Eukaryotic cells respond to the accumulation of unfolded protein within the endoplasmic reticulum (ER) through a signaling pathway that coordinates the increase in the ER protein folding capacity, the activation of the ER-associated protein degradation and the attenuation of protein synthesis. This pathway, designated unfolded protein response (UPR), is activated by several physiological stresses that disturb the ER homeostasis and is sensed by the ER-resident molecular chaperone BiP (Binding protein). We have shown previously that plant BiP, in addition to alleviating the ER stress, improves the water deficit tolerance in tobacco. We have also identified by microarray hybridizations 10 genes which were coordinately up-regulated by ER stressors and osmotic stress. The combination of both stresses promoted a synergistic effect on the induction of the co-regulated genes, as judged by qRT-PCR. These results demonstrated that the osmotic and ER stress responses converge at the level of gene activation. To further characterize this convergent pathway we analyzed directly the effect of BiP overexpression on the induction of the co-regulated genes. We first obtained soybean plants overexpressing the soyBiPD gene under the control of the 35S-CaMV promoter. The transformants were selected by qRT-PCR using transgene-specific primers and the over-accumulation of the protein was confirmed by immunoblottings. Transgenic soybean plants were treated with PEG to induce osmotic stress or tunicamycin, a potent ER stressor, and the induction of the co-regulated genes was assayed by qRT-PCR. While overexpression of BiP inhibited slightly the UPR, it promoted a robust activation of the ER- and osmotic- stress convergent pathway in response to PEG and, to a lesser extent, in response to tunicamycin. These results indicate that this abiotic stress convergent response and UPR function in distinct signal transduction pathways. Based on the functional signature of the co-up-regulated genes, which have been classified primarily as NAC transfactors and apoptosis markers, we are currently addressing the identity of this novel branch of the ER stress response