Bip-Overexpressing Soybean Plants Display Accelerated Hypersensitivity Response (Hr) Affecting The Sa-Dependent Sphingolipid And Flavonoid Pathways

Biotic and abiotic environmental stresses have limited the increase in soybean productivity. Overexpression of the molecular chaperone BiP in transgenic plants has been associated with the response to osmotic stress and drought tolerance by maintaining cellular homeostasis and delaying hypersensitive cell death. Here, we evaluated the metabolic changes in response to the hypersensitivity response (HR) caused by the non-compatible bacteria Pseudomonas syringae pv. tomato in BiP-overexpressing plants. The HR-modified metabolic profiles in BiP-overexpressing plants were significantly distinct from the wild-type untransformed. The transgenic plants displayed a lower abundance of HR-responsive metabolites as amino acids, sugars, carboxylic acids and signal molecules, including p-aminobenzoic acid (PABA) and dihydrosphingosine (DHS), when compared to infected wild-type plants. In contrast, salicylic acid (SA) biosynthetic and signaling pathways were more stimulated in transgenic plants, and both pathogenesis-related genes (PRs) and transcriptional factors controlling the SA pathway were more induced in the BiP-overexpressing lines. Furthermore, the long-chain bases (LCBs) and ceramide biosynthetic pathways showed alterations in gene expression and metabolite abundance. Thus, as a protective pathway against pathogens, HR regulation by sphingolipids and SA may account at least in part by the enhanced resistance of transgenic plants. GmNAC32 transcriptional factor was more induced in the transgenic plants and it has also been reported to regulate flavonoid synthesis in response to SA. In fact, the BiP-overexpressing plants showed an increase in flavonoids, mainly prenylated isoflavones, as precursors for phytoalexins. Our results indicate that the BiP-mediated acceleration in the hypersensitive response may be a target for metabolic engineering of plant resistance against pathogens.