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首页> 外文期刊>Nature >A translocation signal for delivery of oomycete effector proteins into host plant cells
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A translocation signal for delivery of oomycete effector proteins into host plant cells

机译：用于将卵菌效应蛋白转运到宿主植物细胞中的易位信号

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摘要

Bacterial, oomycete and fungal plant pathogens establish disease by translocation of effector proteins into host cells, where they may directly manipulate host innate immunity. In bacteria, translocation is through the type III secretion system, but analogous processes for effector delivery are uncharacterized in fungi and oomycetes. Here we report functional analyses of two motifs, RXLR and EER, present in translocated oomycete effectors. We use the Phytophthora infestans RXLR-EER-containing protein Avr3a as a reporter for translocation because it triggers RXLR-EER-independent hypersensitive cell death following recognition within plant cells that contain the R3a resistance protein. We show that Avr3a, with or without RXLR-EER motifs, is secreted from P. infestans biotrophic structures called haustoria, demonstrating that these motifs are not required for targeting to haustoria or for secretion. However, following replacement of Avr3a RXLR-EER motifs with alanine residues, singly or in combination, or with residues KMIK-DDK—representing a change that conserves physicochemical properties of the protein—P. infestans fails to deliver Avr3a or an Avr3a-GUS fusion protein into plant cells, demonstrating that these motifs are required for translocation. We show that RXLR-EER-encoding genes are transcriptionally upregulated during infection. Bioinformatic analysis identifies 425 potential genes encoding secreted RXLR-EER class proteins in the P. infestans genome. Identification of this class of proteins provides unparalleled opportunities to determine how oomycetes manipulate hosts to establish infection.
机译：细菌，卵菌和真菌植物病原体通过将效应子蛋白转移到宿主细胞中而建立疾病，它们可以直接操纵宿主固有的免疫力。在细菌中，易位是通过III型分泌系统进行的，但在真菌和卵菌细胞中，特异的效应子传递过程并未表征。在这里，我们报告功能的分析，出现在两个移位的卵菌效应子中的RXLR和EER。我们使用疫霉疫霉含有RXLR-EER的蛋白Avr3a作为易位的报告基因，因为它在包含R3a抗性蛋白的植物细胞内被识别后触发了RXLR-EER依赖性超敏细胞死亡。我们显示Avr3a，有或没有RXLR-EER图案，是从被称为haustoria的P. infestans生物营养结构中分泌出来的，表明这些图案对于靶向haustoria或分泌不是必需的。但是，用丙氨酸残基单独或组合或用残基KMIK-DDK取代Avr3a RXLR-EER基序后，代表了保留蛋白质P物理化学性质的变化。侵染未能将Avr3a或Avr3a-GUS融合蛋白传递到植物细胞中，表明这些基序是易位的。我们显示，RXLR-EER编码基因在感染过程中转录上调。生物信息学分析鉴定了425个潜在基因，编码致病疫霉基因组中分泌的RXLR-EER类蛋白。这类蛋白质的鉴定为确定卵菌体如何操纵宿主建立感染提供了无与伦比的机会。

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