In solving a 20-year puzzle about insect metamorphosis, a University of Minnesota research team has taken a big step toward the design of better insecticides and understanding the onset of human puberty.
Led by Michael O’Connor, a professor of genetics, cell biology and development, the researchers studied PTTH, a brain-produced hormone that triggers the mechanism of metamorphosis by acting like a key fitting into a lock. PTTH's “key” identity has been known for 20 years, but it took the O’Connor team to find the “lock,” completing the picture of this seminal event.
Because the onset of human puberty is brought about by a similar mechanism, the finding addresses the question of how a host of organisms, from insects to humans, sense increasing body size and enter the next stage of development on schedule.
“In its overall design, insect metamorphosis is very much like passage through puberty,” says O’Connor. “It, too, is regulated by a [small brain hormone] whose production is controlled by nutritional, environmental, and genetic factors. … [B]oth puberty and metamorphosis accomplish the same goal—to provide reproductive capacity for the species at the appropriate developmental time.”
The discovery also may inform efforts to design environmentally benign insecticides targeting a narrow range of species, such as mosquitoes. The research appears in the December 4 issue of Science.
A common thread
From a squirmy larva turning into a beautiful butterfly to a child becoming an adult, developing organisms sense their body size and use a complex system of hormones and other chemical signals to orchestrate the process. The O’Connor team worked with larvae of fruit flies and silk moths, both of which belong to the large group of insects that undergo a PTTH-based form of metamorphosis. Butterflies, bees, wasps, beetles, and mosquitoes also belong to this group.
PTTH is a neuropeptide—a small brain-derived hormone, similar in function to some human pituitary hormones—released by the brain when insects reach a threshold body weight, a signal that also initiates human puberty. After release from the brain, PTTH is snagged by a “receptor” molecule—the “lock”—in the main insect endocrine organ. The University researchers identified the receptor as an enzyme that works like a master switch, turning on other enzymes that turn on still others and eventually lead to a rash to changes resulting in metamorphosis.
Kill the messenger
Now that the O’Connor team has clarified the mechanism by which PTTH delivers its message, work can begin on ways to scramble the signal and thwart insect development. It helps that the PTTH molecule comes in many forms; even closely related groups of insects often have different versions of it. Someday, insecticides may be designed to interfere with PTTH specific to agricultural pests or carriers of disease without harming bees, butterflies, or other desirable species.
O’Connor says the next step will be to figure out how environmental and nutritional cues control the insect brain’s production of PTTH. — By Deane Morrison
Forget Kafka: U research unlocks secrets about metamorphosis
MinnPost, December 3, 2009