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.
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.
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.