Effector-triggered processing body formation attenuates host translation via ER stress responses and autophagy upon bacterial infection

Compartmentalization of transcripts in biomolecular condensates allows rapid and cost-efficient responses to environmental stimuli. Processing bodies (P-bodies) are dynamic ribonucleoprotein condensates formed by phase separation in the cytosol. P-bodies are involved in translational arrest and mRNA decay and regulate several developmental processes and stress responses. Pathogens have evolved strategies to exploit host degradation pathways for their own benefit, however little is known about how they impact translation. Here we show that upon infection with pathogenic bacteriaPseudomonas syringaepathovartomato(Pst), P-body assembly is enhanced in an effector-dependent manner. Moreover, a P-body-defective mutant is more tolerant to bacterial infection due to altered endoplasmic reticulum (ER) stress responses, suggesting a role of P-bodies as novel susceptibility hubs.Pstinfection is accompanied by a general host translation attenuation, which is both effector-dependent, and deregulated in the P-body-defective mutant. This indicates that P-bodies are required for the bacterial modulation of the plant translation, probably to hinder the defense responses. Additionally, host autophagy is also exploited by the bacteria to modulate P-body dynamics and its subsequent translation attenuation, revealing a complex interplay between P-body formation and disassembly during infection. Altogether, our discoveries provide novel insights on how host translation is targeted by bacteria via effector-triggered P-body formation to promote disease and uncover unknown connections between ER stress responses and autophagy with P-body dynamics.