Plant Science Group, Laboratory of Plant Physiology and Biophysics, Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, University of Glasgow, Bower Building, Glasgow G12 8QQ, UK.
Plant Physiol. 2022 Jun 27;189(3):1639-1661. doi: 10.1093/plphys/kiac149.
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.
植物囊泡运输 SYP132 驱动激素调节的内吞作用，以抑制质膜（PM）H+-ATPase 的密度和功能。针对细菌病原体，它还促进抗菌病相关（PR）蛋白的分泌运输。SYP132 的这两种看似相反的作用引发了关于这两种可能独立的膜运输途径在植物生长和免疫中相互交叉的机制联系的问题。为了研究 SYP132 以及 PM H+-ATPase 1（AHA1）和抗病相关蛋白 1（PR1）在发病过程中的相关运输，我们使用了毒力强的丁香假单胞菌 pv.番茄 DC3000（Pst DC3000）细菌感染拟南芥（Arabidopsis thaliana）植物。SYP132 的过表达通过气孔途径抑制了植物的细菌感染。然而，当细菌渗透到叶组织中以绕过气孔防御时，细菌感染得到增强。跟踪原生 AHA1 和 SYP132 丰度、细胞分布和功能的时变变化，我们发现细菌病原体感染触发了 AHA1 和 SYP132 从质膜内化。AHA1 通过其调节性 SNARE Habc 结构域与 SYP132 结合，这些相互作用影响了 PM H+-ATPase 运输。值得注意的是，使用拟南芥 aha1 突变体，我们发现 AHA1 对于调节 SYP132 的丰度以及 PR1 在质膜上的相关分泌以抵抗病原体至关重要。因此，我们表明，在发病过程中，SYP132 协调 AHA1 以对 AHA1 和 PR1 的运输产生相反的影响。
