Research ArticlePlant biology

The plant cell wall integrity maintenance and immune signaling systems cooperate to control stress responses in Arabidopsis thaliana

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Sci. Signal.  26 Jun 2018:
Vol. 11, Issue 536, eaao3070
DOI: 10.1126/scisignal.aao3070

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Responding to plant cell wall damage

When plant cell walls are damaged by mechanical or biochemical means, the cells initiate adaptive responses to repair the walls and prevent infection. Whereas the cell wall integrity (CWI) maintenance mechanism monitors the status of the cell wall and initiates adaptive cellular responses to damage, pattern-triggered immunity (PTI) induces both cellular and systemic responses that limit infection. Engelsdorf et al. found that osmosensitive alterations in the mechanical properties of the cell wall were important for inducing the adaptive responses to cell wall damage. The receptor-like kinases THE1 and FEI2 and the ion channel MCA1 were required for stimulating CWI-dependent responses to damage. Cell wall damage also induced the expression of host defense peptides that promoted PTI and dampened CWI-dependent processes. The CWI mechanism still elicited damage responses even when PTI was impaired, suggesting that it serves as a failsafe to protect plants even if the immune response is compromised.

Abstract

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.

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