Effective Resistance to Potyvirus Infection Conferred by Expression of Antisense RNA in Transgenic Plants. J. Hammond. Floral and Nursery Plants Research Unit, United States Department of Agriculture, Agricultural Research Service, Beltsville Agricultural Research Center, Beltsville, MD 20705, U.S.A. K. K. Kamo. Floral and Nursery Plants Research Unit, United States Department of Agriculture, Agricultural Research Service, Beltsville Agricultural Research Center, Beltsville, MD 20705, U.S.A. MPMI 8:674-682. Accepted 8 May 1995. This article is in the public domain and not copyrightable. It may be freely reprinted with customary crediting of the source. The American Phytopathological Society, 1995.

Approximately 660 nt including the carboxy-terminal portion of the bean yellow mosaic potyvirus (BYMV) coat protein gene, complete 3 noncoding sequence and a short poly(A) tract were introduced to produce antisense RNA in transgenic Nicotiana benthamiana. Original (R0) transformants were selfed, and homozygous second generation (R2) populations challenged with infected sap, purified virus, or viral RNA. One transgenic line of 10 examined was extremely resistant to infection by mechanical inoculation of 100 µg/ml BYMV or 50 µg/ml BYMV RNA (the highest concentrations tested); no virus could be detected in inoculated leaves of this line. Nine other lines were systemi-cally infected when inoculated with BYMV or BYMV RNA, with initial symptoms indistinguishable from those in nontransgenic plants. One of these lines subsequently developed reduced symptoms and then symptomless, virus-free leaves (complete recovery from BYMV infection), while other lines produced leaves with reduced symptoms and reduced virus liter compared to the controls (partial recovery). No transgenic lines had resistance to infection, nor recovery from symptom expression, following inoculation with pepper mottle or turnip mosaic potyviruses. Antisense RNA from 3' regulatory regions can confer multiple degrees of resistance to potyviruses, including extreme resistance to infection, presumably by interference in virus replication.