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Article|03 May 2023|OPEN
Ralstonia solanacearum type III effector RipAS associates with potato type one protein phosphatase StTOPP6 to promote bacterial wilt
Bingsen Wang1,2,3,4 , Wenfeng He1,2,3,4 , Mengshu Huang1,2,3,4 and Jiachen Feng5 , Yanping Li1,2,3,4 , Liu Yu1,2,3,4 , Yuqi Wang1,2,3,4 , Dan Zhou1,2,3,4 , Chengzhen Meng1,2,3,4 , Dong Cheng1,2,3,4 , Ning Tang5 , Botao Song1,2,3,4 , , Huilan Chen,1,2,3,4 ,
1National Key Laboratory for Germplasm Innovation & Utilization of Horticultural Crops, Huazhong Agricultural University, Wuhan 430070, China
2Key Laboratory of Potato Biology and Biotechnology (HZAU), Ministry of Agriculture and Rural Affairs, Wuhan 430070, China
3Potato Engineering and Technology Research Center of Hubei Province, Huazhong Agricultural University, Wuhan 430070, China
4College of Horticulture and Forestry Science, Huazhong Agricultural University, Wuhan 430070, China
5State Key Laboratory of Crop Stress Adaptation and Improvement, Henan University, Kaifeng 475001, China
*Corresponding author. E-mail:,

Horticulture Research 10,
Article number: uhad087 (2023)
Views: 131

Received: 14 Nov 2022
Accepted: 24 Apr 2023
Published online: 03 May 2023


The bacterial pathogen Ralstonia solanacearum (R. solanacearum) delivered type III secretion effectors to inhibit the immune system and cause bacterial wilt on potato. Protein phosphatases are key regulators in plant immunity, which pathogens can manipulate to alter host processes. Here, we show that a type III effector RipAS can reduce the nucleolar accumulation of a type one protein phosphatase (PP1) StTOPP6 to promote bacterial wilt. StTOPP6 was used as bait in the Yeast two-Hybrid (Y2H) assay and acquired an effector RipAS that interacts with it. RipAS was characterized as a virulence effector to contribute to R. solanacearum infection, and stable expression of RipAS in potato impaired plant resistance against R. solanacearum. Overexpression of StTOPP6 showed enhanced disease symptoms when inoculated with wild strain UW551 but not the ripAS deletion mutant, indicating that the expression of StTOPP6 facilitates the virulence of RipAS. RipAS reduced the nucleolar accumulation of StTOPP6, which occurred during R. solanacearum infection. Moreover, the association also widely existed between other PP1s and RipAS. We argue that RipAS is a virulence effector associated with PP1s to promote bacterial wilt.