P-382 - Target of rapamycin (TOR) regulates sulfur-mediated beneficial plant-microbe interactions

The metabolic communication between beneficial microbes and their host plants plays a crucial role in enhancing plant resilience to environmental stresses. For instance, the endophytic beneficial bacterium Enterobacter sp. SA187 provides sulfur-containing metabolic signals to plants, thereby mitigating salt stress. However, the molecular perception of these sulfur cues by the host plants remains unknown. In this study, we elucidate that SA187 activates the plant TOR (target of rapamycin) pathway, which is essential in mediating the beneficial effects of SA187. Both sulfur (S) deficiency and salt stress reduce TOR activity, which is effectively restored by SA187. We demonstrate that the SA187-produced metabolite 2-keto-4-methylthiobutyric acid (KMBA) is sufficient to activate the TOR pathway at nanomolar concentrations. Furthermore, SA187-driven TOR activation leads to de novo protein translation in host plants. These findings identify TOR as a key molecular sensor of sulfur compounds and an essential mediator of beneficial plant-microbe interaction.