Department of Biology, Washington University in St. Louis, St. Louis, MO 63130, U.S.A.
NSF Center for Engineering Mechanobiology, Washington University in St. Louis, St. Louis, MO 63130, U.S.A.
Mol Plant Microbe Interact. 2022 Jul;35(7):567-582. doi: 10.1094/MPMI-08-21-0207-FI. Epub 2022 Apr 20.
Plants sense and respond to molecular signals associated with the presence of pathogens and their virulence factors. Mechanical signals generated during pathogenic invasion may also be important, but their contributions have rarely been studied. Here, we investigate the potential role of a mechanosensitive ion channel, MscS-like (MSL)10, in defense against the bacterial pathogen in . We previously showed that overexpression of MSL10-GFP, phospho-mimetic versions of MSL10, and the gain-of-function allele all produce dwarfing, spontaneous cell death, and the hyperaccumulation of reactive oxygen species. These phenotypes are shared by many autoimmune mutants and are frequently suppressed by growth at high temperature in those lines. We found that the same was true for all three hypermorphs. In addition, we show that the SGT1/RAR1/HSP90 cochaperone complex was required for dwarfing and ectopic cell death, PAD4 and SID2 were partially required, and the immune regulators EDS1 and NDR1 were dispensable. All hypermorphs exhibited reduced susceptibility to infection by strain DC3000 and DC3000 expressing the avirulence genes or but not DC3000 and showed an accelerated induction of expression compared with wild-type plants. Null mutants were delayed in induction and displayed modest susceptibility to infection by coronatine-deficient pv. . Finally, stomatal closure was reduced in loss-of-function mutants in response to pv. . These data show that MSL10 modulates pathogen responses and begin to address the possibility that mechanical signals are exploited by the plant for pathogen perception.[Formula: see text] Copyright © 2022 The Author(s). This is an open access article distributed under the CC BY-NC-ND 4.0 International license.
植物能够感知和响应与病原体及其毒力因子存在相关的分子信号。在病原体入侵过程中产生的机械信号也可能很重要，但它们的贡献很少被研究。在这里，我们研究了机械敏感离子通道 MscS-like (MSL)10 在防御细菌病原体 中的潜在作用。我们之前曾表明，MSL10-GFP 的过表达、MSL10 的磷酸模拟突变体以及功能获得性等位基因 都会导致矮化、自发性细胞死亡和活性氧的过度积累。这些表型与许多自身免疫突变体共享，并且在这些系中高温生长经常抑制这些表型。我们发现，所有三种 超变体都是如此。此外，我们还表明，SGT1/RAR1/HSP90 共伴侣复合物对于矮化和异位细胞死亡是必需的，PAD4 和 SID2 部分必需，而免疫调节剂 EDS1 和 NDR1 则是可有可无的。所有 超变体对 菌株 DC3000 和表达无毒基因 或 的 DC3000 的感染敏感性降低，但对 DC3000 不敏感，与野生型植物相比，它们表现出更快的 表达诱导。 缺失突变体在 诱导方面延迟，并表现出对冠状缺陷型 pv. 的中度易感性。最后，在对 pv. 响应中，功能丧失突变体的气孔关闭减少。这些数据表明，MSL10 调节病原体反应，并开始探讨植物是否利用机械信号来感知病原体。
