Journal
DEVELOPMENTAL CELL
Volume 47, Issue 3, Pages 294-+Publisher
CELL PRESS
DOI: 10.1016/j.devcel.2018.09.012
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Funding
- Bloomington Drosophila Stock Center [NIH P40 OD018537]
- Transgenic RNAi Project at Harvard Medical School [NIH R24 RR032668]
- Postdoctoral Fellowship for Research Abroad from the Japan Society for the Promotion of Science
- Naito Foundation Subsidy for Dispatch of Young Researchers Abroad
- NIH from NICHD [R00 HD073239]
- W.M. Keck Foundation
- Pew Biomedical Scholars Award from the Pew Charitable Trusts
- EUNICE KENNEDY SHRIVER NATIONAL INSTITUTE OF CHILD HEALTH & HUMAN DEVELOPMENT [R00HD073239] Funding Source: NIH RePORTER
- NATIONAL CENTER FOR RESEARCH RESOURCES [R24RR032668] Funding Source: NIH RePORTER
- OFFICE OF THE DIRECTOR, NATIONAL INSTITUTES OF HEALTH [P40OD018537, P40OD010949] Funding Source: NIH RePORTER
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Steroid hormones are a group of lipophilic hormones that are believed to enter cells by simple diffusion to regulate diverse physiological processes through intracellular nuclear receptors. Here, we challenge this model in Drosophila by demonstrating that Ecdysone Importer (Ecl), a membrane transporter identified from two independent genetic screens, is involved in cellular uptake of the steroid hormone ecdysone. EcI encodes an organic anion transporting polypeptide of the evolutionarily conserved solute carrier organic anion superfamily. In vivo, EcI loss of function causes phenotypes indistinguishable from ecdysone- or ecdysone receptor (EcR)-deficient animals, and EcI knockdown inhibits cellular uptake of ecdysone. Furthermore, EcI regulates ecdysone signaling in a cell-autonomous manner and is both necessary and sufficient for inducing ecdysone-dependent gene expression in culture cells expressing EcR. Altogether, our results challenge the simple diffusion model for cellular uptake of ecdysone and may have wide implications for basic and medical aspects of steroid hormone studies.
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