2011 Fiscal Year Final Research Report
Circumvention of RNA decay in cells infected with SARS coronavirus
| Project/Area Number |
22790431
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Virology
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| Research Institution | Osaka University |
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Principal Investigator |
KAMITANI Wataru 大阪大学, 微生物病研究所, 特任准教授 (60551421)
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| Project Period (FY) |
2010 – 2011
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| Keywords | 分子 / RNA分解 / 翻訳阻害 |
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| Research Abstract |
SARS coronavirus nsp1 protein was shown to suppress host protein syntheses through the degradation of mRNA and the binding to 40S ribosomal subunits. However, SCoV is capable of replicating well in cells impaired the host protein syntheses by the expression of nsp1. To determine the mechanism of an efficient translation of mRNA of SCoV in cells expressing the nsp1, we investigated the effect of the UTRs of SCoV on the evasion from the nsp1-mediated translational suppression. We generated the reporter plasmids carrying a firefly luciferase gene flanked by the 5' UTR and/ or 3' UTR of SCoV and determined the luciferase activity in cells expressing the nsp1. Suppression of luciferase activity by the expression of nsp1 was cancelled by the transfection of the reporter plasmids carrying the 5' UTR of SCoV but not by those possessing the 3' UTR. Protein-RNA binding assay revealed that the positively charged region in the nsp1 responsible for a specific interaction with the stem-loop1 in the 5' UTR.
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