Abstract
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.