Metamorphosis starts with Met

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Abstract
Juvenile hormone (JH) has long been known to be a potent regulator of metamorphosis in most insects, but learning how it acts has been hindered until now by failure to find an entry point for its mechanism of action. Using the beetle Tribolium castaneum, Konopova and Jindra (1) have achieved a result long and fruitlessly sought in Drosophila, which is reported in this issue of PNAS. They have identified a key component of the pathway JH uses in controlling metamorphosis; this component is the gene TcMet. In 1986, Wilson and Fabian (2) screened mutagenized Drosophila for resistance to methoprene, a JH analogue used as an insecticide. The mutants mapped to a region on the X chromosome, and the postulated gene was named Met (for methoprene tolerance). Many optimistically thought that Met would provide a starting point for understanding how JH controls metamorphosis. Drosophila Met mutants are resistant to developing the subtle morphological effects caused by either JH-III or methoprene, and the LD50 against either compound is increased 100-fold. [Confusingly, the name Met had previously been used for another gene (metatarsi irregular) and does not have official standing, having been replaced by the awkward Rst(1)JH (resistance to JH), yet Met is still routinely used.] Early experiments revealed that resistance is not due to decreased penetration, enhanced degradation, or sequestration. Rather, extracts of fat body and accessory glands of Met mutant flies have reduced JH binding activity (3). Met is a member of the bHLH-PAS family because it possesses a basic helix–loop–helix domain and PAS domains (4). “Charter members” of this family in vertebrates are AhR (aryl hydrocarbon receptor) and ARNT (responsible for nuclear translocation of AhR). In the presence of appropriate ligands, such as dioxin, AhR enters the nucleus, heterodimerizes with ARNT, and up-regulates genes …