Short versus long term effects of cyanide on sugar metabolism and transport in dormant walnut kernels.

Tree seed dormancy release by cold stratification accompanies with the embryo increased gluconeogenesis competence. Cyanide also breaks seed dormancy however, integrated information about its effects on carbon metabolism is lacking. Accordingly, the impacts of HCN on germination, lipid gluconeogenesis and sugar transport capacity of walnut (Juglans regia L.) kernels were investigated during 10-days period prior to radicle protrusion. HCN increased walnut kernel germination and within four days of kernel incubation, hastened the decline of starch, reducing and non-reducing sugars and led to greater activities of alkaline invertase and glucose-6-phosphate dehydrogenase. From four days of kernel incubation onwards, starch and non-reducing sugars accumulated only in the HCN treated axes. Cyanide also increased the activities of phosphoenolpyruvate carboxykinase and glyoxysomal succinate oxidase and led to greater acid invertase activity during the aforementioned period. The expressions of both sucrose transporter (JrSUT1) and H+-ATPase (JrAHA1) genes especially in cotyledons and H+-ATPase activity in kernels were significantly enhanced by exposure to cyanide. Thus in short-term HCN led to prevalence of carbohydrate catabolic events such as oxidative pentose phosphate pathway and possibly glycolysis in dormant walnut kernels. Long-term effects however, are increased gluconeogenesis and enhanced sugar transport capacity of kernels as a prerequisite for germination.