Fig. 6

Proposed mechanistic model for paradormancy release by PHC in grapevine buds. Upon application, HC causes immediate cellular hypoxia through the action of released cyanide on aerobic respiration and inhibition of catalase activity and induces H₂O₂ production. ROS (O₂ ^•-, H₂O₂,^.OH) and RNS (NO) are rapidly produced possibly by several enzymatic systems, such as NADPH oxidase, amine oxidase, nitrate reductase and arginine-nitric oxide synthase. H₂O₂ and ethylene act as signaling molecules activating genes involved in antioxidant defense systems. The antioxidant machinery and related pathways (e.g. FSD, POD, DOX, GPX, APX, AOX, HB, etc.) are upregulated to maintain ROS and RNS at sublethal levels to avoid PCD. H₂O₂ in the cell wall induces cell wall loosening and expansion. H₂O₂ also functions in anabolic, signaling and defense pathways and in the synthesis of the other ROSs,^.OH in the presence of H₂O₂ and O₂ ^•- exerts a wall loosening effect, and H₂O₂ also drives peroxidase-mediated cross-linking of structural cell wall components. In the signal transduction pathway, ROS triggers the expression of ROS responsive genes. H₂O₂ and^.OH activate Ca²⁺ channels and initiate a signal transduction and activate protein kinase activity, which in turn activates different transcription factors to regulate ROS scavenging and ROS producing pathways. Finally, these transcription factors control the downstream functional gene expression responsible for dormancy release and growth resumption in grapevine buds. The accumulation of ethylene in the buds promotes cell elongation and parenchyma formation by activating related ERFs