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ARS Home » Midwest Area » Urbana, Illinois » Soybean/maize Germplasm, Pathology, and Genetics Research » Research » Publications at this Location » Publication #163441


item Lim, Hyoun
item Ko, Tae
item Domier, Leslie
item Kim, H
item Hartman, Glen

Submitted to: American Phytopathological Society Abstracts
Publication Type: Abstract Only
Publication Acceptance Date: 4/20/2004
Publication Date: 6/1/2004
Citation: Lim,H.S., Ko, T.S., Domier, L.L., Kim, H.G., Hartman, G.L. 2004. Expression of soybean mosaic virus (SMV) HC-Pro in transgenic soybean plants enhances SMV symptoms. [abstract]. American Phytopathological Society. Phytopathology. 94:S99.

Interpretive Summary:

Technical Abstract: Transgenic soybean lines expressing the helper component-protease (HC-Pro) coding region of SMV G5 were produced by Agrobacterium-mediated transformation of immature soybean cotyledons. Homozygous transgenic lines were recovered with single copy insertions that expressed SMV HC-Pro mRNA at levels ranging from 5 to 34% of that found in SMV-infected plants. Ten days after inoculation with SMV, all HC-Pro transgenic lines had symptoms more severe than uidA transgenic plants. Symptom severity was related to HC-Pro expression levels in the transgenic lines, but SMV RNA titers did not differ among the lines. Similar levels of small interfering RNAs were detected in SMV-infected HC-Pro and uidA transgenic plants. Starting at 20 days after inoculation, new leaves of the transgenic line that expressed the highest level of HC-Pro mRNA no longer showed symptoms, and SMV RNA titers were drastically reduced. The titers of coat-protein and HC-Pro coding regions declined at similar rates suggesting that the HC-Pro coding region was not preferentially targeted. In soybean lines that expressed lower levels of HC-Pro, symptoms remained severe at all sampling dates and no reductions in SMV RNA titers were observed. These results show that HC-Pro enhances SMV symptom severity in transgenic plants and that even potyvirus HC-Pro transgenes are susceptible to virus-induced gene silencing when expressed at high levels.