Originally published as Genetics Published Articles Ahead of Print on October 3, 2005.

Genetics, Vol. 172, 253-264, January 2006, Copyright © 2006
doi:10.1534/genetics.105.046631

Interaction Between Hormonal Signaling Pathways in Drosophila melanogaster as Revealed by Genetic Interaction Between Methoprene-tolerant and Broad-Complex

Thomas G. Wilson^*,1, Yoram Yerushalmi^,2, David M. Donnell^,,3 and Linda L. Restifo^,,

^* Department of Entomology, Ohio State University, Columbus, Ohio 43210, Department of Neurology, University of Arizona, Tucson, Arizona 85721-0077, ARL Division of Neurobiology, University of Arizona, Tucson, Arizona 85721-0077, and Interdisciplinary Program in Insect Science, University of Arizona, Tucson, Arizona 85721-0077

¹ Corresponding author: Department of Entomology, 318 W. 12th Ave., Ohio State University, 400 Aronoff Laboratory, Columbus, OH 43210.
E-mail: wilson.1457{at}osu.edu

Juvenile hormone (JH) regulates insect development by a poorly understood mechanism. Application of JH agonist insecticides to Drosophila melanogaster during the ecdysone-driven onset of metamorphosis results in lethality and specific morphogenetic defects, some of which resemble those in mutants of the ecdysone-regulated Broad-Complex (BR-C). The Methoprene-tolerant (Met) bHLH–PAS gene mediates JH action, and Met mutations protect against the lethality and defects. To explore relationships among these two genes and JH, double mutants were constructed between Met alleles and alleles of each of the BR-C complementation groups: broad (br), reduced bristles on palpus (rbp), and 2Bc. Defects in viability and oogenesis were consistently more severe in rbp Met or br Met double mutants than would be expected if these genes act independently. Additionally, complementation between BR-C mutant alleles often failed when MET was absent. Patterns of BRC protein accumulation during metamorphosis revealed essentially no difference between wild-type and Met-null individuals. JH agonist treatment did not block accumulation of BRC proteins. We propose that MET and BRC interact to control transcription of one or more downstream effector genes, which can be disrupted either by mutations in Met or BR-C or by application of JH/JH agonist, which alters MET interaction with BRC.

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