14-3-3σ is expressed only in cells of epithelial origin and loss of 14-3-3σ has been observed in multiple solid tumors suggesting that it functions as a tumor suppressor. However, the mechanisms by which 14-3-3σ loss leads to tumor progression are not understood. The experiments in this report demonstrate that loss of 14-3-3σ leads to an induction of the epithelial to mesenchymal transition (EMT). The EMT was accompanied by an increase in epithelial markers, a decrease in mesenchymal markers and an increase in migration and invasion were observed in the 14-3-3σ -/- cells.

Work in the laboratory has led to the development of a novel method for the generation of transgenic animals. US and Indian patent applications for the process have been filed and the protocol has been published. Further, our work has shown that loss of 14-3-3γ leads to sterility in male mice due to a defect in desmosome formation between sertoli cells and also between Sertoli cells and spermatocytes. The loss of adhesion seems to be due to a decrease in desomosome formation, due to a defect in the transport of the desmosomal plaque protein, plakoglobin (PG), to the cell border.