Infection-induced mutation rates of plant resistance genes

在植物中，参与抵抗生物胁迫的基因（所谓的R基因）的基因组组成涉及正向（面向同一方向）串联重复的惊人富集。此外，长期以来，R基因簇因其在个体加入物之间的高多样性而闻名。总之，这表明R-基因簇通过正向串联突变的快速积累而进化，但是尚不清楚突变是否确实更频繁地发生，或者这些串联重复是否是这些基因座上强大选择压力的结果。增加的突变率可能是通过同源重组的DNA修复途径介导的，特别是通过在具有局部重复的区域中起作用的那些途径。这是一个有趣的想法，因为已经显示通过同源重组的DNA修复在病原体感染时增加，因此病原体感染可能导致突变率增加，特别是在那些编码对这种应激的应答的基因组区域中。随着高质量基因组组装的出现，我们现在可以通过分析突变积累系中众所周知的难以分析的R基因簇中的实际突变率来验证这一假设。

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.