Danger-associated peptide signaling in Arabidopsis requires clathrin
Danger-associated peptide signaling in Arabidopsis requires clathrin
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DOI：
10.1073/pnas.1605588113
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发表时间：
2016-09-27
影响因子：
11.1
通讯作者：
Russinova, Eugenia
中科院分区：
文献类型：
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作者：
Ortiz-Morea, Fausto Andres;Savatin, Daniel V.;Russinova, Eugenia
拟南芥内源性激发肽（AtPes）在病原体或创伤引起细胞损伤后释放到质外体中，通过直接结合膜定位的富含亮氨酸重复序列受体激酶PEP受体1（PEPR 1）和PEPR 2来诱导先天免疫。虽然PEPR介导的信号成分和反应已被广泛研究，亚细胞定位和动态的活性PEPR的贡献仍然在很大程度上是未知的。我们使用活细胞成像的荧光标记和生物活性的pep 1可视化的拟南芥根分生组织中的PEPR的细胞内行为。我们发现AtPep 1以受体依赖的方式修饰质膜并与PEPR共内化。AtPep 1-PEPR 1复合物向液泡的运输既不需要跨高尔基体网络/早期内体（TGN/EE）定位的液泡H+-ATP酶活性，也不需要布雷菲德菌素A敏感的ADP-核糖基化因子-鸟嘌呤交换因子（ARF-GEFs）的功能。此外，AtPep 1和不同的TGN/EE标记共定位只有很少，这意味着这种受体-配体对的细胞内途径在很大程度上是独立的TGN/EE. Inducible过表达的拟南芥网格蛋白外套拆卸因子，Eclin 2，抑制网格蛋白介导的内吞作用（CME），损害AtPep 1-PEPR 1的内化和妥协AtPep 1介导的反应。我们的研究结果表明，在PM网格蛋白功能是需要诱导植物防御反应，可能通过CME的细胞表面定位的信号成分。
The Arabidopsis thaliana endogenous elicitor peptides (AtPeps) are released into the apoplast after cellular damage caused by pathogens or wounding to induce innate immunity by direct binding to the membrane-localized leucine-rich repeat receptor kinases, PEP RECEPTOR1 (PEPR1) and PEPR2. Although the PEPR-mediated signaling components and responses have been studied extensively, the contributions of the subcellular localization and dynamics of the active PEPRs remain largely unknown. We used live-cell imaging of the fluorescently labeled and bioactive pep1 to visualize the intracellular behavior of the PEPRs in the Arabidopsis root meristem. We found that AtPep1 decorated the plasma membrane (PM) in a receptor-dependentmanner and cointernalized with PEPRs. Trafficking of the AtPep1-PEPR1 complexes to the vacuole required neither the trans-Golgi network/early endosome (TGN/EE)-localized vacuolar H+-ATPase activity nor the function of the brefeldin A-sensitive ADP-ribosylation factor-guanine exchange factors (ARF-GEFs). In addition, AtPep1 and different TGN/EE markers colocalized only rarely, implying that the intracellular route of this receptor-ligand pair is largely independent of the TGN/EE. Inducible overexpression of the Arabidopsis clathrin coat disassembly factor, Auxilin2, which inhibits clathrin-mediated endocytosis (CME), impaired the AtPep1-PEPR1 internalization and compromised AtPep1-mediated responses. Our results show that clathrin function at the PM is required to induce plant defense responses, likely through CME of cell surface-located signaling components.