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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Ralstonia solanacearum 效应子 RipI 通过与本塞姆氏烟草中的 bHLH93 转录因子相互作用来诱导防御反应。


青枯雷尔斯顿菌将一组效应子释放到植物细胞中，改变宿主的防御反应。效应蛋白 RipI 在感染过程中的作用尚未阐明。在这项研究中，我们证明，在本塞姆氏烟草中，RipI 的瞬时过度表达会诱导过敏反应 (HR)，上调 HR 标记基因hin1 。删除R. solanacearum ripI会导致番茄 ( Solanum lycopersicum ) 植物的毒力增加。通过酵母双杂交和下拉实验，我们发现了本塞姆氏烟草转录因子 bHLH93 和 RipI 之间的相互作用，两者都可以定位于拟南芥原生质体的细胞核中。沉默bHLH93显着减弱 RipI 诱导的 HR 并诱导PDF1.2防御基因的表达。这些数据表明青枯菌效应子 RipI 通过与 bHLH93 转录因子相互作用诱导宿主防御反应。