title: Fitness penalty in susceptible host is associated with virulence of Soybean mosaic virus on Rsv1-genotype soybean: a consequence of perturbation of HC-Pro and not P3.
abstract: The multigenic Rsv1 locus in the soybean plant introduction (PI) 'PI96983' confers extreme resistance against the majority of Soybean mosaic virus (SMV) strains, including SMV-N, but not SMV-G7 and SMV-G7d. In contrast, in susceptible soybean cultivars lacking a functional Rsv1 locus, such as 'Williams82' (rsv1), SMV-N induces severe disease symptoms and accumulates to a high level, whereas both SMV-G7 and SMV-G7d induce mild symptoms and accumulate to a significantly lower level. Gain of virulence by SMV-N on Rsv1-genotype soybean requires concurrent mutations in both the helper-component proteinase (HC-Pro) and P3 cistrons. This is because of the presence of at least two resistance (R) genes, probably belonging to the nucleotide-binding leucine-rich repeat (NB-LRR) class, within the Rsv1 locus, independently mediating the recognition of HC-Pro or P3. In this study, we show that the majority of experimentally evolved mutational pathways that disrupt the avirulence functions of SMV-N on Rsv1-genotype soybean also result in mild symptoms and reduced accumulation, relative to parental SMV-N, in Williams82 (rsv1). Furthermore, the evaluation of SMV-N-derived HC-Pro and P3 chimeras, containing homologous sequences from virulent SMV-G7 or SMV-G7d strains, as well as SMV-N-derived variants containing HC-Pro or P3 point mutation(s) associated with gain of virulence, reveals a direct correlation between the perturbation of HC-Pro and a fitness penalty in Williams82 (rsv1). Collectively, these data demonstrate that gain of virulence by SMV on Rsv1-genotype soybean results in fitness loss in a previously susceptible soybean genotype, this being a consequence of mutations in HC-Pro, but not in P3.
authors.affiliation: Department of Entomology and Plant Pathology, University of Tennessee, Knoxville, TN, 37996, USA.
authors.forename: B
authors.initials: B
authors.lastname: Khatabi
authors.forename: R-H
authors.initials: RH
authors.lastname: Wen
authors.forename: M R
authors.initials: MR
authors.lastname: Hajimorad
mesh_terms: D003546:Cysteine Endopeptidases / Q000235:genetics / Q000378:metabolism; D056084:Genetic Fitness; D016679:Genome, Viral / Q000235:genetics; D005838:Genotype; D054884:Host-Pathogen Interactions / Q000235:genetics*; D008969:Molecular Sequence Data; D009154:Mutation / Q000235:genetics*; D010641:Phenotype; D010935:Plant Diseases / Q000235:genetics / Q000821:virology; D017800:Potyvirus / Q000472:pathogenicity*; D013025:Glycine max / Q000235:genetics* / Q000821:virology*; D014764:Viral Proteins / Q000235:genetics* / Q000378:metabolism; D014771:Virion / Q000378:metabolism; D014774:Virulence
chemical_list: D014764:Viral Proteins; D003546:Cysteine Endopeptidases; C072775:HC-Pro protein, potyvirus