Selective autophagy functions not only in nutrient recycling and stress adaptation but also in the degradation of pathogen-derived virulence effectors during effector‑triggered immunity (ETI). However, how vacuolar sorting receptors (VSRs) coordinate endomembrane trafficking and selective autophagy during ETI remained poorly understood. In a recent study, we identified four pathogen‑inducible VSRs (VSR1, VSR5, VSR6, VSR7) that play important roles in regulating vacuolar cargo sorting, tonoplast - plasma membrane fusion, and hypersensitive cell death during ETI. Importantly, upon pathogen invasion and immune activation, VSR1 dynamically relocalized from the prevacuolar compartment/multivesicular body (PVC/MVB) to ATG8-positive autophagosomes. Moreover, loss of VSR function impaired autophagic flux and disrupted degradation of bacterial effectors. These observations illustrated a model in which pathogen-responsive VSRs function as a trafficking hub, integrating secretory and effector-phagy to enable rapid and effective plant immunity during ETI.Abbreviations: VSRs, vacuolar sorting receptors; TGN, trans-Golgi network; PVC/MVB, prevacuolar compartment/multivesicular body; ETI, effector‑triggered immunity; P. syringae,Pseudomonas syringae; PM, plasma membrane; NLR, nucleotide-binding leucine-rich repeat; HR, hypersensitive response; ECS, extracellular space; NPR1, nonexpressor of pathogenesis-related genes 1; AP, adaptor protein; PLCPs, pathogen-inducible papain-like cysteine proteases; ATG, autophagy-related; NBR1, neighbor of BRCA1 gene 1 protein; FLS2, FLAGELLIN-SENSING 2.
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