Zhu, S.; Gonzalez-Fuente, M.; Leger, O.; Langin, G.; Xu, K.; Aydin, N.; Schulz, N.; Solansky, P.; Denyer, T.; Del Chiaro, A.; Dagdas, Y.; Timmermans, M.; Üstün, S.

Plant immune responses must balance effective pathogen restriction to prevent excessive tissue damage and rely on potentiation between pattern-triggered immunity (PTI) and effector-triggered immunity (ETI). However, how these immune responses are spatially organized across different cell-types and coordinated by intracellular pathways remains incompletely understood. Here, we show that autophagy functions as a central organizer of this spatial immune response 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 supressing abscisic acid (ABA) signaling through selective degradation of the ABA receptor PYL4. In contrast, in mesophyll cells, autophagy restricts immune activation and is required for effective immune execution: its loss enhances expression of the EDS1-PAD4-ADR1 immune pathway but compromises canonical PTI outputs, likely impacting PTI-ETI potentiation. This uncoupling reveals that immune activation alone is insufficient for effective defense. Together, our findings resolve the longstanding ambiguity surrounding the role of autophagy in plant immunity and establish autophagy as a spatial organizer that partitions immune strategies between stomata and mesophyll during bacterial infection.