Journal
PLANT JOURNAL
Volume 115, Issue 3, Pages 662-677Publisher
WILEY
DOI: 10.1111/tpj.16252
Keywords
Arabidopsis thaliana; FLD; H3K4me2/me3; infection memory; RRTF1; systemic acquired resistance
Categories
Ask authors/readers for more resources
Plants develop systemic acquired resistance (SAR) to enhance their defense response during subsequent infections, and epigenetic modifications of defense-related genes play a role in this process. RSI1/FLD is a key gene involved in the activation of SAR in Arabidopsis. RRTF1 is identified as an epigenetic target of RSI1 and negatively regulates basal defense and SAR.
Plants can retain a memory of previous pathogen infections to mount a more robust defense response during subsequent infections by developing systemic acquired resistance (SAR). However, the mechanism through which plants develop and retain infection memory is not known. Experiments have shown the association of epigenetic modifications of specific defense-related genes with SAR. RSI1/FLD codes for a histone demethylase and is required for the activation of SAR in Arabidopsis. Here we report the identification of RRTF1 as an epigenetic target of RSI1. RRTF1 expression is higher in pathogen-free distal tissues of the rsi1 mutant. Experiments with loss-of-function and overexpression lines suggest RRTF1 is a negative regulator of basal defense against virulent and avirulent pathogens as well as SAR. Enhanced expression of RRTF1 in a wild-type (WT) background specifically impairs SAR without impacting local resistance. RSI1 is recruited at the RRTF1 locus in a SAR-inducible manner and contributes to H3K4me2 and H3K4me3 demethylation. Introduction of the rrtf1 mutation rescues the loss-of-SAR phenotype of rsi1 plants. However, these plants fail to retain infection memory beyond 7 days post-primary inoculation, whereas WT plants retain memory for at least 11 days. Our results demonstrate that RSI1 and RRTF1 form a functional module for retaining infection memory in Arabidopsis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available