חיפוש מתקדם
Rafaeli, A., Department of Stored Products, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Gileadi, C., Department of Stored Products, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
The biochemical second messenger system during pheromonotropic and pheromonostatic activities was assessed and compared. The involvement of G- proteins was implicated by the stimulatory action of sodium fluoride (NaF), at a range of 1-2 mM, on both pheromone biosynthesis and intracellular cAMP levels in isolated intersegmental membranes of Helicoverpa armigera. However, cholera toxin did not mimic the pheromonotropic response of PBAN. The stimulatory action of NaF was significantly inhibited by adrenergic agonists (tyramine and clonidine) as was observed at low levels of PBAN. At high levels of PBAN, although cAMP production was inhibited, pheromone biosynthesis was unaffected by clonidine. A similar phenomenon was observed with the ionophore, thapsigargin, in which adrenergic agonists did not inhibit pheromone biosynthesis but reduced intracellular cAMP to basal levels. Thus pheromonotropic activity exhibited both cAMP-independent and cAMP-dependent stimulatory responses. The calcium calmodulin inhibitor, W7, inhibited pheromone biosynthesis and intracellular cAMP production which was induced either by Hez-PBAN, NaF or thapsigargin. The pheromonostatic activity by clonidine was prevented in the presence of pertussis toxin, thereby indicating the involvement of inhibitory G-protein (G1) in the inhibitory action of adrenergic agonists on the activity of Hez-PBAN. From the results we hypothesized that negative regulation of pheromonotropic activity occurs at the membrane receptor level by the interaction of an adrenergic receptor.
פותח על ידי קלירמאש פתרונות בע"מ -
הספר "אוצר וולקני"
אודות
תנאי שימוש
Down regulation of pheromone biosynthesis: Cellular mechanisms of pheromonostatic responses
26
Rafaeli, A., Department of Stored Products, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Gileadi, C., Department of Stored Products, Volcani Center, P.O. Box 6, Bet Dagan 50250, Israel
Down regulation of pheromone biosynthesis: Cellular mechanisms of pheromonostatic responses
The biochemical second messenger system during pheromonotropic and pheromonostatic activities was assessed and compared. The involvement of G- proteins was implicated by the stimulatory action of sodium fluoride (NaF), at a range of 1-2 mM, on both pheromone biosynthesis and intracellular cAMP levels in isolated intersegmental membranes of Helicoverpa armigera. However, cholera toxin did not mimic the pheromonotropic response of PBAN. The stimulatory action of NaF was significantly inhibited by adrenergic agonists (tyramine and clonidine) as was observed at low levels of PBAN. At high levels of PBAN, although cAMP production was inhibited, pheromone biosynthesis was unaffected by clonidine. A similar phenomenon was observed with the ionophore, thapsigargin, in which adrenergic agonists did not inhibit pheromone biosynthesis but reduced intracellular cAMP to basal levels. Thus pheromonotropic activity exhibited both cAMP-independent and cAMP-dependent stimulatory responses. The calcium calmodulin inhibitor, W7, inhibited pheromone biosynthesis and intracellular cAMP production which was induced either by Hez-PBAN, NaF or thapsigargin. The pheromonostatic activity by clonidine was prevented in the presence of pertussis toxin, thereby indicating the involvement of inhibitory G-protein (G1) in the inhibitory action of adrenergic agonists on the activity of Hez-PBAN. From the results we hypothesized that negative regulation of pheromonotropic activity occurs at the membrane receptor level by the interaction of an adrenergic receptor.
Scientific Publication
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