RT Journal Article
SR Electronic
T1 Intra-strain elicitation and suppression of plant immunity by <em>Ralstonia solanacearum</em> type-III effectors in <em>Nicotiana benthamiana</em>
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 780890
DO 10.1101/780890
A1 Yuying Sang
A1 Wenjia Yu
A1 Haiyan Zhuang
A1 Yali Wei
A1 Lida Derevnina
A1 Gang Yu
A1 Jiamin Luo
A1 Alberto P. Macho
YR 2019
UL http://biorxiv.org/content/early/2019/12/15/780890.abstract
AB Effector proteins delivered inside plant cells are powerful weapons for bacterial pathogens, but this exposes the pathogen to potential recognition by the plant immune system. Therefore, the effector repertoire of a given pathogen must be balanced for a successful infection. Ralstonia solanacearum is an aggressive pathogen with a large repertoire of secreted effectors. One of these effectors, RipE1, is conserved in most R. solanacearum strains sequenced to date. In this work, we found that RipE1 triggers immunity in N. benthamiana, which requires the immune regulator SGT1, but not EDS1 or NRCs. Interestingly, RipE1-triggered immunity induces the accumulation of salicylic acid (SA) and the overexpression of several genes encoding phenylalanine-ammonia lyases (PALs), suggesting that the unconventional PAL-mediated pathway is responsible for the observed SA biosynthesis. Surprisingly, RipE1 recognition also induces the expression of jasmonic acid (JA)-responsive genes and JA biosynthesis, suggesting that both SA and JA may act cooperatively in response to RipE1. Finally, we found that RipE1 expression leads to the accumulation of glutathione in plant cells, which precedes the activation of immune responses. R. solanacearum encodes another effector, RipAY, which is known to inhibit immune responses by degrading cellular glutathione. Accordingly, we show that RipAY inhibits RipE1-triggered immune responses. This work shows a strategy employed by R. solanacearum to counteract the perception of its effector proteins by the plant immune system.