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. 2019 May 16;9:7464. doi: 10.1038/s41598-019-42849-9

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© The Author(s) 2019

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Model: The role of secCl within the tyramine/leucokinin diuretic pathway. A model describing the role of secCl within the signaling pathways of the diuretic hormones tyramine (Tyr) and Drosophila leucokinin (DK). Diuretic hormones bind to their respective GPCRs on the basolateral membrane of stellate cells, which triggers the release of calcium from intracellular stores via the PLC/IP3 pathway. Through an unknown mechanism, this rise in intracellular [Ca⁺⁺] results in the activation of ClC-a (orange), and secCl (red). ClC-a, localized to the basolateral membrane, provides necessary Cl⁻ entry into the cell from the hemolymph and secCl, localized to the apical membrane, provides a route for Cl⁻ exit into the lumen. FSRs increase as a consequence of increased chloride secretion.