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Caspase‐dependent induction of apoptosis in barramundi, Lates calcarifer (Bloch), muscle cells by grouper iridovirus
Author(s) -
Chiou P P,
Chen YC,
Lai YS
Publication year - 2009
Publication title -
journal of fish diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.819
H-Index - 85
eISSN - 1365-2761
pISSN - 0140-7775
DOI - 10.1111/j.1365-2761.2009.01083.x
Subject(s) - barramundi , biology , apoptosis , iridovirus , microbiology and biotechnology , programmed cell death , caspase , grouper , lates , cell culture , virology , virus , genetics , fish <actinopterygii> , fishery
We recently reported that grouper iridovirus (GIV) can induce apoptosis in barramundi, Lates calcarifer , muscle (BM) and swim bladder (BSB) cell lines. In this paper, we further characterize the molecular mechanism underlying apoptotic death in BM cells triggered by GIV. DNA‐laddering and apoptotic cells were observed in BM cells infected with UV‐irradiated or untreated GIV but was absent in cells infected with heat‐inactivated GIV, indicating the involvement of viral protein in the apoptosis event. In GIV‐infected BM cells, the conversion of procaspase‐3 to caspase‐3 was evident and the level of caspase‐8 and ‐9 increased as early as 30 min post‐infection. When treated with a pancaspase inhibitor, the GIV‐induced apoptosis event was abolished. These observations indicate that GIV‐induced apoptosis is caspase‐dependent, and that both the external and internal routes in the caspase‐dependent pathway are likely involved in the apoptosis process.