Figure 6

Molecular pathways and effectors susceptible to the proposed treatments with salicylic acid and 2,6-dichloro-isonicotinic acid. (I) SA upregulates PAL activity at three stages: PAL mRNA accumulation, PAL protein synthesis and phenolic compound accumulation. PAL involvement in synthesis of endogenous SA could accelerate the treatment effects. SA could also induce JA synthesis via a non-canonical pathway. (II) SA activation of SOD, GR and GST as well as its effect on downregulation of AO could alleviate oxidative stress associated with tobamovirus infections. (III) SA induced PAL could have a major effect on the phenylpropanoid pathway associated with ROI scavenging, thereby reducing oxidative stress, as well as instigation of systemic acquired resistance. Co-treatments with 2,6-dichloro-isonicotinic acid and SA, which additively activate systemic acquired resistance against tobamoviruses, could strengthen the SA effects. SA salicylic acid, PAL phenylalanine ammonia lyase, JA jasmonic acid, SOD superoxide dismutase, GR glutathione reductase, GST glutathione S-transferase, AO l-ascorbate oxidase, ROI reactive oxygen intermediates. A⁴⁵; B³⁹; C⁴⁶; D¹⁵; E¹⁹; F⁴⁷; G¹⁶; H²⁵; I⁴³; J⁴⁸; K¹⁴.