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Molecular Plant Pathology

Modifications of the Tobacco Mosaic Virus Coat Protein Gene Affecting Replication, Movement, and Symptomatology. W. O. Dawson, Department of Plant Pathology, University of California, Riverside, CA 92521; P. Bubrick, and G. L. Grantham. Department of Plant Pathology, University of California, Riverside, CA 92521. Phytopathology 78:783-789. Accepted for publication 5 January 1988. Copyright 1988 The American Phytopathological Society. DOI: 10.1094/Phyto-78-783.

A series of tobacco mosaic virus (TMV) mutants with insertions and/or deletions in the coat protein gene were made by modification of the cDNA of the genome (pTMV204) followed by in vitro transcription. All mutants multiplied as free-RNA viruses and moved from cell to cell in inoculated leaves of Xanthi tobacco, although the mutants established systemic infections less efficiently than wild-type TMV. This included mutants that had the entire coat protein gene removed, deletions that extended 28 nucleotides into the 3’-nontranslated region, as well as a mutant containing the bacterial chloramphenicol acetyltransferase gene substituted for the coat protein gene. Most of the mutants produced coat protein-related polypeptides in vivo, although the size and amount of protein found in inoculated leaves varied considerably among different mutants. In general, polypeptides that contained the normal coat protein carboxyl terminus tended to accumulate in greater amounts. Three types of responses were observed in mutant-infected Xanthi tobacco: no symptoms, yellowing, and necrosis. Most mutants that produced no or low amounts of coat protein failed to induce symptoms. The mutants that retained the carboxyl terminus of the coat protein induced yellowing symptoms. All mutants including those completely lacking the coat protein gene induced local lesions in Xanthi-nc. Two mutants also induced necrotic local lesions in Xanthi tobacco as well as almost all host plants tested. These results demonstrate that the TMV coat protein gene has a multifunctional role during infection that includes encapsidation, symptom expression, and differential elicitation of resistant genes.

Additional keywords: construction of virus mutants, hypersensitive reaction, modification of genome of TMV, recombinant viral genetics.