Cyanide Metabolism in Apple Embryos During Dormancy Breakage Is Modulated by NO or HCN Application

Hydrogen cyanide (HCN) is an N-containing gasotransmitter with a regulatory function in plants and animals. Despite its toxicity, HCN acts as a signalling molecule in plants, influencing development, pathogen defence, and stress responses, with particular emphasis on biotic stress and seed dormancy/germination. Around 3000 species across > 130 families produce HCN from cyanogenic compounds. This study investigated how nitric oxide (NO) and HCN impact the activity of enzymes involved in HCN metabolism during dormancy breakage of apple (Malus domestica Borkh.) embryos. Based on earlier findings that HCN exposure elevates NO emission and alters the phytoglobin-NO cycle, we examined whether NO affects HCN metabolism. We measured the activities of β-glucosidases, β-cyanoalanine synthase (β-CAS), and sulfurtransferases (STRs) (HCN-detoxifying enzymes), and the transcript levels of their corresponding gene homologues. Both NO and HCN stimulated β-glucosidase activity and enhanced β-CAS and STR activities. Although both N-containing gasotransmitters increased β-CAS transcripts, they differentially implicated transcript levels of STR homologues. Additionally, only HCN increased the transcript levels of mitochondrial cysteine synthase (OASTL-C). These results, together with our previous work, potentially link NO and HCN in the metabolic network during dormancy breakage of apple embryos.