UV-mediated apoptosis is a highly complex process in which different molecular pathways are involved. These include DNA damage,triggering of cell death receptors and the broken of mitochondria. It has been reported that DNA damage which is induced by UV irradiation can active the tumor suppressor p53 and trigger a cascade response of cell apoptosis. One of the most importment thing is the expression of PUMA is upregulated. However,the mechanism of PUMA-mediated apoptosis and Bax translocation after UV irradiation remains unclear. In this study,the fluorescence resonance energy transfer (FRET) technique was used to study the dynamic interaction among PUMA,Bax and Bcl-Xl in living single-cells. ASTC-a-1 cells were transiently co-transfected with GFP-PUMA and YFP-Bcl-Xl or CFP-Bcl-Xl and YFP-Bax,followed with 120 mJ/cm2 UV irradiation. We found that the FRET intensity of GFP-PUMA and YFP-Bcl-Xl increased while the FRET intensity of CFP-Bcl-Xl and YFP-Bax dicreased suggesting PUMA has a more strong interaction with Bcl-Xl than Bax. At the same time,GFP-Bax translocated to the mitochondria from the cytosol in typical cells started at about 7 h after UV irradiation. Taken together,the results indicated that PUMA promotes Bax translocation by competitive binding to Bcl-Xl during UV-induced apoptosis.