Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells. Issue 2 (August 2015)
- Record Type:
- Journal Article
- Title:
- Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells. Issue 2 (August 2015)
- Main Title:
- Giant seaperch iridovirus infection upregulates Bas and Bak expression, leading to apoptotic death of fish cells
- Authors:
- Chen, Xin-Yu
Wen, Chiu-Ming
Hui, Cho-Fat
Chen, Ming-Chyuan
Wu, Jen-Leih
Hsueh, Tsai-Ching
Lei, Wei-Han
Hong, Jiann-Ruey - Abstract:
- 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. Graphical abstract: Highlights: Iridovirus (GSIV) induces host cell apoptosis by an ill-understood process. GSIV can upregulate the pro-apoptotic death genes Bax and Bak at the middle replication stage. Pro-apoptotic gene Bax and Bak gene upregulation could be blocked by protein synthesis inhibitor cycloheximide. The GSIV-induced Bax/Bak-mediated cell death may reduce by theAbstract: 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. Graphical abstract: Highlights: Iridovirus (GSIV) induces host cell apoptosis by an ill-understood process. GSIV can upregulate the pro-apoptotic death genes Bax and Bak at the middle replication stage. Pro-apoptotic gene Bax and Bak gene upregulation could be blocked by protein synthesis inhibitor cycloheximide. The GSIV-induced Bax/Bak-mediated cell death may reduce by the anti-apoptotic gene Bcl-xL in fish cells. … (more)
- Is Part Of:
- Fish & shellfish immunology. Volume 45:Issue 2(2015:Aug.)
- Journal:
- Fish & shellfish immunology
- Issue:
- Volume 45:Issue 2(2015:Aug.)
- Issue Display:
- Volume 45, Issue 2 (2015)
- Year:
- 2015
- Volume:
- 45
- Issue:
- 2
- Issue Sort Value:
- 2015-0045-0002-0000
- Page Start:
- 848
- Page End:
- 857
- Publication Date:
- 2015-08
- Subjects:
- Iridovirus -- Pro-apoptotic gene -- Bax -- Bak -- Bcl-xL -- Upregulation -- Overexpression
Fishes -- Immunology -- Periodicals
Shellfish -- Immunology -- Periodicals
Poissons -- Immunologie -- Périodiques
Crustacés -- Immunologie -- Périodiques
571.9617 - Journal URLs:
- http://www.sciencedirect.com/science/journal/10504648 ↗
http://firstsearch.oclc.org ↗
http://firstsearch.oclc.org/journal=1050-4648;screen=info;ECOIP ↗
http://www.sciencedirect.com/science/journal/latest/10504648 ↗
http://www.elsevier.com/journals ↗ - DOI:
- 10.1016/j.fsi.2015.06.003 ↗
- Languages:
- English
- ISSNs:
- 1050-4648
- Deposit Type:
- Legaldeposit
- View Content:
- Available online (eLD content is only available in our Reading Rooms) ↗
- Physical Locations:
- British Library DSC - 3934.880000
British Library DSC - BLDSS-3PM
British Library HMNTS - ELD Digital store - Ingest File:
- 25299.xml