Phytophthora infestans RXLR-WY Effector AVR3a Associates with Dynamin-Related Protein 2 Required for Endocytosis of the Plant Pattern Recognition Receptor FLS2.
Phytophthora infestans RXLR-WY Effector AVR3a Associates with Dynamin-Related Protein 2 Required for Endocytosis of the Plant Pattern Recognition Receptor FLS2.
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DOI：
10.1371/journal.pone.0137071
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发表时间：
2015
期刊：
影响因子：
3.7
通讯作者：
Kamoun S
中科院分区：
文献类型：
--
作者：
Chaparro-Garcia A;Schwizer S;Sklenar J;Yoshida K;Petre B;Bos JI;Schornack S;Jones AM;Bozkurt TO;Kamoun S
病原体利用效应子抑制植物基础防御，称为 PTI（病原体相关分子模式触发免疫）。然而，我们对丝状植物病原体（即真菌和卵菌）抑制 PTI 的了解仍然不完整。先前的研究表明，辅助受体 BAK1/SERK3 有助于针对马铃薯病原体致病疫霉的基础免疫。此外，BAK1/SERK3是致病疫霉诱发素INF1（一种具有PAMP特征的蛋白质）诱导的细胞死亡所必需的。已知致病疫霉宿主转位的 RXLR-WY 效应子 AVR3a 通过结合植物 E3 连接酶 CMPG1 来抑制 INF1 介导的细胞死亡。相比之下，AVR3aKI-Y147del（AVR3a C 端酪氨酸的缺失突变体）无法结合 CMPG1，并且不会抑制 INF1 介导的细胞死亡。在这里，我们使用激发子/受体对 flg22/FLS2 作为模型，研究了 AVR3a 及其变体对本塞姆氏烟草中额外的 BAK1/SERK3 依赖性 PTI 反应的干扰程度。我们发现所有测试的 AVR3a 变体都会抑制 flg22 触发的防御反应并减少激活的 FLS2 的内化。此外，我们发现 AVR3a 与 Dynamin 相关蛋白 2 (DRP2) 相关，DRP2 是一种参与受体介导的内吞作用的植物 GTP 酶。有趣的是，DRP2 的沉默会损害配体诱导的 FLS2 内化，但不会影响生长受体 BRI1 的内化。我们的结果表明，AVR3a 与参与免疫受体介导的内吞作用的关键细胞运输和膜重塑复合物相关。我们得出的结论是，AVR3a 是一种多功能效应器，可以通过至少两种不同的途径抑制 BAK1/SERK3 介导的免疫。
Pathogens utilize effectors to suppress basal plant defense known as PTI (Pathogen-associated molecular pattern-triggered immunity). However, our knowledge of PTI suppression by filamentous plant pathogens, i.e. fungi and oomycetes, remains fragmentary. Previous work revealed that the co-receptor BAK1/SERK3 contributes to basal immunity against the potato pathogen Phytophthora infestans. Moreover BAK1/SERK3 is required for the cell death induced by P. infestans elicitin INF1, a protein with characteristics of PAMPs. The P. infestans host-translocated RXLR-WY effector AVR3a is known to supress INF1-mediated cell death by binding the plant E3 ligase CMPG1. In contrast, AVR3aKI-Y147del, a deletion mutant of the C-terminal tyrosine of AVR3a, fails to bind CMPG1 and does not suppress INF1-mediated cell death. Here, we studied the extent to which AVR3a and its variants perturb additional BAK1/SERK3-dependent PTI responses in N. benthamiana using the elicitor/receptor pair flg22/FLS2 as a model. We found that all tested variants of AVR3a suppress defense responses triggered by flg22 and reduce internalization of activated FLS2. Moreover, we discovered that AVR3a associates with the Dynamin-Related Protein 2 (DRP2), a plant GTPase implicated in receptor-mediated endocytosis. Interestingly, silencing of DRP2 impaired ligand-induced FLS2 internalization but did not affect internalization of the growth receptor BRI1. Our results suggest that AVR3a associates with a key cellular trafficking and membrane-remodeling complex involved in immune receptor-mediated endocytosis. We conclude that AVR3a is a multifunctional effector that can suppress BAK1/SERK3-mediated immunity through at least two different pathways.