Wheat streak mosaic virus Coat Protein Deletion Mutants Elicit More Severe Symptoms Than Wild-Type Virus in Multiple Cereal Hosts

• Published in: Molecular plant-microbe interactions Vol. 30; no. 12; pp. 974 - 983
• Main Authors: Tatineni, Satyanarayana, Elowsky, Christian, Graybosch, Robert A
• Format: Journal Article
• Language: English
• Published: United States The American Phytopathological Society 01-12-2017
• Subjects: Amino Acids - metabolism; Capsid Proteins - metabolism; Chloroplasts - metabolism; Edible Grain - virology; Gene Deletion; Genome, Viral; Host-Pathogen Interactions; Plant Diseases - genetics; Plant Diseases - virology; Plant Viral Movement Proteins - metabolism; Potyviridae - genetics; Potyviridae - metabolism; RNA, Viral - metabolism; Triticum - virology
• ISSN: 0894-0282; 1943-7706
• DOI: 10.1094/MPMI-07-17-0182-R

Previously, we reported that 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. In this study, we demonstrated that WSMV mutants with deletion of CP amino acids 58 to 84 but not of 36 to 57 induced severe chlorotic streaks and spots, followed by acute chlorosis in wheat, maize, barley, and rye compared with mild to moderate chlorotic streaks and mosaic symptoms by wild-type virus. Deletion of CP amino acids 58 to 84 from the WSMV genome accelerated cell-to-cell movement, with increased accumulation of genomic RNAs and CP, compared with the wild-type virus. Microscopic examination of wheat tissues infected by green fluorescent protein-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 altered in wheat infected by mutants causing acute chlorosis, compared with mutants eliciting wild-type symptoms. All deletion mutants accumulated CP-specific major protein similarly to that in wild-type virus; however, mutants that elicit acute chlorosis failed to accumulate a 31-kDa minor protein compared with 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 the WSMV genome enhanced accumulation of CP and genomic RNA, altered CP-specific protein profiles, and caused severe symptom phenotypes in multiple cereal hosts.