The
wild-type strain (Cl-WT) of Clover
yellow vein virus (ClYVV) systemically induces
cell death in pea cv. Plant introduction (PI) 118501 but not in PI 226564. A single incompletely
dominant gene, Cyn1, controls systemic
cell death in PI 118501. Here, we show that
activation of the
salicylic acid (SA)
signaling pathway enhances ClYVV
virulence in
susceptible pea
cultivars. The kinetics of
virus accumulation was not significantly different between PI 118501 (Cyn1) and PI 226564 (cyn1); however, the SA-responsive
chitinase gene (SA-CHI) and the
hypersensitive response (HR)-related gene homologous to
tobacco HSR203J were induced only in PI 118501 (Cyn1). Two
mutant viruses with
mutations in P1/HCPro, which is an RNA-silencing suppressor, reduced the ability to induce
cell death and SA-CHI expression. The application of SA and of its analog
benzo (1,2,3) thiadiazole-7-carbothioic acid S-methyl
ester (BTH) partially complemented the reduced
virulence of
mutant viruses. These results suggest that high
activation of the SA
signaling pathway is required for ClYVV
virulence. Interestingly, BTH could enhance Cl-WT
symptoms in PI 226564 (cyn1). However, it could not enhance
symptoms induced by
White clover mosaic virus and
Bean yellow mosaic virus. Our report suggests that the SA
signaling pathway has opposing functions in compatible interactions, depending on the virus-host combination.
