Protein-RNA control networks at the plant-pathogen interface.

Plant immunity depends on coordinated control of signaling gain, molecular persistence, RNA fate, interorganismal exchange and timely attenuation, defining testable routes to durable disease control. Plant immunity is often reviewed as a sequence of receptor activation, transcriptional reprogramming, and antimicrobial output. That organization is useful, but it obscures a central mechanistic problem: immune performance depends on coupled control of protein abundance, RNA fate, interorganismal exchange and response termination. Here, we develop an evidence-weighted protein-RNA control-loop framework that is explicitly differentiated from receptor-, proteostasis-, RNA-silencing- and extracellular-vesicle-centered reviews. The framework organizes plant-pathogen interactions around five experimentally tractable control variables: signaling gain, molecular persistence, RNA routing, interorganismal exchange and memory versus cost. We evaluate how pattern-recognition receptors and nucleotide-binding leucine-rich-repeat receptors set signaling gain; ubiquitination, SUMOylation, proteasomal turnover and autophagy determine persistence; RNA-binding proteins, alternative splicing, N6-methyladenosine (m6A), translation and decay route immune messages; and vesicular or non-vesicular ribonucleoprotein carriers mediate cross-kingdom RNA exchange. For each layer, we distinguish association from physical mechanism, causal perturbation, and crop-level validation. Receptor synergy, resistosome signaling, selected proteolytic circuits and several cross-kingdom RNA interference mechanisms are strongly supported, whereas generalized roles for immune m6A, stress-granule routing, vesicle-exclusive RNA transport and durable epigenetic memory remain incompletely demonstrated. The framework yields testable predictions and a stage-gated roadmap for engineered receptors, host- and spray-induced gene silencing, proteostasis or RNA-binding-protein engineering, and multi-omics breeding. Durable resistance should therefore be judged not by maximal defense activation, but by sufficient gain, correct routing, appropriate persistence and timely attenuation with acceptable yield and environmental costs.