Strain-specific P3 of Soybean mosaic virus elicits Rsv1-mediated extreme resistance, but absence of P3 elicitor function alone is insufficient for virulence on Rsv1-genotype soybean.

When challenged by mechanical inoculation, the Rsv1 gene of soybean invokes extreme resistance (ER) against Soybean mosaic virus (SMV) strain N, but not SMV-G7 and its experimentally evolved variant, SMV-G7d. SMV-G7 provokes a lethal systemic hypersensitive response (LSHR), whereas SMV-G7d induces systemic mosaic. Thus, for Rsv1-genotype soybean, SMV-G7 and SMV-G7d are both virulent virus strains. The elicitor function of SMV-G7 provoking Rsv1-mediated LSHR was recently mapped to P3, and the influence of amino acids 823, 953, and 1112 of the precursor polypeptide of SMV-G7d on evasion of Rsv1-mediated recognition provoking LSHR was demonstrated. We have now extended this study to SMV-N. Initially, amino acids corresponding to those of SMV-G7d at these positions were substituted, individually or in combinations. All the mutants remained replication competent on rsv1-genotype soybean; however, none lost the elicitor function provoking Rsv1-mediated ER. Subsequently, P3 of SMV-N was precisely replaced with P3 of SMV-G7 or SMV-G7d and vice versa. All the chimeras were replication competent on rsv1-genotype soybean, but surprisingly SMV-N/G7P3 and SMV-N/G7dP3 failed to gain virulence on Rsv1-genotype soybeans. However, SMV-G7/NP3 and SMV-G7d/NP3 lost virulence, and this loss of virulence function was mapped to the N-terminus domain of SMV-N P3. The data indicate that SMV strain-specific P3 provokes Rsv1-mediated ER; however, virulence on Rsv1-genotype soybean is not solely a consequence of the absence of the P3 elicitor functions provoking Rsv1-mediated ER and LSHR.