The hormonal control of insect metamorphosis was shown by Wigglesworth (1934), who studied Rhodnius prolixus, a blood-sucking bug that has five instars. When the 1st instar larva of Rhodnius was decapitated and fused with the 5th instar larva, the minute first instar developed the cuticle, body structure, and genitalia of the adult.
Wigglesworth also showed that corporaallata located near the insect brain, produce a hormone that retards metamorphosis by producing juvenile hormone. This hormone inhibits the genes that promote development of adult characteristics (e.g. wings, reproductive organs, and external genitalia), causing the insect to remain nymph or larva.
The molting process is initiated in the brain, where neurosecretorycells release prothoracicotropic hormone (PTTH) in response to neural, hormonal, or environmental factors. PTTH is a homodimer of two polypeptides of 109 amino acids. PTTH stimulates the production of ecdysone by the prothoracic glands.
The second major hormone in insect development is juvenile hormone (JH). JH is secreted by corpora allata. The secretory cells of corpora allata are active during larval molts but are inactive during the metamorphic molt. This hormone is responsible for preventing metamorphosis.
When an immature insect has grown sufficiently to require a larger exoskeleton, sensory input from the body activates certain neurosecretory cells in the brain. These neurons respond by secreting brain hormone which stimulates corpora cardiaca to release the prothoracicotropic hormone (PTTH) into circulatory system, which then stimulates the prothoracic glands to secrete the molting hormone, ecdysone.
Agrochemical research over the last two decades has resulted in the discovery of chemically novel insecticides that mimic the action of the two insect growth and developmental hormones, the steroidal 20-hydroxyecdysone (20E) and the juvenile hormone (JH).
Aromatic non-terpenoidal insecticides, such as fenoxycarb and pyriproxyfen, mimic the action of Juvenile Hormones.
INSECT GROWTH REGULATORS
Insect juvenile hormones (JH) control metamorphosis and development. Studies have shown that maintenance of JH at a high level prevents the development of larvae and nymphs into adults. They remain as juveniles, often continuing to grow, and sometimes producing what are known as super-larvae.
Analogues of juvenile hormones have been synthesized and exploited commercially and are called Insect Growth Regulators (IGRs). The best known juvenile hormone analogues are methoprene, hydroprene and fenoxycarb. These substances do not kill adult insects but they prevent juvenile stages from completing their development. When used as pesticides, they stop insect larvae from developing into adults and because they affect biochemical processes unique to insects they are safe for non-target animals and the environment.
Chitin inhibitors disrupt the synthesis of chitin on body. They act against the larval stages which fail to survive the next molt. Death is caused by incomplete ecdysis and cuticle malformation. The best known chitin inhibitors are the benzoylphenylureas, which include diflubenzuron and its analogues teflubenzuron, flufenoxuron and triflumuron.
Bowers (1976) discovered that extract from the plant Ageratum houstonianum causes premature metamorphosis in some Hemiptera. It was subsequently shown that the active molecules precocenes destroyed the glands corpora allata, which produce JH. Screening led to the discovery of anti-JHs such as fluoromevalonate, which showed activity against virtually all the Lepidoptera but little effect on other insects.
The pheromones (from the Greek pherein = to transfer and hormon = to excite), are chemicals produced as messengers that affect the behavior of other individuals of insects or other animals. Pheromones regulate many types of insect behavior. Sexpheromones are produced by one sex (usually the female) to attract the other sex for mating. Mass attacks by certain bark beetles are coordinated by aggregationpheromones that attract other beetles to the same tree. Alarmpheromones are produced by honey bees and aphids to help in colony defense. Trailpheromones are produced by ants to help other worker ants find food sources.
The first chemical identification of a pheromone took place in the late 1950s, by Butenandt, who identified the pheromone of silk moth, Bombyx mori, as (10E,12Z)-hexadecadien-1-ol or bombykol. Synthetic sex pheromones are available for many pest insects and are used for pest suppression.
In 1960, chemist Morton Beroza of the U.S. Department of Agriculture suggested using sex pheromones to jam the insect mating communication system. He reasoned that if an agricultural field is supplied with many sources of sex pheromones of a pest species, most males of would follow the false trails.
In Mexico the pinworm causes extensive damage to the tomato crop. Then growers began broadcasting the pinworm’s sex pheromone in tomato fields by using plastic tubes attached to tomato stems. Results were dramatic and only about 4 percent of the females were able to mate and lay fertilized eggs.
Pheromone traps have been also been developed in which female synthetic pheromones are placed. Males are attracted and killed in the trap. Indian Meal Moths and striped stem borer (Chilo suppressalis) of rice crop have been successfully controlled by the pheromone trap method.
Commercial pheromones are now available for many pests, e.g. European old house borer (Hylotrupes bajulus); Western corn root worm (Diabrotica virgifera); Codling moth (Cydia pomonella); Plum fruit moth (Grapholita funebrana); European grape berry moth (Eupoecilia ambiguella); European grapevine moth (Lobesia botrana); Clothes Moth (Tiheola bisselliella); Confused Flour Beetle (Tribolium castaneum);