GSBS Student Publications

Student Author(s)

Caitlin Quigley

GSBS Program

Neuroscience

UMMS Affiliation

Department of Neurobiology; Hong-Sheng Li Lab; Graduate School of Biomedical Sciences, MD/PhD Program

Date

1-23-2015

Document Type

Article

Disciplines

Behavioral Neurobiology | Cellular and Molecular Physiology | Genetics | Molecular and Cellular Neuroscience | Molecular Genetics

Abstract

Most organisms are able to maintain systemic water homeostasis over a wide range of external or dietary osmolarities. The excretory system, composed of the kidneys in mammals and the Malpighian tubules and hindgut in insects, can increase water conservation and absorption to maintain systemic water homeostasis, which enables organisms to tolerate external hypertonicity or desiccation. However, the mechanisms underlying the maintenance of systemic water homeostasis by the excretory system have not been fully characterized. In the present study, we found that the putative Na(+)/Cl(-)-dependent neurotransmitter/osmolyte transporter inebriated (ine) is expressed in the basolateral membrane of anterior hindgut epithelial cells. This was confirmed by comparison with a known basolateral localized protein, the alpha subunit of Na(+)-K(+) ATPase (ATPalpha). Under external hypertonicity, loss of ine in the hindgut epithelium results in severe dehydration without damage to the hindgut epithelial cells, implicating a physiological failure of water conservation/absorption. We also found that hindgut expression of ine is required for water conservation under desiccating conditions. Importantly, specific expression of ine in the hindgut epithelium can completely restore disrupted systemic water homeostasis in ine mutants under both conditions. Therefore, ine in the Drosophila hindgut is essential for the maintenance of systemic water homeostasis.

Rights and Permissions

Citation: Sci Rep. 2015 Jan 23;5:7993. doi: 10.1038/srep07993. Link to article on publisher's site

DOI of Published Version

10.1038/srep07993

Comments

This work is licensed under a Creative Commons Attribution 4.0 International License. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder in order to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

Related Resources

Link to Article in PubMed

Journal Title

Scientific reports

PubMed ID

25613130

Creative Commons License

Creative Commons Attribution 4.0 License
This work is licensed under a Creative Commons Attribution 4.0 License.

 
 

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