SNARE SYP132 mediates divergent traffic of plasma membrane H+-ATPase AHA1 and antimicrobial PR1 during bacterial pathogenesis.
SNARE SYP132 mediates divergent traffic of plasma membrane H+-ATPase AHA1 and antimicrobial PR1 during bacterial pathogenesis.
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DOI：
10.1093/plphys/kiac149
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发表时间：
2022-06-27
期刊：
影响因子：
7.4
通讯作者：
Karnik, Rucha Anil
中科院分区：
文献类型：
--
作者：
Baena, Guillermo;Xia, Lingfeng;Waghmare, Sakharam;Karnik, Rucha Anil
囊泡转运蛋白SYP 132（vesicle trafficking SYNTAXIN OF plants 132，SYP 132）是一种通过囊泡转运抑制质膜H+-ATP酶密度和功能的蛋白质。在响应细菌病原体时，它还促进抗菌剂病程相关（PR）蛋白的分泌运输。SYP 132的这些看似相反的作用引发了关于这两个可能独立的膜运输途径之间的机械联系的问题，这些途径与植物生长和免疫交叉。为了研究SYP 132和致病过程中PM H+-ATP酶1（AHA 1）和致病相关蛋白1（PR 1）的相关运输，我们使用了致病性假单胞菌pv.番茄DC 3000（Pst DC 3000）细菌感染拟南芥（Arabidopsis thaliana）植物。SYP 132过表达抑制细菌通过气孔途径感染植物。然而，当细菌渗透到叶片组织中以绕过气孔防御时，细菌感染增强。追踪天然AHA 1和SYP 132丰度、细胞分布和功能的时间依赖性变化，我们发现细菌病原体感染触发AHA 1和SYP 132从质膜内化。AHA 1通过其调节SNARE Habc结构域与SYP 132结合，这些相互作用影响PM H+-ATP酶的运输。值得注意的是，使用拟南芥aha 1突变体，我们发现，AHA 1是必不可少的调节SYP 132丰度和相关的分泌PR 1在质膜上的病原体防御。因此，我们表明，在发病过程中SYP 132协调AHA 1与交通的AHA 1和PR 1的相反效果。SNARE SYP 132和质膜H+-ATPase AHA 1之间的协调在发病过程中调节SNARE丰度，对AHA 1和抗菌剂发病相关蛋白1的运输具有相反的作用。
The vesicle trafficking SYNTAXIN OF PLANTS132 (SYP132) drives hormone-regulated endocytic traffic to suppress the density and function of plasma membrane (PM) H+-ATPases. In response to bacterial pathogens, it also promotes secretory traffic of antimicrobial pathogenesis-related (PR) proteins. These seemingly opposite actions of SYP132 raise questions about the mechanistic connections between the two, likely independent, membrane trafficking pathways intersecting plant growth and immunity. To study SYP132 and associated trafficking of PM H+-ATPase 1 (AHA1) and PATHOGENESIS-RELATED PROTEIN1 (PR1) during pathogenesis, we used the virulent Pseudomonas syringae pv. tomato DC3000 (Pst DC3000) bacteria for infection of Arabidopsis (Arabidopsis thaliana) plants. SYP132 overexpression suppressed bacterial infection in plants through the stomatal route. However, bacterial infection was enhanced when bacteria were infiltrated into leaf tissue to bypass stomatal defenses. Tracking time-dependent changes in native AHA1 and SYP132 abundance, cellular distribution, and function, we discovered that bacterial pathogen infection triggers AHA1 and SYP132 internalization from the plasma membrane. AHA1 bound to SYP132 through its regulatory SNARE Habc domain, and these interactions affected PM H+-ATPase traffic. Remarkably, using the Arabidopsis aha1 mutant, we discovered that AHA1 is essential for moderating SYP132 abundance and associated secretion of PR1 at the plasma membrane for pathogen defense. Thus, we show that during pathogenesis SYP132 coordinates AHA1 with opposing effects on the traffic of AHA1 and PR1. Coordination between SNARE SYP132 and plasma membrane H+-ATPase AHA1 moderates SNARE abundance during pathogenesis with opposing effects on trafficking of AHA1 and antimicrobial pathogenesis-related protein 1.
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