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<i>Caspase-8</i>, a member of the caspase family, is an initiating caspase and plays a crucial role in apoptosis. In this study, the full-length cDNA of <i>caspase8-like</i> (<i>CASP8-like</i>) was isolated from <i>Crassostrea hongkongensis</i> (<i>C. hongkongensis</i>) by RACE-PCR. <i>ChCASP8-like</i> contained a 1599-bp open reading frame (ORF) encoding 533 amino acids with two conserved death effector domains (DEDs) and a cysteine aspartase cysteine structural domain (CASc). Amino acid sequence comparison showed that <i>ChCASP8-like</i> shared the highest identity (85.4%) with <i>CASP8-like</i> of <i>C. angulata</i>. The tissue expression profile showed that <i>ChCASP8-like</i> was constitutively expressed in gills, hepatopancreas, mantle, adductor muscle, hemocytes and gonads, and was significantly upregulated in hemocytes, hepatopancreas and gills under hyper-salinity stress. The apoptosis-related genes, including <i>ATR</i>, <i>CHK1</i>, <i>BCL-XL</i>, <i>CASP8-like</i>, <i>CASP9</i> and <i>CASP3,</i> were significantly activated by hyper-salinity stress, but were remarkably inhibited by <i>ChCASP8-like</i> silencing. The caspase 8 activity was increased by 1.7-fold after hyper-salinity stress, and was inhibited by 9.4% by <i>ChCASP8-like</i> silencing. Moreover, <i>ChCASP8-like</i> silencing clearly alleviated the apoptosis resulting from hyper-salinity stress. These results collectively demonstrated that <i>ChCASP8-like</i> played a crucial role in inducing apoptosis against hyper-salinity stress.