title: Steroid Hormone Signaling Is Essential for Pheromone Production and Oenocyte Survival.
abstract: Many of the lipids found on the cuticles of insects function as pheromones and communicate information about age, sex, and reproductive status. In Drosophila, the composition of the information-rich lipid profile is dynamic and changes over the lifetime of an individual. However, the molecular basis of this change is not well understood. To identify genes that control cuticular lipid production in Drosophila, we performed a RNA interference screen and used Direct Analysis in Real Time and gas chromatography mass spectrometry to quantify changes in the chemical profiles. Twelve putative genes were identified whereby transcriptional silencing led to significant differences in cuticular lipid production. Amongst them, we characterized a gene which we name spidey, and which encodes a putative steroid dehydrogenase that has sex- and age-dependent effects on viability, pheromone production, and oenocyte survival. Transcriptional silencing or overexpression of spidey during embryonic development results in pupal lethality and significant changes in levels of the ecdysone metabolite 20-hydroxyecdysonic acid and 20-hydroxyecdysone. In contrast, inhibiting gene expression only during adulthood resulted in a striking loss of oenocyte cells and a concomitant reduction of cuticular hydrocarbons, desiccation resistance, and lifespan. Oenocyte loss and cuticular lipid levels were partially rescued by 20-hydroxyecdysone supplementation. Taken together, these results identify a novel regulator of pheromone synthesis and reveal that ecdysteroid signaling is essential for the maintenance of cuticular lipids and oenocytes throughout adulthood.
authors.affiliation: Temasek Life Sciences Laboratory, National University of Singapore, Singapore, Singapore.
authors.forename: Yin Ning
authors.initials: YN
authors.lastname: Chiang
authors.affiliation: Temasek Life Sciences Laboratory, National University of Singapore, Singapore, Singapore.
authors.forename: Kah Junn
authors.initials: KJ
authors.lastname: Tan
authors.affiliation: Howard Hughes Medical Institute and Laboratory of Molecular Biology, University of Wisconsin, Madison, Wisconsin, United States of America.
authors.forename: Henry
authors.identifier: 0000-0001-5056-2755
authors.initials: H
authors.lastname: Chung
authors.affiliation: Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
authors.forename: Oksana
authors.identifier: 0000-0001-5126-2412
authors.initials: O
authors.lastname: Lavrynenko
authors.affiliation: Max Planck Institute of Molecular Cell Biology and Genetics, Dresden, Germany.
authors.forename: Andrej
authors.initials: A
authors.lastname: Shevchenko
authors.affiliation: Pacific Biosciences Research Center, University of Hawai'i at Mānoa, Honolulu, Hawaii, United States of America.
authors.forename: Joanne Y
authors.identifier: 0000-0003-4851-912X
authors.initials: JY
authors.lastname: Yew
mesh_terms: D000818:Animals; D004331:Drosophila melanogaster / Q000235:genetics* / Q000378:metabolism*; D004441:Ecdysterone / Q000235:genetics / Q000378:metabolism; D005260:Female; D006838:Hydrocarbons / Q000378:metabolism; D008055:Lipids / Q000235:genetics; D008297:Male; D010088:Oxidoreductases / Q000235:genetics / Q000378:metabolism; D010675:Pheromones / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference / Q000502:physiology; D012098:Reproduction; D012727:Sex Characteristics; D015398:Signal Transduction / Q000235:genetics*; D013256:Steroids / Q000378:metabolism*
chemical_list: D006838:Hydrocarbons; D008055:Lipids; D010675:Pheromones; D013256:Steroids; D004441:Ecdysterone; D010088:Oxidoreductases