|Qu, Feng - UNIVERSITY OF NEBRASKA|
|Morris, T.J. - UNIVERSITY OF NEBRASKA|
Submitted to: Phytopathology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: April 25, 2007
Publication Date: October 1, 2007
Citation: Stenger, D.C., Young, B.A., Qu, F., Morris, T., French, R.C. 2007. Wheat streak mosaic virus lacking HC-Pro is competent to produce disease synergism in double infections with maize chlorotic mottle virus. Phytopathology 97:1213-1221. Interpretive Summary: Mixed infections of crop plants with two unrelated viruses may result in disease symptoms far more severe that that produced by the respective viruses in single infections. This phenomenon is referred to as disease synergism. Often, one of the viruses involved is a member of the potyvirus family. Previously, others have shown that the HC-Pro gene of potyviruses is responsible for disease synergism and that pathogenicity enhancement by HC-Pro occurs via suppression of RNA silencing pathways used by the plants as a defense against viral infection. In the experiments reported here, it was demonstrated that a deletion mutant of wheat streak mosaic virus (WSMV) completely lacking HC-Pro was able to produce disease synergism in corn dually infected with maize chlorotic mottle virus. Additional experiments indicated that WSMV HC-Pro did not function as a suppressor of RNA silencing. Collectively, the experiments indicate that HC-Pro function differs among members of the potyvirus family and that WSMV likely utilizes a different gene to induce synergistic disease and suppress RNA silencing.
Technical Abstract: Single infections of maize plants with the tritimovirus Wheat streak mosaic virus (WSMV) or the machlomovirus Maize chlorotic mottle virus (MCMV) are characterized by systemic chlorosis but not necrosis. Co-infection of maize with both viruses results in disease synergism and induction of corn lethal necrosis disease (CLND). Here, we report that a WSMV construct, in which the HC-Pro coding region was completely deleted, was equally effective as WSMV encoding HC-Pro in producing CLND in mixed infections with MCMV. These results indicated that, unlike potyvirus HC-Pro, WSMV HC-Pro was dispensable for pathogenicity enhancement. Elevated viral titers, commonly observed in mixed infections relative to single infections, also were observed regardless of whether or not HC-Pro was encoded by the WSMV construct paired with MCMV. MCMV titer was increased in mixed infections with WSMV up to 2-fold two weeks post inoculation and up to 4-fold one month post inoculation. Titer of WSMV in mixed infections with MCMV was increased 3- to 6-fold two weeks post inoculation but was not elevated in mixed infections one month post inoculation. We further demonstrated that WSMV HC-Pro did not suppress post-transcriptional gene silencing (PTGS) using a Agrobacterium-mediated co-infiltration assay in which potyvirus HC-Pro acts as a strong suppressor of PTGS. Collectively, the results define significant differences in HC-Pro function among divergent genera of the family Potyviridae and suggest that the tritimovirus WSMV utilizes a gene other than HC-Pro to suppress PTGS and mediate synergistic interactions with unrelated viruses in mixed infections.