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In Vitro Disassembly of Influenza A Virus Capsids by Gradient Centrifugation
Published on: March 27, 2016
Voltage-dependent anion channel proteins associate with dynamic Bamboo mosaic virus-induced complexes
Hsiang-Chi Lee1, Ying-Ping Huang2, Ying-Wen Huang2,3
1PhD Program in Microbial Genomics, National Chung Hsing University and Academia Sinica, Taichung 40227, Taiwan.
Mitochondrial voltage-dependent anion channels (VDACs) are crucial for Bamboo mosaic virus (BaMV) infection. These proteins aggregate and traffic with BaMV, promoting virus accumulation through interaction with viral protein TGBp1.
Area of Science:
- Plant virology
- Molecular biology
- Cell biology
Background:
- Viral infection cycles rely on host factors associated with cellular membranes.
- Understanding these interactions is key to controlling plant viral diseases like Bamboo mosaic virus (BaMV).
Purpose of the Study:
- To identify membrane-associated host factors involved in the BaMV infection cycle.
- To elucidate the role of identified host factors in BaMV replication and accumulation.
Main Methods:
- Purification of membrane-associated viral complexes from infected plants.
- Proteomic analysis to identify host factors (VDACs).
- Loss- and gain-of-function experiments to assess VDAC roles.
- Yeast two-hybrid and pull-down assays for protein interactions.
- Confocal microscopy for cellular localization and aggregation studies.
Main Results:
- Four voltage-dependent anion channel (VDAC) isoforms were identified in BaMV complexes.
- NbVDAC2, -3, and -4 are essential for efficient BaMV accumulation.
- NbVDACs aggregate and traffic with BaMV virions to a novel replication complex.
- BaMV triple gene block protein 1 (TGBp1) interacts with NbVDACs and induces their aggregation.
Conclusions:
- Mitochondrial NbVDACs are integral components of the BaMV replication complex, likely via TGBp1 interaction.
- NbVDACs promote BaMV accumulation, highlighting the role of mitochondrial proteins in virus infection.
- This study reveals a novel mechanism of host-pathogen interaction involving VDACs in plant virus infection.
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