Ralstonia solanacearum effector RipAK suppresses homodimerization of the host transcription factor ERF098 to enhance susceptibility and the sensitivity of pepper plants to dehydration

Author:

Liu Kaisheng123,Shi Lanping123,Luo Hongli123,Zhang Kan123,Liu Jianxin123,Qiu Shanshan123,Li Xia123,He Shuilin123ORCID,Liu Zhiqin123ORCID

Affiliation:

1. Key Laboratory of Applied Genetics of Universities in Fujian Province Fujian Agriculture and Forestry University Fuzhou 350002 China

2. Key Laboratory of Ministry of Education for Genetics, Breeding and Multiple Utilization of Crops Fujian Agriculture and Forestry University Fuzhou 350002 China

3. College of Agriculture Fujian Agriculture and Forestry University Fuzhou 350002 China

Abstract

SUMMARYPlants have evolved a sophisticated immune system to defend against invasion by pathogens. In response, pathogens deploy copious effectors to evade the immune responses. However, the molecular mechanisms used by pathogen effectors to suppress plant immunity remain unclear. Herein, we report that an effector secreted by Ralstonia solanacearum, RipAK, modulates the transcriptional activity of the ethylene‐responsive factor ERF098 to suppress immunity and dehydration tolerance, which causes bacterial wilt in pepper (Capsicum annuum L.) plants. Silencing ERF098 enhances the resistance of pepper plants to R. solanacearum infection not only by inhibiting the host colonization of R. solanacearum but also by increasing the immunity and tolerance of pepper plants to dehydration and including the closure of stomata to reduce the loss of water in an abscisic acid signal‐dependent manner. In contrast, the ectopic expression of ERF098 in Nicotiana benthamiana enhances wilt disease. We also show that RipAK targets and inhibits the ERF098 homodimerization to repress the expression of salicylic acid‐dependent PR1 and dehydration tolerance‐related OSR1 and OSM1 by cis‐elements in their promoters. Taken together, our study reveals a regulatory mechanism used by the R. solanacearum effector RipAK to increase virulence by specifically inhibiting the homodimerization of ERF098 and reprogramming the transcription of PR1, OSR1, and OSM1 to boost susceptibility and dehydration sensitivity. Thus, our study sheds light on a previously unidentified strategy by which a pathogen simultaneously suppresses plant immunity and tolerance to dehydration by secreting an effector to interfere with the activity of a transcription factor and manipulate plant transcriptional programs.

Funder

Natural Science Foundation of Fujian Province

National Natural Science Foundation of China

Publisher

Wiley

Subject

Cell Biology,Plant Science,Genetics

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