Evidence that RNA silencing functions as an antiviral defense mechanism in fungi
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- Gert C. Segers
- Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, Rockville, MD 20850
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- Xuemin Zhang
- Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, Rockville, MD 20850
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- Fuyou Deng
- Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, Rockville, MD 20850
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- Qihong Sun
- Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, Rockville, MD 20850
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- Donald L. Nuss
- Center for Biosystems Research, University of Maryland Biotechnology Institute, Shady Grove Campus, Rockville, MD 20850
抄録
<jats:p> The role of RNA silencing as an antiviral defense mechanism in fungi was examined by testing the effect of dicer gene disruptions on mycovirus infection of the chestnut blight fungus <jats:italic>Cryphonectria parasitica. C. parasitica</jats:italic> dicer-like genes <jats:italic>dcl-1</jats:italic> and <jats:italic>dcl-2</jats:italic> were cloned and shown to share a high level of predicted amino acid sequence identity with the corresponding dicer-like genes from <jats:italic>Neurospora crassa</jats:italic> [Nc <jats:italic>dcl-1</jats:italic> (50.5%); Nc <jats:italic>dcl-2</jats:italic> (38.0%)] and <jats:italic>Magnaporthe oryzae</jats:italic> [ <jats:italic>MDL-1</jats:italic> (45.6%); <jats:italic>MDL-2</jats:italic> (38.0%)], respectively. Disruption of <jats:italic>dcl-1</jats:italic> and <jats:italic>dcl-2</jats:italic> resulted in no observable phenotypic changes relative to wild-type <jats:italic>C. parasitica</jats:italic> . Infection of Δ <jats:italic>dcl-1</jats:italic> strains with hypovirus CHV1-EP713 or reovirus MyRV1-Cp9B21 resulted in phenotypic changes that were indistinguishable from that exhibited by wild-type strain <jats:italic>C. parasitica</jats:italic> EP155 infected with these same viruses. In stark contrast, the Δ <jats:italic>dcl-2</jats:italic> and Δ <jats:italic>dcl-1</jats:italic> /Δ <jats:italic>dcl-2</jats:italic> mutant strains were highly susceptible to mycovirus infection, with CHV1-EP713-infected mutant strains becoming severely debilitated. Increased viral RNA levels were observed in the Δ <jats:italic>dcl-2</jats:italic> mutant strains for a hypovirus CHV1-EP713 mutant lacking the suppressor of RNA silencing p29 and for wild-type reovirus MyRV1-Cp9B21. Complementation of the Δ <jats:italic>dcl-2</jats:italic> strain with the wild-type <jats:italic>dcl-2</jats:italic> gene resulted in reversion to the wild-type response to virus infection. These results provide direct evidence that a fungal dicer-like gene functions to regulate virus infection. </jats:p>
収録刊行物
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- Proceedings of the National Academy of Sciences
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Proceedings of the National Academy of Sciences 104 (31), 12902-12906, 2007-07-31
Proceedings of the National Academy of Sciences
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詳細情報 詳細情報について
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- CRID
- 1362544419551859328
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- NII論文ID
- 80018422140
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- ISSN
- 10916490
- 00278424
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