Moth sex-pheromone biosynthesis is inhibited by the herbicide diclofop

Pheromones of nocturnal moths are derived from fatty acids produced as a result of the activity of acetyl-CoA carboxylase. This timely production is initiated in nocturnal moths by a tropic peptide, pheromone biosynthesis activating neuropeptide released into the hemolymph. In monocotyledonous plants, specific plastid acetyl-CoA carboxylase is inhibited by herbicides that target the eukaryotic form of the enzyme. We report evidence that these herbicides can also target pheromone biosynthesis by a moth, thereby implicating the acetyl-CoA carboxylase as a key regulatory enzyme in the pheromone biosynthetic pathway. These findings, whilst indicating the possible action of such herbicides on non-target organisms, also suggest a novel alternative method of insect pest management, which precludes sex-pheromone production and mating success, thereby reducing insect population growth.