Function of Nitric Oxide in Chitosan Oligosaccharide-Induced Resistance to Tobacco Mosaic Virus

Abstract

Chitosan oligosaccharide (COS) has been shown to protect plants against viral invasion.To study its antiviral mechanism, nitric oxide (NO) signaling was investigated in the process of resistance to tobacco mosaic virus (TMV) in tobacco plants induced by COS.Results show that COS and NO donor sodium nitroprusside could induce NO generation quantified by Griess reagent in tobacco leaves with no TMV infection.However, the NO levels were not markedly different in various samples after TMV infection.The content of S-nitrosothiols, an important signal molecule downstream of NO was also determined, and results indicate that they may not be involved in the COS-induced antiviral process.In addition, western blotting experiments show that COS and sodium nitroprusside were observed to inhibit TMV multiplication and movement, which were blocked by NO scavenger cPTIO.COS and sodium nitroprusside-induced callose deposition were also reversed by treatment with cPTIO in aniline blue assay.The expression of -1, 3-glucanase, which has been proved to control callose degradation, was regulated by COS and NO.Another protein, calreticulin related with TMV movement was also modulated by COS and NO.Collectively, these observations suggest that NO participates in COS-induced resistance to TMV by regulating calreticulin and -1, 3-glucanase expression.