The woody plant-degrading pathogen Lasiodiplodia theobromae effector LtCre1 targets the grapevine sugar-signaling protein VvRHIP1 to suppress host immunity

Author:

Xing Qikai1,Zhou Xiangui2,Cao Yang1,Peng Junbo1,Zhang Wei1,Wang Xuncheng1ORCID,Wu Jiahong1,Li Xinghong1,Yan Jiye1ORCID

Affiliation:

1. Beijing Key Laboratory of Environment Friendly Management on Fruits Pests in North China, Institute of Plant Protection, Beijing Academy of Agriculture and Forestry Sciences , Beijing 100097 , China

2. State Key Laboratory of Protein and Plant Gene Research, School of Advanced Agricultural Sciences and School of Life Sciences, Peking-Tsinghua Center for Life Sciences, Peking University , 100871 Beijing , China

Abstract

Abstract Lasiodiplodia theobromae is a causal agent of Botryosphaeria dieback, which seriously threatens grapevine production worldwide. Plant pathogens secrete diverse effectors to suppress host immune responses and promote the progression of infection, but the mechanisms underlying the manipulation of host immunity by L. theobromae effectors are poorly understood. In this study, we characterized LtCre1, which encodes a L. theobromae effector that suppresses BAX-triggered cell death in Nicotiana benthamiana. RNAi-silencing and overexpression of LtCre1 in L. theobromae showed impaired and increased virulence, respectively, and ectopic expression in N. benthamiana increased susceptibility. These results suggest that LtCre1 is as an essential virulence factor for L. theobromae. Protein–protein interaction studies revealed that LtCre1 interacts with grapevine RGS1-HXK1-interacting protein 1 (VvRHIP1). Ectopic overexpression of VvRHIP1 in N. benthamiana reduced infection, suggesting that VvRHIP1 enhances plant immunity against L. theobromae. LtCre1 was found to disrupt the formation of the VvRHIP1–VvRGS1 complex and to participate in regulating the plant sugar-signaling pathway. Thus, our results suggest that L. theobromae LtCre1 targets the grapevine VvRHIP1 protein to manipulate the sugar-signaling pathway by disrupting the association of the VvRHIP1–VvRGS1 complex.

Funder

National Natural Science Foundation of China

Outstanding Scientist of Beijing Academy of Agriculture and Forestry Sciences

Promotion and Innovation Foundation of Beijing Academy of Agriculture and Forestry Sciences

China Agriculture Research System of MOF and MARA

Publisher

Oxford University Press (OUP)

Subject

Plant Science,Physiology

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