Abstract

Complementary DNA clones from which infectious RNA can be transcribed were used to map the genetic determinants for oat (Avena sativa L.) pathogenicity of barley stripe mosaic virus (BSMV). Pseudorecombinant analysis of BSMV strains NDI8 (nonpathogenic to oat) and CV42 (pathogenic to oat) indicated that the ability to systemically infect oat mapped to RNA α. A homologous recombinant of ND18 (18αTKTKIN), possessing nucleotides 2218 to 2454 from CV42 RNA α, induced symptoms on oat similar to those generated by wild-type CV42. Six amino acids encoded by the αa gene differ between ND18 (PQSQTK) and CV42 (TKTKIN) in this region. Fine structure recombinants that encoded subsets of the six amino acid changes either were slow in their infection phenotype (18αTKTK and 18αTQSQIN) relative to recombinant 18αTKTKIN or were not infectious (18αKTKIN and 18αKTK) to inoculated oat plants. Neither coat protein antigen nor viral RNA was detected in inoculated plants that did not display symptoms. All recombinants infected isolated oat protoplasts, however, as determined by Northern and Western blots of extracts from inoculated oat protoplasts. The accumulation of viral genomic RNAs in protoplasts among the recombinants tested was similar, except for that of recombinant 18αTKTK which was reduced by 30%. The data support an earlier suggestion (Y. Zheng. and M. C. Edwards, 1990. J. Gen. Virol. 71. 1865-1868) that resistance of oat to BSMV strain ND18 is due to restricted virus movement in planta and provide evidence that the αa protein itself may be involved in the movement of BSMV in the infected plant.

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