Infection-induced mutation rates of plant resistance genes

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In plants, the genomic make-up of genes involved in resistance against biotic stress (so-called R-genes) involves a striking enrichment of forward (facing the same direction) tandem duplications. Moreover, for a long time R-gene clusters are known for their high diversity between individual accessions. Together this suggests that R-gene clusters evolve through rapid accumulation of forward tandem mutations, however it is not clear whether the mutations indeed occur more frequently or whether these tandem duplications are the results of strong selection pressure on these loci. Increased mutation rates could potentially be mediated by DNA repair pathways through homologous recombination, in particular by those pathways that act in regions with local repeats. This is an intriguing idea, as DNA repair through homologous recombination has been shown to be increased upon pathogen infection and in consequence pathogen infection could lead to increased mutation rates specifically in those genomic regions which encode the response to exactly this stress. With the advent of high-quality genome assemblies, we can now test this hypothesis by analysing the actual mutation rates in the notoriously-difficult-to-analyse R-gene clusters within mutation accumulation lines.