| Summary: | The physiological responses and molecular mechanisms of apoptosis in Japanese flounder under hypoxic stress remain unclear. In the present study, we performed acute hypoxia stress on Japanese flounder (2.39 ± 0.84 mg/L) and detected gills responses in histomorphology and molecular mechanisms. The results showed that the volume of the interlamellar cell mass decreased and the gill lamellae prolonged, indicating the expansion of the respiratory surface area. Additionally, the fluorescence signal of apoptosis increased under hypoxic stress. In addition, the expression of two genes (<i>EPAS1</i> and <i>Bad</i>) related to apoptosis increased about four-fold and two-fold, respectively, at 6 h of hypoxia. Meanwhile, the result of the dual-luciferase reporter assay showed that EPAS1 is a transcription factor, which could regulate <i>(p <</i> 0.05) the expression of the <i>Bad</i> gene, and we identified the binding site of EPAS1 was the AATGGAAAC sequence located near −766. DNA methylation assay showed that hypoxia affected the methylation status of CpG islands of <i>EPAS1</i> and <i>Bad</i> genes. All results indicated that hypoxia could activate the <i>EPAS1/Bad</i> signal pathway to induce gill apoptosis of Japanese flounder. Our study provides new light on understanding the molecular mechanism of hypoxia-induced apoptosis in Japanese flounder.
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