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© Research
Publication : The New phytologist

Quantitative resistance to clubroot infection mediated by transgenerational epigenetic variation in Arabidopsis.

Scientific Fields
Diseases
Organisms
Applications
Technique

Published in The New phytologist - 01 Apr 2019

Liégard B, Baillet V, Etcheverry M, Joseph E, Lariagon C, Lemoine J, Evrard A, Colot V, Gravot A, Manzanares-Dauleux MJ, Jubault M,

Link to Pubmed [PMID] – 30393890

Link to DOI – 10.1111/nph.15579

New Phytol 2019 04; 222(1): 468-479

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 (QTLepi ) 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 QTLepi were detected across the five chromosomes, with a bona fide epigenetic origin for 16 of them. The effect of five QTLepi was dependent on temperature conditions. Six QTLepi co-localized with previously identified clubroot resistance genes and QTL in Arabidopsis. Co-localization of clubroot resistance QTLepi 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.

https://pubmed.ncbi.nlm.nih.gov/30393890