A Receptor Pair with an Integrated Decoy Converts Pathogen Disabling of Transcription Factors to Immunity
A Receptor Pair with an Integrated Decoy Converts Pathogen Disabling of Transcription Factors to Immunity
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DOI：
10.1016/j.cell.2015.04.025
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发表时间：
2015-05-21
期刊：
影响因子：
64.5
通讯作者：
Deslandes, Laurent
中科院分区：
文献类型：
--
作者：
Le Roux, Clementine;Huet, Gaelle;Deslandes, Laurent
微生物病原体通过递送干扰防御的毒力因子（效应物）感染宿主细胞。在植物中，细胞内的核苷酸结合/富含亮氨酸的重复受体（NLR）检测特定的效应干扰和触发免疫的未知机制。拟南芥相互作用的NLR对，RRS 1-R与RPS 4，赋予对不同病原体的抗性，包括表达乙酰转移酶效应子PopP 2的青枯雷尔氏菌细菌。我们表明，PopP 2直接乙酰化一个关键的赖氨酸内的一个额外的C-末端WRKY转录因子结构域的RRS 1-R，结合DNA。这破坏了RRS 1-R DNA结合并激活RPS 4依赖性免疫。PopP 2使用相同的赖氨酸乙酰化策略靶向多种防御促进WRKY转录因子，导致防御基因表达和抗病所需的WRKY-DNA结合和反式激活功能丧失。因此，RRS 1-R在DNA处整合了具有NLR复合物的效应靶标，以将有效的细菌毒力活性转换为防御基因激活。
Microbial pathogens infect host cells by delivering virulence factors (effectors) that interfere with defenses. In plants, intracellular nucleotide-binding/leucine-rich repeat receptors (NLRs) detect specific effector interference and trigger immunity by an unknown mechanism. The Arabidopsis-interacting NLR pair, RRS1-R with RPS4, confers resistance to different pathogens, including Ralstonia solanacearum bacteria expressing the acetyltransferase effector PopP2. We show that PopP2 directly acetylates a key lysine within an additional C-terminal WRKY transcription factor domain of RRS1-R that binds DNA. This disrupts RRS1-R DNA association and activates RPS4-dependent immunity. PopP2 uses the same lysine acetylation strategy to target multiple defense-promoting WRKY transcription factors, causing loss of WRKY-DNA binding and transactivating functions needed for defense gene expression and disease resistance. Thus, RRS1-R integrates an effector target with an NLR complex at the DNA to switch a potent bacterial virulence activity into defense gene activation.