Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells

Xin Yu Chen, Chiu Ming Wen, Cho Fat Hui, Ming Chyuan Chen, Jen Leih Wu, Tsai Ching Hsueh, Wei Han Lei, Jiann-Ruey Hong

Research output: Contribution to journalArticlepeer-review

8 Citations (Scopus)

Abstract

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.

Original languageEnglish
Pages (from-to)848-857
Number of pages10
JournalFish and Shellfish Immunology
Volume45
Issue number2
DOIs
Publication statusPublished - 2015 Aug 1

All Science Journal Classification (ASJC) codes

  • Environmental Chemistry
  • Aquatic Science

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