Autophagy acts as a spatial organizer of cell-type-specific plant immunity

Summary Effective plant immunity requires precise spatial coordination of immune responses across cell-types to restrict pathogens while preventing tissue damage, yet the intracellular pathways that organize this spatial architecture remain unknown. Here we show that autophagy serves as a spatial coordinator of immunity, partitioning and calibrating immune strategies across tissues during Pseudomonas syringae infection in Arabidopsis thaliana . Combining single-cell transcriptomics, cell-type-specific complementation, and live-cell imaging, we uncover distinct and opposing roles of autophagy across tissues. In guard cells, autophagy promotes pathogen-induced stomatal reopening by suppressing abscisic acid (ABA) signalling in part via autophagic turnover of the guard cell ABA receptor PYL4. In contrast, in mesophyll cells, autophagy restricts immune activation while simultaneously enabling effective immune execution: its loss enhances EDS1-PAD4-ADR1 pathway expression yet compromises PTI outputs. Mechanistically, bacterial infection triggers autophagic EDS1 turnover, supporting a model in which controlled EDS1 recycling facilitates HR elicitation. Cell-type-specific complementation reveals that PTI competence may involve coordinated autophagy across tissues, whereas mesophyll-autonomous autophagy is partially sufficient for HR execution. Together, these findings establish a framework in which spatial control of proteostasis orchestrates multicellular immune coordination, with broad implications for understanding how conserved degradation pathways regulate layered immunity across organisms.