Mechanosensitive ion channels in plant immunity: initiators of systemic Ca2⁺ and electrical signaling

Abstract

Plants constantly encounter mechanical forces such as wind, rain, touch, and soil resistance. These forces can function as biological signals that influence growth, immune responses, and adaptation. Mechanical stimuli are converted into electrical and Ca²⁺ signals through mechanosensitive ion channels, generating local Ca²⁺ signatures that may either remain local or propagate as waves through vascular tissues and neighboring cells. This review critically evaluates the evidence that mechanosensitive ion channels initiate or gate systemic Ca²⁺ and electrical signaling in plant immunity, while distinguishing established mechanisms from testable hypotheses. Recent molecular and electrophysiological studies support this framework. JUE1, an MscS-like mechanosensitive channel gene in Torenia, is required for rapid propagation of touch-induced Ca²⁺ waves within the stigma and for stigma movement, but the study does not establish JUE1 as the initial force sensor or a mediator of whole-plant systemic signaling. OSCA/TMEM63 channels provide a structural model for force-from-lipid gating; plant OSCAs were first linked to hyperosmolality-induced Ca²⁺ responses. Together, these findings support the view that mechanosensitive channels act as core molecular hardware for plant electromechanical signaling, but they do not imply that a single channel family explains all systemic responses. We propose a framework that separates (i) force encoding at the channel level, (ii) local Ca²⁺/electrical signatures, (iii) propagation through excitable tissues, and (iv) decoding into growth and defense outputs. Connecting channel biophysics with systemic signaling should advance predictive plant mechanobiology and support strategies for improving resilience and immunity.