Vanisulfane Induced Plant Resistance toward Potato Virus Y via the Salicylic-Depended Acid Signaling Pathway

Abstract

Vanisulfane is a plant resistance inducer that exhibits potent activity against potato virus Y (PVY), but its mechanism of action against this virus remains unclear. Our results showed that when we used 400 μg/mL of vanisulfane, it provided an impressive level of control (63.55%) against PVY in Nicotiana benthamiana L. Meanwhile, vanisulfane increased activities of catalase (CAT), superoxide dismutase (SOD), peroxidase (POD), and phenylalanine ammonia lyase (PAL) as well as inducing H2O2 accumulation and Ca2+ influx to mediate PVY resistance. Furthermore, combined transcriptome and proteome analyses revealed that vanisulfane upregulated the POD52, APX, and PR-1 genes and proteins in the salicylic acid (SA) signaling pathway. Experiments demonstrated that vanisulfane triggered the accumulation of SA, upregulated the expression of ICS1 and PR-1 genes, and induced resistance against PVY in transgenic Arabidopsis plants. Consequently, it can be concluded that vanisulfane mediates the SA-dependent signaling pathway to confer PVY resistance in plants.

Expression and antiviral application of exogenous lectin (griffithsin) in sweetpotatoes

“…Pathogenesis-related gene expression can be induced by SA ( Baebler et al., 2014 ; Liang et al., 2024 ). Similarly, in Arabidopsis thaliana , vanisulfane can trigger salicylic acid accumulation, upregulate the expression of ICS1 and PR1 , and induce resistance to PVY in transgenic Arabidopsis ( Zhang et al., 2023 ). Treatment of Arabidopsis leaves with benzazol- S -methyl acid significantly increased the expression of the systemic acquired resistance-related genes PR1 , SID2 , and ALD1 and inhibited Plantago mosaic virus infection after 1 day ( Ito et al., 2024 ).…”

Recent Advances and Outlook of Benzopyran Derivatives in the Discovery of Agricultural Chemicals

“…Song et al developed a new antiviral agent vanisulfane that is presently being commercialized. 57 Simultaneously, the active fragment of this new antiviral agent vanisulfane was rationally grafted upon a benzopyran skeleton to obtain compound 10 by the active splicing principle (Figure 4), which exhibited excellent anti-TMV activity (EC 50 = 9.3 mg/L) that was 14.53-fold higher than that of ribavirin (EC 50 = 135.2 mg/L). 58 In addition, compound 10 caused misfolding and fragmentation of TMV proteins, leading to loss of TMV infectivity in the host.…”