Genome-wide mapping of heteroduplex DNA (a recombination intermediate) formed during mitotic recombination in yeast demonstrates that the "classical" model of double-strand DNA break repair is inadequate to explain several aspects of mitotic recombination.
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.
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.
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.