TY - JOUR
T1 - Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells
AU - Chen, Xin Yu
AU - Wen, Chiu Ming
AU - Hui, Cho Fat
AU - Chen, Ming Chyuan
AU - Wu, Jen Leih
AU - Hsueh, Tsai Ching
AU - Lei, Wei Han
AU - Hong, Jiann-Ruey
PY - 2015/8/1
Y1 - 2015/8/1
N2 - The giant seaperch iridovirus (GSIV) induces host cell apoptosis by a poorly-understood process. In this study, GSIV is shown to upregulate the pro-apoptotic death genes Bax and Bak at the middle replication stage, and factors in the grouper fin cell line (GF-1) are shown to modulate this process. Studying the mechanism of cell death, we found that upregulated, de novo-synthesized Bax and Bak proteins formed heterodimers. This up-regulation process correlated with mitochondrial membrane potential (MMP) loss, increased caspase-3 activity, and increased apoptotic cell death. All effects were diminished by treatment of infected GF-1 cells with the protein synthesis inhibitor cycloheximide. Interestingly, overexpression of the anti-apoptotic gene Bcl-xL also diminished GSIV-induced mitochondria-mediated cell death, increasing host cell viability and decreasing MMP loss at the early replication stage. Our data suggest that GSIV induces GF-1 apoptotic cell death through up-regulation of the pro-apoptotic genes Bax and Bak, which are regulated by Bcl-xL overexpression on mitochondria in GF-1 cells.
AB - The giant seaperch iridovirus (GSIV) induces host cell apoptosis by a poorly-understood process. In this study, GSIV is shown to upregulate the pro-apoptotic death genes Bax and Bak at the middle replication stage, and factors in the grouper fin cell line (GF-1) are shown to modulate this process. Studying the mechanism of cell death, we found that upregulated, de novo-synthesized Bax and Bak proteins formed heterodimers. This up-regulation process correlated with mitochondrial membrane potential (MMP) loss, increased caspase-3 activity, and increased apoptotic cell death. All effects were diminished by treatment of infected GF-1 cells with the protein synthesis inhibitor cycloheximide. Interestingly, overexpression of the anti-apoptotic gene Bcl-xL also diminished GSIV-induced mitochondria-mediated cell death, increasing host cell viability and decreasing MMP loss at the early replication stage. Our data suggest that GSIV induces GF-1 apoptotic cell death through up-regulation of the pro-apoptotic genes Bax and Bak, which are regulated by Bcl-xL overexpression on mitochondria in GF-1 cells.
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U2 - 10.1016/j.fsi.2015.06.003
DO - 10.1016/j.fsi.2015.06.003
M3 - Article
C2 - 26067170
AN - SCOPUS:84934935299
VL - 45
SP - 848
EP - 857
JO - Fish and Shellfish Immunology
JF - Fish and Shellfish Immunology
SN - 1050-4648
IS - 2
ER -