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Pathogenicity of Pepper mild mottle virus Is Controlled by the RNA Silencing Suppression Activity of Its Replication Protein but Not the Viral Accumulation

April 2007 , Volume 97 , Number  4
Pages  412 - 420

Shinya Tsuda , Kenji Kubota , Ayami Kanda , Takehiro Ohki , and Tetsuo Meshi

First, third, and forth authors: National Agricultural Research Center, Tsukuba, Ibaraki 305-8666, Japan; second author: National Agricultural Research Center for Kyushu Okinawa Region, Koshi, Kumamoto 861-1192, Japan; and fifth author: National Institute of Agrobiological Sciences, Tsukuba, Ibaraki 305-8602, and CREST, JST, Kawaguchi 322-0012, Japan

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Accepted for publication 6 October 2006.

Pepper mild mottle virus (PMMoV) infects pepper plants, causing mosaic symptoms on the upper developing leaves. We investigated the relationship between a virus pathogenicity determinant domain and the appearance of mosaic symptoms. Genetically modified PMMoV mutants were constructed, which had a base substitution in the 130K replication protein gene causing an amino acid change or a truncation of the 3′ terminal pseudoknot structure. Only one substitution mutant (at amino acid residue 349) failed to cause symptoms, although its accumulation was relatively high. Conversely, the pseudoknot mutants showed the lower accumulation, but they still caused mosaic symptoms as severe as the wild-type virus. Therefore, the level of virus accumulation in a plant does not necessarily correlate with the development of mosaic symptoms. The activity to suppress posttranscriptional gene silencing (PTGS) was impaired in the asymptomatic mutant. Consequently, pathogenicity causing mosaic symptoms should be controlled by combat between host PTGS and its suppression by the 130K replication protein rather than virus accumulation.

Additional keywords: attenuated virus, cross protection, GFP, methyl bromide.

© 2007 The American Phytopathological Society