to differences in intragenic recombination rate, linked to variation in meiotic transcription level.