Abstract
Summary Quantitative disease resistance, often influenced by environmental factors, is thought to be the result of DNA sequence variants segregating at multiple loci. However, heritable differences in DNA methylation, so‐called transgenerational epigenetic variants, also could contribute to quantitative traits. Here, we tested this possibility using the well‐characterized quantitative resistance of Arabidopsis to clubroot, a Brassica major disease caused by Plasmodiophora brassicae.For that, we used the epigenetic recombinant inbred lines (epiRIL) derived from the cross ddm1‐2 × Col‐0, which show extensive epigenetic variation but limited DNA sequence variation. Quantitative loci under epigenetic control (QTL epi) mapping was carried out on 123 epiRIL infected with P. brassicae and using various disease‐related traits.EpiRIL displayed a wide range of continuous phenotypic responses. Twenty QTL epi were detected across the five chromosomes, with a bona fide epigenetic origin for 16 of them. The effect of five QTL epi was dependent on temperature conditions. Six QTL epi co‐localized with previously identified clubroot resistance genes and QTL in Arabidopsis.Co‐localization of clubroot resistance QTL epi with previously detected DNA‐based QTL reveals a complex model in which a combination of allelic and epiallelic variations interacts with the environment to lead to variation in clubroot quantitative resistance.
Highlights
Clubroot caused by the protist Plasmodiophora brassicae is a major disease of Brassicaceae including the three most economically important Brassica species, B. napus, B. rapa and B. oleracea (Dixon, 2009), and the model plant Arabidopsis thaliana (Koch et al, 1991)
Twenty Quantitative loci under epigenetic control (QTLepi) were detected across the five chromosomes, with a bona fide epigenetic origin for 16 of them
Six QTLepi co-localized with previously identified clubroot resistance genes and quantitative trait loci (QTL) in Arabidopsis, revealing that quantitative resistance to clubroot in natural accessions could be controlled by both nucleotidic and epigenetic variations
Summary
Clubroot caused by the protist Plasmodiophora brassicae is a major disease of Brassicaceae including the three most economically important Brassica species, B. napus, B. rapa and B. oleracea (Dixon, 2009), and the model plant Arabidopsis thaliana (Koch et al, 1991). Current approaches to generating resistant varieties rely mainly on a few loci controlling qualitative resistance, with the inevitable outcome of rapid adaptation of the pathogen populations (Diederichsen et al, 2009). In this context, diversification and access to other sources of clubroot resistance variability is becoming necessary
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