A Plant Phosphoswitch Platform Repeatedly Targeted by Type III Effector Proteins Regulates the Output of Both Tiers of Plant Immune Receptors
A Plant Phosphoswitch Platform Repeatedly Targeted by Type III Effector Proteins Regulates the Output of Both Tiers of Plant Immune Receptors
复制标题
DOI：
10.1016/j.chom.2014.09.004
复制
发表时间：
2014-10-08
影响因子：
30.3
通讯作者：
Dangl, Jeffery L.
中科院分区：
文献类型：
--
作者：
Chung, Eui-Hwan;El-Kasmi, Farid;Dangl, Jeffery L.
植物通过两层功能互连的免疫受体来检测微生物。免疫检测受到同样复杂的病原体机制的抑制。小的质膜拴系蛋白RIN4负向调节微生物相关分子模式(MAMP)触发的反应，这些反应在细菌鞭毛蛋白感知上被解除抑制。我们证明了鞭毛肽MamP flg22的识别触发了丝氨酸141(PS141)磷酸化的RIN4的积累，从而介导了几种免疫输出的去抑制。RIN4是四种细菌III型效应蛋白的靶标，在鞭毛蛋白感知后暂时递送。其中，AvrB与宿主激酶作用，增加苏氨酸166处磷酸化的RIN4水平(PT166)。RIN4 pT166是RIN4 pS141的上位基因。我们的结果解释了独立效应器的进化，该效应拮抗RIN4 pS141和特定植物细胞内NLR蛋白RPM1的积累，而RPM1是由AvrB介导的RIN4 pT166积累激活的。
Plants detect microbes via two functionally interconnected tiers of immune receptors. Immune detection is suppressed by equally complex pathogen mechanisms. The small plasma-membrane-tethered protein RIN4 negatively regulates microbe-associated molecular pattern (MAMP)-triggered responses, which are derepressed upon bacterial flagellin perception. We demonstrate that recognition of the flagellin peptide MAMP flg22 triggers accumulation of RIN4 phosphorylated at serine 141 (pS141) that mediates derepression of several immune outputs. RIN4 is targeted by four bacterial type III effector proteins, delivered temporally after flagellin perception. Of these, AvrB acts with a host kinase to increase levels of RIN4 phosphorylated at threonine 166 (pT166). RIN4 pT166 is epistatic to RIN4 pS141. Thus, AvrB contributes to virulence by enhancing "rerepression'' of immune system outputs. Our results explain the evolution of independent effectors that antagonize accumulation of RIN4 pS141 and of a specific plant intracellular NLR protein, RPM1, which is activated by AvrB-mediated accumulation of RIN4 pT166.