Submitted to: General and Comparative Endocrinology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/3/2009
Publication Date: 4/1/2010
Citation: Jones, D., Jones, G., Teal, P.E., Hammac, C., Messmer, L., Osborne, K., Belgacem, Y.H., Martin, J. 2010. Suppressed production of methyl farnesoid hormones yields developmental defects and lethality in Drosophila larvae. General and Comparative Endocrinology. 165:244-254. Interpretive Summary: Hormones, chemicals used by all organisms to regulate physiological functions, have been studied in insects for many decades. One set of hormones all derived from the chemical methyl farnesoic acid are keys to maintenance of larval characters and in adults play major roles in reproductive development. However, no clear knowledge existed, until now, for their functioning in larval maturation and metamorphosis of larvae to pupal and adult stages in insects. An international team of scientists including scientists from the University of Kentucky, Laboratoire de Neurobiologie Cellulaire et Moleculaire (France) and a member from the Chemistry Unit at the Center for Medical Agricultural and Veterinary Entomology, USDA, ARS Gainesville Floridahave addressed this in the fruit fly. Their results support the ides that larval methyl farnesoid hormones are necessary for larval survival and morphogenetic transformation through the larval and pupal metamorphic processes.
Technical Abstract: A long-unresolved question in the developmental biology of Drosophila melanogaster has been whether methyl farnesoid hormones secreted by the ring gland are necessary for larval maturation and metamorphosis. In this study, we have used RNAi techniques to inhibit 3-Hydroxy-3-Methylglutaryl CoA Reductase (HMGCR) expression selectively in the corpora allatal cells that produce the circulating farnesoid hormones. The developing larvae manifest a number of developmental, metabolic and morphogenetic derangements. These defects included the exhibition of an ‘‘ultraspiracle” death phenotype at the 1st to 2nd larval molt, similar to that exhibited by animals that are null for the farnesoid receptor ultraspiracle. The few larvae surviving past a second lethal period at the 2nd to 3rd instar larval molt, again with‘‘ultraspiracle” phenotype, often became developmentally arrested after either attaining a misformed puparium or after formation of the white pupa. Survival past the ‘‘ultraspiracle” lethal phenotype could be rescued by dietary provision of an endogenous dedicated precursor to the three naturally secreted methyl farnesoid hormones. In addition to these developmental and morphogenetic defects, most larvae that survived to the late second instar exhibited a posterior-originating melanization of the tracheal system. These results support the hypothesis that larval methyl farnesoid hormones are necessary for larval survival and morphogenetic transformation through the larval and pupal metamorphic processes.