Julian Preiner, Irene Steccari, Eva Oburger, Stefanie Wienkoop
Molybdenum (Mo) serves an important biological role as part of cofactors of various enzymes in all domains of life. In plants, it is critical for nitrogen metabolism and integral to rhizobial enzymes such as nitrogenase, which is essential for plant-rhizobia symbiosis. However, like other transition metals, Mo can be toxic at excess concentrations. Its chemical analog tungsten (W) has no biological function in eukaryotes and is known to be toxic, primarily by inhibiting molybdoenzymes. Previously, we found that soybean ( Glycine max ) in symbiosis with N 2 -fixing rhizobia ( Bradyrhizobium japonicum ) (N fix plants) had greater capacity to synthesize protective compounds in response to W-induced stress than KNO 3 -fertilized (N fed) plants. This shotgun metabolomic and proteomic study investigates the response of N fed and N fix plants to excess Mo (0.5 mM Na 2 MoO 4 ), whether the metabolic plasticity observed upon W-stress is also present in Mo-exposed N fix plants and the key drivers of this plasticity. Our results show that, similar to W, excess Mo elicits a strong metabolic response in symbiotic soybean plants, disrupting plant growth, photosynthesis, nitrogen metabolism and the translocation of essential nutrients including Fe, Cu, Mn and S. Furthermore, excess Mo elicits a profile of protective compounds that is qualitatively similar to, but quantitatively distinct from, that seen under W stress. Notably, while this defense response was more pronounced in symbiotic plants (N fix) under W and Mo stress, it did not result in restored plant growth. Together, these findings demonstrate that the deployment of protective compounds is largely independent of whether the excess metal is essential for plant growth. The fact that this response is associated with the plant-rhizobia symbiosis highlights the importance of biotic interactions for shaping a plant’s chemical defense against abiotic stress.