Connexin 43 (Cx43) is one of the gap junction proteins which are compounds of transmembrane proteins and transports the small-molecular-weight chemicals up to 2 kDa. Lacking of Cx43 influences the junctional protein, induces autophagy and apoptosis in somatic cells. However, the function of Cx43 in porcine early embryos is still unknown. Aim to find out the molecular mechanism of Cx43 on the developmental competence in early porcine embryos, Cx43 dsRNA (1 ㎍/㎕) was microinjected into the parthenogenetically activated porcine zygotes. Blastocyst rate (treatment, 8.8±1.6% vs. control, 38.6±4.3%) and total cell numbers in the blastocyst (treatment, 20.7±3.5 vs. control, 39.8±4.1) were significantly reduced following Cx43 knocking down. Results from FITC-dextran and Western blot assay show that knock down (KD) of Cx43 significantly increased membrane permeability through down regulation of genes which are component of both adherence and tight junction in the porcine blastocyst. Reactive oxygen species (ROS) was significantly increased in the Cx43 KD group compared to control. In addition, KD of Cx43 activated Caspase 3 and significantly increased ATG8 expression, induced autophagy and apoptosis. Results suggest that KD of Cx43 influences preimplantation porcine embryo development via increasing membrane permeability and ROS generation, and inducing autophagy and apoptosis.