Department of Biology, Høgskoleringen 5, Realfagbygget, Norwegian University of Science and Technology, 7491 Trondheim, Norway.
Department of Biology, Imperial College London, South Kensington Campus, SW7 2AZ London, UK.
Sci Signal. 2018 Jun 26;11(536):eaao3070. doi: 10.1126/scisignal.aao3070.
Cell walls surround all plant cells, and their composition and structure are modified in a tightly controlled, adaptive manner to meet sometimes opposing functional requirements during growth and development. The plant cell wall integrity (CWI) maintenance mechanism controls these functional modifications, as well as responses to cell wall damage (CWD). We investigated how the CWI system mediates responses to CWD in CWD induced by cell wall-degrading enzymes or an inhibitor of cellulose biosynthesis elicited similar, turgor-sensitive stress responses. Phenotypic clustering with 27 genotypes identified a core group of receptor-like kinases (RLKs) and ion channels required for the activation of CWD responses. A genetic analysis showed that the RLK FEI2 and the plasma membrane-localized mechanosensitive Ca channel MCA1 functioned downstream of the RLK THE1 in CWD perception. In contrast, pattern-triggered immunity (PTI) signaling components, including the receptors for plant elicitor peptides (Peps) PEPR1 and PEPR2, repressed responses to CWD. CWD induced the expression of and , which encode the precursors of Pep1 and Pep3, and the release of PROPEP3 into the growth medium. Application of Pep1 and Pep3 repressed CWD-induced phytohormone accumulation in a concentration-dependent manner. These results suggest that Pep-mediated signaling suppresses CWD-induced defense responses controlled by the CWI mechanism. This suppression was alleviated when PTI signaling downstream of PEPR1 and PEPR2 was impaired. Defense responses controlled by the CWI maintenance mechanism might thus compensate to some extent for the loss of PTI signaling elements.
细胞壁包围着所有植物细胞，其组成和结构以一种紧密控制的、适应性的方式进行修饰，以满足生长和发育过程中有时相互矛盾的功能要求。植物细胞壁完整性（CWI）维持机制控制着这些功能修饰，以及对细胞壁损伤（CWD）的反应。我们研究了 CWI 系统如何介导对细胞壁降解酶或纤维素生物合成抑制剂诱导的 CWD 的反应。使用 27 个基因型进行的表型聚类确定了一组核心受体样激酶（RLK）和离子通道，这些激酶和通道对于 CWD 反应的激活是必需的。遗传分析表明，RLK FEI2 和位于质膜的机械敏感 Ca 通道 MCA1 在 CWD 感知中作为 RLK THE1 的下游发挥作用。相比之下，模式触发免疫（PTI）信号成分，包括植物激发肽（Peps）受体 PEPR1 和 PEPR2，抑制了对 CWD 的反应。CWD 诱导了编码 Pep1 和 Pep3 前体的基因和的表达，并将 PROPEP3 释放到生长培养基中。Pep1 和 Pep3 的应用以浓度依赖的方式抑制了 CWD 诱导的植物激素积累。这些结果表明，Pep 介导的信号抑制了由 CWI 机制控制的 CWD 诱导的防御反应。当 PEPR1 和 PEPR2 下游的 PTI 信号受损时，这种抑制作用会减轻。因此，由 CWI 维持机制控制的防御反应可能在某种程度上补偿了 PTI 信号元件的缺失。
