Ralstonia solanacearum releases a set of effectors into plant cells that modify the host defence reaction. The role of the effector protein RipI during infection has not been elucidated. In this study, we demonstrated that transient overexpression of RipI induces the hypersensitive response (HR), up‐regulating the HR marker gene hin1, in Nicotiana benthamiana. Deletion of R. solanacearum ripI led to increased virulence in tomato (Solanum lycopersicum) plants. Through yeast two‐hybrid and pull‐down assays, we identified an interaction between the N. benthamiana transcription factor bHLH93 and RipI, both of which could be localized in the nucleus of Arabidopsis protoplasts. Silencing of bHLH93 markedly attenuated the RipI‐induced HR and induced expression of the PDF1.2 defence gene. These data demonstrate that the R. solanacearum effector RipI induces a host defence reaction by interacting with the bHLH93 transcription factor.

中文翻译：

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青枯雷尔氏菌的效应子RipI通过与本氏烟草中的bHLH93转录因子相互作用来诱导防御反应。

青枯雷尔氏菌将一组效应子释放到植物细胞中，从而改变宿主的防御反应。尚未阐明效应蛋白RipI在感染过程中的作用。在这项研究中，我们证明RIPI的那个瞬时过表达诱导过敏反应（HR），上调的HR标记基因HIN1，在本塞姆氏烟草。R. solanacearum ripI的删除导致番茄（Solanum lycopersicum）植物的毒力增加。通过酵母双杂交和下拉实验，我们鉴定了本氏烟草转录因子bHLH93和RipI之间的相互作用，两者都可以位于拟南芥的核内。原生质体。bHLH93的沉默显着减弱了RipI诱导的HR，并诱导了PDF1.2防御基因的表达。这些数据证明，青枯雷尔氏菌效应子RipI通过与bHLH93转录因子相互作用诱导宿主防御反应。