Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection

• Main Authors: Chen,Chin-Wen, 陳瑾玟
• Other Authors: Yu-Shen Lai
• Format: Others
• Language: zh-TW
• Published: 2008
• Online Access: http://ndltd.ncl.edu.tw/handle/12272147415756602881

碩士 === 國立宜蘭大學 === 生物技術研究所碩士班 === 96 === By definition, viruses are unable to replicate within a host cell. Virus infection can trigger events that lead to apoptosis, however some viruses are known to encode gene products or induce host gene products that block apoptosis and use the host-cell macro-molecular machinery and energy supplies to replicate. In previous studies, it was suggested that GIV could induced apoptosis in barramundi muscle cells via caspase-3, -8, -9 activation pathway. In this study, a proteomic method was applied to identify alterations in protein expression profile in barramundi muscle cells and being an indicator of apoptosis after GIV infection. From this screening, 7 novel proteins were identfied, including Initiation factor 4A 1B （eIF4A1B）, Proteasome 20S, ADP-ribosylation factor 1 （Arf-1）, Ribose 5 phosphate isomerase（RPIA）, Tyrosine Hydroxylase（TH）, RAN binding protein 1, and Phosphoglycerate mutase 1（PGAM1）, were overexpressed in GIV-infected barramundi muscle cells. In addition, we also determined these genes expression levels by real-time PCR. The results showed that except Initiation factor 4A 1B （eIF4A1B）but, ADP-ribosylation factor 1（Arf-1）, Ribose 5 phosphate isomerase （RPIA）and Tyrosine Hydroxylase （TH）were up regulated conpared to the mock-infected cells. However, the Phosphoglycerate mutase 1（PGAM1） expression only rises slightly is heightened in comparison to the mock-infected cells. Summarized our results indicated that GIV could induce host genes expression level, by GIV infection and supports viral, and replication virus-infected cells of premature death. Our results provide an information for understanding of GIV viral replcation in the host cells and possible mechenisms apoptosis regulatory systems.