Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection
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-m...
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ndltd-TW-096NIU071080042015-11-30T04:02:34Z http://ndltd.ncl.edu.tw/handle/12272147415756602881 Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection 以蛋白質體學探討石斑魚虹彩病毒誘發金目鱸肌肉細胞株之表現 Chen,Chin-Wen 陳瑾玟 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. Yu-Shen Lai 賴裕順 2008 學位論文 ; thesis 87 zh-TW |
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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.
|
author2 |
Yu-Shen Lai |
author_facet |
Yu-Shen Lai Chen,Chin-Wen 陳瑾玟 |
author |
Chen,Chin-Wen 陳瑾玟 |
spellingShingle |
Chen,Chin-Wen 陳瑾玟 Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
author_sort |
Chen,Chin-Wen |
title |
Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
title_short |
Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
title_full |
Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
title_fullStr |
Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
title_full_unstemmed |
Study On The Genes Expression of Barramundi (Lates calcarifer)Muscle Cell Line Induced By Grouper Iridovirus Infection |
title_sort |
study on the genes expression of barramundi (lates calcarifer)muscle cell line induced by grouper iridovirus infection |
publishDate |
2008 |
url |
http://ndltd.ncl.edu.tw/handle/12272147415756602881 |
work_keys_str_mv |
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