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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #299587

Title: Sequence variability in HC-Pro coding regions of Korean Soybean mosaic virus isolates is associated with differences in RNA silencing suppression

Author
item LI, MEI-JIA - Chungnam National University
item KIM, JUNG-KYU - Chungnam National University
item SEO, EUN-YOUNG - Chungnam National University
item HWANG, EUI-IL - Korea Tomorrow And Global Corporation
item Domier, Leslie
item Hammond, John
item YOUN, YOUNG-NAM - Chungnam National University
item LIM, HYOUN-SUB - Chungnam National University

Submitted to: Archives of Virology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/17/2013
Publication Date: 1/1/2014
Citation: Li, M., Kim, J., Seo, E., Hwang, E., Domier, L.L., Hammond, J., Youn, Y., Lim, H. 2014. Sequence variability in HC-Pro coding regions of Korean Soybean mosaic virus isolates is associated with differences in RNA silencing suppression. Archives of Virology. 159:(4)1373-1383.

Interpretive Summary: Soybean mosaic virus (SMV) is an important viral pathogen affecting soybean production in Korea and other Asian countries. The genetic and pathogenic variability of SMV isolates from seven Korean provinces was investigated and compared with those of previously characterized SMV isolates from China, Korea and the United States. The analysis identified a SMV isolate with reduced virulence that contained mutations in viral genes that are required to counteract the antiviral defenses of soybean plants. When a subset of the mutations present in the less virulent SMV isolate was introduced into a virulent SMV isolate, the modified virus had low virulence, but quickly reverted back to the non-mutant state. The observation that the original SMV isolate with low virulence was genetically stable in nature suggested that a combination of mutations worked together to stabilized the virus’s genome. The results of these studies will be of interest to other scientist who are studying the interactions between viruses and plants that cause disease symptoms. The results will also be useful to scientist who are working to develop virus-based systems to disrupt soybean gene expression.

Technical Abstract: Soybean mosaic virus (SMV), a member of the family Potyviridae, is an important viral pathogen affecting soybean production in Korea. The variability in helper component proteinase (HC-Pro) sequences and pathogenicity of SMV tissue samples from seven Korean provinces was investigated and compared with those of previously characterized SMV isolates from Korea and the United States. Phylogenetic analysis separated 16 representative new Korean SMV isolates into two groups. Fourteen of the new Korean SMV samples belonged to Group II and were very similar to U.S. strain SMV G7 and Chinese isolate C14. One isolate in Group II, A297-13, differed at three amino acid positions (L54F, N286D, D369N) in the HC-Pro coding sequence from the severe isolates and SMV 413, showed very weak silencing suppressor activity, and produced only mild symptoms in soybean. To test the role of each of the amino acid substitutions in RNA silencing and viral RNA accumulation, a series of point mutations was constructed. Substitution of N for D at position 286 in HC-Pro of SMV A297-12 significantly reduced silencing suppression activity. When the mutant HC-Pro of A297-13 was introduced into an infectious clone of SMV 413, accumulation of viral RNA was reduced to less than 3% of the level of an infectious clone of SMV 413 containing the HC-Pro of A297-12 at 10 days post inoculation (dpi), but increased to 40% of A297-12 at 40 dpi and finally RNA accumulated to a similar level as A297-12 at 50 dpi. However, at 50 dpi the D at position 286 of HC-Pro was found to have reverted to N. The results showed that a naturally occurring novel mutation in HC-Pro significantly reduced silencing suppression activity and accumulation of transgene and viral RNAs, and that there was strong selection for revision to wild type when the mutation was introduced into an infectious clone of SMV.