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 (epi
RIL
) 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 epi
RIL
infected with
P. brassicae
and using various disease‐related traits.
Epi
RIL
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.
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