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 Arabidopsis thaliana. 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 Ca²⁺ 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 (AtPeps) PEPR1 and PEPR2, repressed responses to CWD. CWD induced the expression of PROPEP1 and PROPEP3, which encode the precursors of AtPep1 and AtPep3, and the release of PROPEP3 into the growth medium. Application of AtPep1 and AtPep3 repressed CWD-induced phytohormone accumulation in a concentration-dependent manner. These results suggest that AtPep-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，它们的组成和结构以严格控制的自适应方式进行修饰，以满足生长和发育过程中有时相反的功能要求。植物细胞壁完整性（CWI）维护机制控制着这些功能的修改，以及对细胞壁损伤（CWD）的响应。我们调查了CWI系统如何介导拟南芥对CWD的反应。由细胞壁降解酶或纤维素生物合成抑制剂诱导的CWD引起类似的，对胸腺敏感的应激反应。具有27个基因型的表型聚类确定了激活CWD响应所需的受体样激酶（RLK）和离子通道的核心组。遗传分析表明，在CWD感知中，RLK FEI2和质膜定位的机械敏感Ca ²⁺通道MCA1在RLK THE1的下游起作用。相比之下，模式触发的免疫（PTI）信号传导成分，包括植物激发子肽（在Peps）的受体PEPR1和PEPR2，抑制了对CWD的应答。CWD诱导PROPEP1和PROPEP3的表达，它们编码At的前体。Pep1和At Pep3，并将PROPEP3释放到生长培养基中。At Pep1和At Pep3的应用以浓度依赖的方式抑制了CWD诱导的植物激素蓄积。这些结果表明，At Pep介导的信号传导抑制了CWI机制控制的CWD诱导的防御反应。当PEPR1和PEPR2下游的PTI信号传导受损时，这种抑制作用得以缓解。因此，由CWI维护机制控制的防御响应可能会在一定程度上补偿PTI信号元素的丢失。