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作 者:Bingsen Wang Wenfeng He Mengshu Huang Jiachen Feng Yanping Li Liu Yu Yuqi Wang Dan Zhou Chengzhen Meng Dong Cheng Ning Tang Botao Song Huilan Chen
机构地区:[1]National Key Laboratory for Germplasm Innovation&Utilization of Horticultural Crops,Huazhong Agricultural University,Wuhan 430070,China [2]Key Laboratory of Potato Biology and Biotechnology(HZAU),Ministry of Agriculture and Rural Affairs,Wuhan 430070,China [3]Potato Engineering and Technology Research Center of Hubei Province,Huazhong Agricultural University,Wuhan 430070,China [4]College of Horticulture and Forestry Science,Huazhong Agricultural University,Wuhan 430070,China [5]State Key Laboratory of Crop Stress Adaptation and Improvement,Henan University,Kaifeng 475001,China
出 处:《Horticulture Research》2023年第6期228-237,共10页园艺研究(英文)
基 金:This work was funded by the National Natural Science Foundation of China(32201789);the China Agriculture Research System of MOF and MARA(CARS-09).
摘 要: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.
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