Repressive control of immune receptor genes by convergent epigenetic mechanisms

TORRES, JOSÉ ROBERTO; ALVAREZ M.E.; CAMBIAGNO D.A.

VIRTUAL

Congreso; Reunión Argentina de Fisiología Vegetal; 2021

RAFV

Genes encoding PRR and NLR immune receptors determine the ability of a plant to resist microbial infections. Their repression is driven by diverse mechanisms avoiding there harmful hyperactivity. We studied the epigenetic control on their expression in met1, cmt3, mom1, suvh4/5/6 and ddm1 mutants, impaired in deposition of the repressive 5-methyl cytosine (5-mC) and histone 3 lysine 9 dimethylation (H3K9me2) marks. At optimal growth conditions, none of the mutants showed basal expression of the defense gene marker PR1, but all of them had greater resistance to Pseudomonas syringae pv. tomato than wild type plants. Moreover, PR1 was induced in an earlier and/or stronger manner in these mutants, suggesting they are primed to stimulate immune cascades and defenses. The analysis of multiple available transcriptomes of each mutant, showed spontaneous activation of particular PRR/NLR gene subsets in uninfected conditions. We found 37 "mutant-specific" PRR/NLR genes likely activated at early infection stages. Specific epigenetic features at their promoters could explain their up-regulation in the mutants. As expected, suvh4/5/6 and ddm1 expressed PRR/NLR genes carrying 5-mC and H3K9me2 marks in uninfected wild type plants. Surprisingly, all mutants activated genes harboring the repressive H2A.Z/H3K27me3 marks at their promoters, which depend on the activity of REF6 demethylase and the chromatin remodeler PIE1, respectively. Therefore, MET1, CMT3, MOM1, SUVH4/5/6 and DDM1, together with REF6 and PIE1, would contribute to establish chromatin states that prevent constitutive PRR/NLR gene activation, but facilitate their priming by modulating epigenetic marks at their promoters.