PRJNA718691
A comprehensive genome-wide investigation of the epigenome and transcriptome of self-fertilized descendants of the mock-treated (MM), Pst-treated (PP) parents and their reciprocally crossed F1 progenies
Systemic acquired resistance (SAR) is an induced immune mechanism in plants, involving epigenetic regulation by chromatin remodeling and DNA methylation, which also can be inherited to progeny following disease pressure by Pseudomonas syringae pv. tomato DC3000 (PstDC3000). Intersexual epigenetic conflict sometimes leads to unequal expression of maternal and paternal alleles in offspring, resulting in parent-of-origin effects. To better understand the epigenetic contributions of maternal and paternal alleles in plant defense, we characterized Arabidopsis thaliana (Ler) epigenomes and transcriptomes in response to challenge against Pseudomonas syringae pv. tomato DC3000 (Pst). Samples from self-fertilized F1 descendants of the mock-treated (MM), Pst-treated (PP) parents and their reciprocally crossed progenies (MP and PM) were analyzed for their genome-wide inherited DNA methylation. In addition, the response and transcriptome change against Pst treatment were analyzed among the F1 descendants. In reciprocal crosses, we identified widespread increase in CHH methylation of transposon elements (TE) in the more disease resistant descendant MP when compared to descendants PM, MM and PP, suggesting a contribution from the Pst-primed paternal genome on CHH hypermethylation in MP. When the F1 descendants were challenged with Pst, a higher level of TE expression was maintained in the MP at 6 and 24 hours after treatment when compared to the other F1 descendants. Our data suggested that altered glutathione signaling in MP contributes to global translation reprogramming and stress tolerance. These findings will facilitate the selection of maternal and paternal parents and affect the performance of disease resistance in breeding.