Mutational Analysis of the Virion-sense Genes of Maize Streak Virus

1 John Innes Institute, AFRC Institute of Plant Science Research, Colney Lane, Norwich NR4 7UH, U.K. 2 Institute of Applied Microbiology, University of Agriculture and Forestry, Peter Jordanstrasse 82, A1190 Vienna, Austria and 3 Department of Plant Pathology, University of California, Riverside, Ca...

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Published in:Journal of general virology 1989-09, Vol.70 (9), p.2309-2323
Main Authors: Boulton, Margaret I, Steinkellner, Herta, Donson, Jonathan, Markham, Peter G, King, Donna I, Davies, Jeffrey W
Format: Article
Language:English
Subjects:
Amino Acid Sequence
Base Sequence
Capsid - genetics
Chromosome Deletion
DNA Transposable Elements
Genes
Genes, Viral
Molecular Sequence Data
Mutation
Plant Viruses - genetics
Plasmids
Rhizobium - genetics
Virion - genetics
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Summary:1 John Innes Institute, AFRC Institute of Plant Science Research, Colney Lane, Norwich NR4 7UH, U.K. 2 Institute of Applied Microbiology, University of Agriculture and Forestry, Peter Jordanstrasse 82, A1190 Vienna, Austria and 3 Department of Plant Pathology, University of California, Riverside, California 92521, U.S.A. Insertion and deletion mutagenesis of the two virion-sense genes, V1 and V2, of maize streak virus (MSV) prevents symptomatic infections following Agrobacterium -mediated ‘agroinoculation’ of maize seedlings. These genes code for an M r 10900 protein and for coat protein, respectively. Mutants containing insertions or deletions in the coat protein gene, V2, were able to replicate to low levels, producing dsDNA although virion ssDNA was not detected and symptoms were not observed. Hence, unlike the bipartite geminiviruses, MSV requires coat protein to produce symptomatic systemic infection. Mutations in gene V1 which considerably shortened the M r 10900 protein (V1 gene) resulted either in low levels of replication, in which all the DNA forms associated with a wild-type infection were produced, or in no infection, in which case coat protein production may also have been affected. A V1 mutant generated in vivo with 11 of the 14 N-terminal amino acids altered, was viable and produced symptoms typical of a wild-type infection. Infectivity, assessed by replication and symptom expression, was restored by co-inoculating constructs containing single mutations in different open reading frames, thus rescue can occur by trans-complementation of gene products. The experiments showed that the mutations did not affect the nucleotide sequence requirements for replication and that in all cases intermolecular recombination eventually resulted in dominant wild-type virus. Keywords: MSV, mutagenesis, complementation, recombination Received 6 March 1989; accepted 26 April 1989.
ISSN:0022-1317
1465-2099
DOI:10.1099/0022-1317-70-9-2309