The inner ear structures are derived from the otic vesicle (OV) which is formed by thickening and invagination of the otic placode of the surface ectoderm. A number of neuroblasts, which arise from epithelial cells of the otic vesicle, delaminate and differentiate into neurons of the cochleovestibular ganglion (CVG). We have found that transforming growth factor-BEta2 (Tgfbeta2 ) was expressed in the otic epithelium at the OV stages between Embryonic days (E) 9.5 and 11.5 and that anteroventrolateral localization of its expression in the OV overlapped with that of NeuroD, which is a marker of delaminating CVG precursors. The expression of TGFbeta type I and type II receptors in the otic epithelium and the nuclear localization of phosphorylated-Smad2 in both the otic epithelium and CVG suggested that TGFbeta2 signaling plays some roles in CVG formation. In order to examine the roles of TGFbeta2 in differentiation of the inner ear, otic vesicle explants of E10.5 mouse embryos were treated in vitro with TGFbeta2 or the TGFbeta type I receptor kinase inhibitor, SB431542. Addition of TGFbeta2 peptide to the culture led to Enlargement of the CVG, while the inhibitor reduced its size. These findings strongly imply that TGFbeta2 contributes to the development of the CVG in mouse embryos.