For many bacterial species, recombination dominates genome evolution and phylogenetic patterns that have so far been assumed to reflect clonal relationships, in fact reflect variation in recombination rates across lineages.
Mutation of Glycine 34 to Arginine within the N-terminal tail of histone H3 alters post-translational modifications on Lysine 36 and is associated with a delay in replication restart, defective homologous recombination and an increase in genomic instability.
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.
Random sequence RNA pools display an innate capacity for ligation and recombination, enabling them to “bootstrap” themselves towards higher compositional, informational and structural complexity.
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 DNA recombination landscape is locally influenced by the kinetochore to minimize potentially deleterious pericentromeric crossover recombination.
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.
Although Rad51 is the central protein involved in recombinational DNA repair, multiple auxiliary factors potentiate its activity by binding to a single, evolutionarily conserved motif.
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.
