Biological Science: Research Developments and Innovations Vol. 5

Small RNAs have moved from being viewed mainly as intracellular regulators of plant gene expression to candidate mobile effectors exchanged between plants and their pathogens. This critical narrative review evaluates the evidence that small RNAs mediate cross-kingdom communication during plant disease, with emphasis on fungal and oomycete pathosystems in which donor origin, recipient machinery, molecular targets and disease phenotypes can be assessed mechanistically. Literature published from 2004 to 18 July 2026 was considered through searches of multidisciplinary and life-science scholarly sources, supplemented by citation tracing and verification of bibliographic metadata and digital object identifiers. The strongest evidence supports bidirectional RNA interference in a limited set of systems rather than a universal mechanism. Pathogen-derived small RNAs can exploit host Argonaute complexes to suppress immunity, while plant-derived microRNAs and small interfering RNAs can silence pathogen virulence or fitness genes. Recent work has strengthened causal models by identifying fungal RNA-dependent RNA polymerase and Argonaute requirements, clathrin-mediated entry of fungal extracellular vesicles, plant RNA-binding proteins associated with exported small RNAs, pathogen effectors that antagonise host RNA transport, and host competing endogenous RNA modules that buffer pathogen small-RNA activity. At the same time, major uncertainties remain. Mixed-tissue sequencing can misassign RNA origin, target prediction is frequently treated as stronger evidence than it warrants, silencing mutants can be pleiotropic, and extracellular-vesicle preparations may contain substantial non-vesicular ribonucleoprotein-associated RNA. Negative results in the wheat-Zymoseptoria tritici system and interspecific differences in environmental RNA uptake show that cross-kingdom RNA interference is conditional on recipient competence and pathosystem biology. Host-induced and spray-induced gene silencing are therefore best understood as exploitable RNA-silencing technologies whose success does not by itself prove a natural trafficking route. Progress now depends on quantitative, cell-resolved and genetically reversible demonstrations of RNA origin, transport, target engagement and disease relevance across diverse crops and pathogens.