Insect metamorphosis is a strange and stirring phenomenon. Complex metamorphosis, that is, the process as it occurs in beetles, butterflies, bees, and flies. Whereas grasshoppers, say, just get larger at each successive molt, a moth completely reorganizes itself at every life stage. Gross anatomy, internal organs, physiological processes—everything changes when it transforms from larva to pupa, and again from pupa to adult.
Some years back a third-grader posed me an impossible question. I was trying to explain that the crane fly we were looking at wouldn’t bite, even if it did resemble a mosquito on steroids; that the adults didn’t even eat. They did all their eating as larvae, then (via the pupa stage) became adults without functional mouthparts.
“Why do they do that?” the kid asked. He had me there. I couldn’t even really tell him how they did that.
Now I could at least give him a partial version of how, thanks to Ian and Dianne Duncan of Washington University in St. Louis, Missouri. The Duncans and their colleagues just published a paper entitled “Control of Target Gene Specificity During Metamorphosis by the Steroid Response Gene E93” in Proceedings of the National Academy of Sciences that provides at least a key to the mystery, using (of course) fruit flies, the lab rats of the insect world.
The researchers knew going in that the bodies of both larval and adult fruit flies developed through signaling systems, chains of molecules that transfer a signal from receptors on the surface of cells to target genes inside the cells’ nuclei. Their main finding was that the flies have a steroid hormone that triggers a gene that in turn redirects the signal systems so that they switch on a different set of genes. Think of it as extreme puberty.
At each stage—larva to pupa, pupa to adult—the master gene tweaks the performance of almost 900 target genes. That breaks down to 200 in the larva stage, another 400 in the prepupa, and 350 in the pupa. “…the genes controlled at each stage were almost completely different,” Ian Duncan told a reporter. “So they realized there were global changes of rules from each stage to the next.”
Dianne Duncan came up with a wonderful analogy for the process: “It’s as if two teams were playing soccer, and at halftime the referee comes out and hands out a new set of rules. Now you’ve got the same players, the same field, the same goals, but the teams are playing hockey not soccer. The rules are different, so the game is different.” I’ll bet people would pay to see that.
The exemplary gene in their study was one dubbed E93, which is switched on by the hormone when the larva becomes a pupa. E93, in conjunction with the epidermal growth factor receptor (EGFR) pathway, in turn activates the Distal-less gene, which is responsible for forming spots near the fly’s leg bristles. E93 determines the timing of the change; EGFR species the location.
Leg spots are not that big a deal. But the Duncans say E93 also affects the remodeling of the pupal brain. Ian Duncan: “Presumably E93 is doing the same thing in the nervous system that it is doing in the leg; it’s affecting the responsiveness of genes.”
Lest you think this is only about fruit flies, Dianne Duncan points out that human frontal lobes are remodeled during puberty: “There’s so much cell death and rewiring during this period, it’s astonishing that we get through it as well as we do.”
Now that I think of it, I still wouldn’t be prepared to attempt to explain puberty to a third-grader. But I expect he would have appreciated the soccer/hockey image.