Location: Wheat, Sorghum and Forage ResearchTitle: Coat protein deletion mutants elicit more severe symptoms than wild-type virus in multiple cereal hosts
|Tatineni, Satyanarayana - Ts|
|ELOWSKY, CHRISTIAN - University Of Nebraska|
Submitted to: Molecular Plant-Microbe Interactions
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 8/23/2017
Publication Date: 11/11/2017
Publication URL: http://handle.nal.usda.gov/10113/5855449
Citation: Tatineni, S., Elowsky, C., Graybosch, R.A. 2017. Coat protein deletion mutants elicit more severe symptoms than wild-type virus in multiple cereal hosts. Molecular Plant-Microbe Interactions. 30(12):974-983. https://doi.org/10.1094/MPMI-07-17-0182-R.
Interpretive Summary: Wheat streak mosaic virus (WSMV) is the most economically important wheat virus in the Great Plains region. Viruses rely on host proteins for replication, movement, and disease development because of their smaller genomes with fewer genes. Disruption of interactions between host and viral factors without affecting cellular functions of host factors would provide effective control mechanisms for viral diseases. In this study, WSMV bearing deletions in the coat protein gene produced severe symptoms on wheat, most likely due to efficient virus-host interactions. These results will facilitate identification of wheat proteins involved in interactions with WSMV coat protein, followed by disruption of these interactions by silencing host genes through RNA-interference technology in transgenic wheat would provide WSMV-resistant wheat. Results presented in this study also suggest that deployment of resistance based on WSMV coat protein antagonism needs to be proceeded with caution because resistance may be overcome as WSMV can infect wheat with deletions within the coat protein gene.
Technical Abstract: The coat protein (CP) of Wheat streak mosaic virus (WSMV; genus Tritimovirus, family Potyviridae) tolerates deletion of amino acids 36 to 84 for efficient systemic infection of wheat. This study demonstrates that deletion of CP amino acids 58 to 84, but not 36 to 57, from WSMV genome induced severe chlorotic streaks and spots, followed by acute chlorosis in wheat, maize, barley, and rye compared to mild to moderate chlorotic streaks and mosaic symptoms by wild-type virus. Deletion of CP amino acids 58 to 84 from WSMV genome increased fitness of mutants with accelerated cell-to-cell movement and increased accumulation of genomic RNAs and CP compared to the wild-type virus. Microscopic examination of wheat tissues infected by GFP-tagged mutants revealed that infection by mutants lacking CP amino acids 58 to 84 caused degradation of chloroplasts, resulting in acute macroscopic chlorosis. The profile of CP-specific proteins was changed in wheat infected by mutants causing acute chlorosis compared to mutants eliciting wild-type symptoms. All deletion mutants accumulated CP-specific major protein similar to the wild-type virus; however, mutants that elicit acute chlorosis failed to accumulate a 31-kDa minor protein compared to wild-type virus or mutants lacking amino acids 36 to 57. Taken together, these data suggest that deletion of CP amino acids 58 to 84 from WSMV genome enhanced viral fitness, altered CP-specific protein profiles, and caused severe symptom phenotypes in multiple cereal hosts.