Phytophthora infestans effector SFI3 targets potato UBK to suppress early immune transcriptional responses
Phytophthora infestans effector SFI3 targets potato UBK to suppress early immune transcriptional responses
复制标题
致病疫霉效应子 SFI3 以马铃薯 UBK 为靶点，抑制早期免疫转录反应。
DOI：
10.1111/nph.15635
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发表时间：
2019-04-01
期刊：
影响因子：
9.4
通讯作者：
Birch, Paul R. J.
中科院分区：
文献类型：
--
作者：
He, Qin;McLellan, Hazel;Birch, Paul R. J.
马铃薯枯萎病病原体致病疫霉分泌一系列RXLR效应物以促进疾病。最近的证据表明，一些效应抑制早期模式触发免疫（PTI）的微生物相关的分子模式（MAMPs）的看法。致病疫霉效应子PiSFI 3/Pi 06087/PexRD 16先前已显示抑制MAMP触发的pFRK 1-荧光素酶报告基因活性。PiSFI 3如何抑制免疫力尚不清楚。我们采用酵母双杂交（Y2 H）测定，免疫共沉淀，RNA干扰和病毒诱导的基因沉默（VIGS）的转录沉默，和X射线晶体学结构导向突变，研究PiSFI 3在靶向植物U盒激酶蛋白（StUBK）抑制免疫的功能。我们发现PiSFI 3在宿主细胞核中是活跃的，并且在酵母和植物中与StUBK相互作用。UBK是马铃薯和本氏烟草中特异性PTI途径的正调控因子。重要的是，它有助于被PiSFI 3抑制的早期转录反应。PiSFI 3形成不寻常的反式同源二聚体。破坏二聚化的突变阻止了PiSFI 3的核仁定位，并减弱了其与StUBK的相互作用及其增强致病疫霉叶定殖的能力。PiSFI 3是一种“WY-domain”RXLR效应物，其形成一种新的反式同源二聚体，这是其通过与U盒激酶蛋白StUBK相互作用抑制PTI的能力所必需的。
The potato blight agent Phytophthora infestans secretes a range of RXLR effectors to promote disease. Recent evidence indicates that some effectors suppress early pattern-triggered immunity (PTI) following perception of microbe-associated molecular patterns (MAMPs). Phytophthora infestans effector PiSFI3/Pi06087/PexRD16 has been previously shown to suppress MAMP-triggered pFRK1-Luciferase reporter gene activity. How PiSFI3 suppresses immunity is unknown. We employed yeast-two-hybrid (Y2H) assays, co-immunoprecipitation, transcriptional silencing by RNA interference and virus-induced gene silencing (VIGS), and X-ray crystallography for structure-guided mutagenesis, to investigate the function of PiSFI3 in targeting a plant U-box-kinase protein (StUBK) to suppress immunity. We discovered that PiSFI3 is active in the host nucleus and interacts in yeast and in planta with StUBK. UBK is a positive regulator of specific PTI pathways in both potato and Nicotiana benthamiana. Importantly, it contributes to early transcriptional responses that are suppressed by PiSFI3. PiSFI3 forms an unusual trans-homodimer. Mutation to disrupt dimerization prevents nucleolar localisation of PiSFI3 and attenuates both its interaction with StUBK and its ability to enhance P. infestans leaf colonisation. PiSFI3 is a 'WY-domain' RXLR effector that forms a novel trans-homodimer which is required for its ability to suppress PTI via interaction with the U-box-kinase protein StUBK.