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Genomic Segments RNA1 and RNA2 of Prunus necrotic ringspot virus Codetermine Viral Pathogenicity to Adapt to Alternating Natural Prunus Hosts

May 2013 , Volume 26 , Number  5
Pages  515 - 527

Hongguang Cui,1,2 Ni Hong,3 Guoping Wang,1 and Aiming Wang2

1National Key Laboratory of Agromicrobiology, Huazhong Agricultural University, Wuhan, Hubei 430070, People's Republic of China; 2Southern Crop Protection and Food Research Centre, Agriculture and Agri-Food Canada, 1391 Sandford St., London, ON, N5V 4T3, Canada; 3College of Plant Science and Technology, Hubei Crop Disease Monitoring and Safety Control Key Laboratory, Huazhong Agricultural University, Wuhan, Hubei 430070, People's Republic of China


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Accepted 19 January 2013.

Prunus necrotic ringspot virus (PNRSV) affects Prunus fruit production worldwide. To date, numerous PNRSV isolates with diverse pathological properties have been documented. To study the pathogenicity of PNRSV, which directly or indirectly determines the economic losses of infected fruit trees, we have recently sequenced the complete genome of peach isolate Pch12 and cherry isolate Chr3, belonging to the pathogenically aggressive PV32 group and mild PV96 group, respectively. Here, we constructed the Chr3- and Pch12-derived full-length cDNA clones that were infectious in the experimental host cucumber and their respective natural Prunus hosts. Pch12-derived clones induced much more severe symptoms than Chr3 in cucumber, and the pathogenicity discrepancy between Chr3 and Pch12 was associated with virus accumulation. By reassortment of genomic segments, swapping of partial genomic segments, and site-directed mutagenesis, we identified the 3′ terminal nucleotide sequence (1C region) in RNA1 and amino acid K at residue 279 in RNA2-encoded P2 as the severe virulence determinants in Pch12. Gain-of-function experiments demonstrated that both the 1C region and K279 of Pch12 were required for severe virulence and high levels of viral accumulation. Our results suggest that PNRSV RNA1 and RNA2 codetermine viral pathogenicity to adapt to alternating natural Prunus hosts, likely through mediating viral accumulation.



© 2013 The American Phytopathological Society