Mechanisms of Trichoderma-induced plant immunity: An RNA-epigenetic perspective

Abstract

Root-associated beneficial microbes can enhance plant resistance at the systemic level without triggering constitutive defense activation, yet how such durable and low-cost immune states are established remains poorly understood. Plant-Trichoderma spp. mutualism represents a well-characterized model of beneficial plant-microbe interactions in which induced resistance is maintained despite the absence of sustained transcriptional defense outputs. Accumulating evidence implicates small RNAs, including microRNAs (miRNAs), small interfering RNAs (siRNAs), and long non-coding RNAs (lncRNAs), as central regulators of immune priming during Trichoderma-plant interactions. Such RNA-mediated processes shape defense responsiveness, hormonal sensitivity, and chromatin-associated regulation. In parallel, epigenetic modifications have been linked to the persistence and reversibility of primed immune states. However, these regulatory layers are often examined separately, limiting mechanistic understanding of how immune states are both stabilized and flexibly reprogrammed. In this conceptual review, we synthesize recent advances to examine Trichoderma-induced systemic immunity through an integrated RNA-epigenetic perspective. By viewing RNA-mediated regulation and epigenetic modification as components of a functional continuum, we illustrate how immune priorities defined by small RNAs can be consolidated into chromatin states that preserve inducibility without imposing constitutive costs. This framework provides a coherent explanation for how Trichoderma-induced immunity is organized across molecular layers in plants.