摘要Genetic studies with mouse models have shown that fibroblast growth factor receptor 2-Ⅲb (FGFR2-Ⅲb) plays crucial roles in lung development and differentiation.To evaluate the effect of FGFR2-Ⅲb in pig lung development,we employed somatic cell nuclear transfer (SCNT) technology to generate transgenic pig fetuses overexpressing the transmembrane (dnFGFR2-Ⅲb-Tm) and soluble (dnFGFR2-Ⅲb-HFc) forms of the dominant-negative human FGFR2-Ⅲb driven by the human surfactant protein C (SP-C) promoter,which was specifically expressed in lung epithelia.Eight dnFGFR2-Ⅲb-Tm transgenic and twelve dnFGFR2-Ⅲb-HFc transgenic pig fetuses were collected from three and two recipient sows,respectively.Repression of FGFR2-Ⅲb in lung epithelia resulted in smaller lobes and retardation of alveolarization in both forms of dnFGFR2-Ⅲb transgenic fetuses.Moreover,the dnFGFR2-Ⅲb-HFc transgenic ones showed more deterioration in lung development.Our results demonstrate that disruption of FGFR2-Ⅲb signaling in the epithelium impedes normal branching and alveolarization in pig lungs,which is less severe than the results observed in transgenic mice.The dnFGFR2-Ⅲb transgenic pig is a good model for the studies of blastocyst complementation as well as the mechanisms of lung development and organogenesis.