Insect development and metamorphosis are regulated by two major hormones, juvenile
hormone and ecdysteroids. Despite being the key regulator of insect developmental
transitions, the metabolic pathway of the primary steroid hormone, 20-hydroxyecdysone
(20E), especially its inactivation pathway, is still not completely elucidated. A
cytochrome P450 enzyme, CYP18A1, has been shown to play key roles in insect steroid
hormone inactivation through 26-hydroxylation. Here, we identified two CYP18 (BmCYP18A1
and BmCYP18B1) orthologs in the lepidopteran model insect, Bombyx mori. Interestingly,
BmCYP18A1 gene is predominantly expressed in the middle silk gland (MSG) while BmCYP18B1
expresses ubiquitously in B. mori. BmCYP18A1 is induced by 20E in vitro, suggesting
its role in 20E metabolism. Using the binary Gal4/UAS transgenic system, we ectopically
overexpressed BmCYP18A1 in a MSG-specific manner with a Sericin1-Gal4 (Ser-Gal4) driver
or in a ubiquitous manner with an Actin3-Gal4 (A3-Gal4) driver. Ectopic overexpression
of BmCYP18A1 in MSG or in all tissues resulted in developmental arrestment of transgenic
animals during the final instar larval stage. The 20E titers in the transgenic animals
expressing BmCYP18A1 were lower compared to the levels in the control animals. Although
the biological significance of MSG-specific expression of BmCYP18A1 is unclear, our
results provide the first evidence that BmCYP18A1, which is conserved in most arthropods,
is involved in a tissue-specific steroid hormone inactivation in B. mori.