Summary Steroid hormones are a large family of cholesterol derivatives regulating development and physiology in both the animal and plant kingdoms, but little is known concerning mechanisms of their secretion from steroidogenic tissues. Here, we present evidence that in Drosophila, endocrine release of the steroid hormone ecdysone is mediated through a regulated vesicular trafficking mechanism. Inhibition of calcium signaling in the steroidogenic prothoracic gland results in the accumulation of unreleased ecdysone, and the knockdown of calcium-mediated vesicle exocytosis components in the gland caused developmental defects due to deficiency of ecdysone. Accumulation of synaptotagmin-labeled vesicles in the gland is observed when calcium signaling is disrupted, and these vesicles contain an ABC transporter that functions as an ecdysone pump to fill vesicles. We propose that trafficking of steroid hormones out of endocrine cells is not always through a simple diffusion mechanism as presently thought, but instead can involve a regulated vesicle-mediated release process.
Bibliographical noteFunding Information:
We thank Vienna Drosophila Resource Center, Bloomington Drosophila Stock Center, NIG-FLY at National Institute of Genetics, Transgenic RNAi Project at Harvard Medical School, and K. Broadie for fly stocks; Drosophila Genomics Resource Center for cDNA clones; members of M.B.O. lab for fruitful discussion; and M.J. Shimell, A. Peterson, J. Simon, and S. Conner for critical reading of the manuscript. GCaMP5 imaging and analysis was performed at the University Imaging Centers, University of Minnesota. This study was supported by a postdoctoral fellowship from the Japan Society for the Promotion of Science to N.Y., NIH grants K99/R00 HD073239 from the Eunice Kennedy Shriver National Institute of Child Health and Human Development (NICHD) to N.Y., and R01 GM093301 from the National Institute of General Medical Sciences (NIGMS) to M.B.O.
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