Calcium-ROS-NO signalling integration in plant immunity: mechanistic interactions and feedback regulation

This review establishes Ca²⁺, ROS and NO signalling as an integrated feedback network that links pathogen perception, calcium decoding, local and systemic defence, and maintenance of immune homeostasis across tissues. Calcium (Ca²⁺) signalling is a central component of plant immune responses and provides a mechanistic link between pathogen perception and downstream defence activation. Immune stimuli generate distinct spatial and temporal Ca²⁺ signatures that are decoded by calcium sensor proteins, including calcium-dependent protein kinases, calcineurin B-like protein-interacting protein kinases, calmodulins and calmodulin-like proteins. These sensors regulate defence gene expression, hormone signalling, reactive oxygen species (ROS) production and programmed cell death. Recent structural and functional studies have further demonstrated that nucleotide-binding leucine-rich repeat (NLR) resistosomes can function as Ca²⁺-permeable channels, providing a direct connection between effector recognition and Ca²⁺ influx during effector-triggered immunity. Increasing evidence also shows extensive bidirectional communication amongst Ca²⁺, ROS and nitric oxide (NO). Ca²⁺-dependent activation of NADPH oxidases promotes ROS production, whereas ROS and NO can modulate Ca²⁺ fluxes and signalling components through redox-dependent mechanisms. These reciprocal interactions generate feedback circuits that regulate the intensity, duration and spatial propagation of immune responses. This review summarizes current knowledge of Ca²⁺ channels and sensor proteins involved in plant immunity and integrates recent findings on Ca²⁺-ROS-NO crosstalk. Particular emphasis is placed on feedback regulation and unresolved mechanisms governing the spatio-temporal coordination of these signals. Understanding this integrated signalling network will advance mechanistic approaches for improving crop disease resistance whilst limiting detrimental effects of excessive immune activation.