TheRAD51paralogueHvXRCC2regulates meiosis and recombination in barley

Abstract

Using a positional candidate-gene approach we show that semi-steriledesynaptic8mutants are associated with deletions in or complete knockout of the barley homolog ofXRCC2(X-Ray Repair Cross Complementing 2). In barleyXRCC2mutants, the initial meiotic progression is normal, albeit with a small delay in initiation, with completion of synapsis. However, the absence ofHvXRCC2subsequently leads to a dramatic reduction in the number of crossovers, chromosome mis-segregation, and infertility, suggesting thatHvXRCC2plays a major role in recombination. This mutant phenotype is congruent with that reported in mammalian studies but contrasts with theXRCC2mutant in Arabidopsis which is fertile, exhibits normal chromosome pairing and correct chromosome segregation, and is associated with an increased rate of crossovers. This indicates that theXRCC2mutant phenotype in Arabidopsis is not representative of all plants and thatXRCC2is not a good candidate for the modulation of recombination in barley.HighlightThe mutants of the barley homolog ofXRCC2exhibit delays in replication leading to defective meiosis, altered RAD51 orthologue behaviour, and significant reduction in the number of crossovers as in canonical mammalianXRCC2mutants but unlike those in Arabidopsis.