Journal article
The Drosophila NKCC Ncc69 is required for normal renal tubule function
American Journal of Physiology: Cell Physiology, Vol.303(8), pp.C883-C894
10/01/2012
DOI: 10.1152/ajpcell.00201.2012
PMCID: PMC3774093
PMID: 22914641
Abstract
Rodan AR, Baum M, Huang CL. The Drosophila NKCC Ncc69 is required for normal renal tubule function. Am J Physiol Cell Physiol 303: C883-C894, 2012. First published August 22, 2012; doi:10.1152/ajpcell.00201.2012.-Epithelial ion transport is essential to renal homeostatic function, and it is dysregulated in several diseases, such as hypertension. An understanding of the insect renal (Malpighian) tubule yields insights into conserved epithelial ion transport processes in higher organisms and also has implications for the control of insect infectious disease vectors. Here, we examine the role of the Na+-K+-2Cl(-) (NKCC) cotransporter Ncc69 in Drosophila tubule function. Ncc69 mutant tubules have decreased rates of fluid secretion and K+ flux, and these phenotypes were rescued by expression of wild-type Ncc69 in the principal cells of the tubule. Na+ flux was unaltered in Ncc69 mutants, suggesting Na+ recycling across the basolateral membrane. In unstimulated tubules, the principal role of the Na+-K+-ATPase is to generate a favorable electrochemical gradient for Ncc69 activity: while the Na+-K+-ATPase inhibitor ouabain decreased K+ flux in wild-type tubules, it had no effect in Ncc69 mutant tubules. However, in the presence of cAMP, which stimulates diuresis, additional Na+-K+-ATPase-dependent K+ transport pathways are recruited. In studying the effects of capa-1 on wild-type and Ncc69 mutant tubules, we found a novel antidiuretic role for this hormone that is dependent on intact Ncc69, as it was abolished in Ncc69 mutant tubules. Thus, Ncc69 plays an important role in transepithelial ion and fluid transport in the fly renal tubule and is a target for regulation in antidiuretic states.
Details
- Title: Subtitle
- The Drosophila NKCC Ncc69 is required for normal renal tubule function
- Creators
- Aylin R. Rodan - The University of Texas Southwestern Medical CenterMichel Baum - The University of Texas Southwestern Medical CenterChou-Long Huang - The University of Texas Southwestern Medical Center
- Resource Type
- Journal article
- Publication Details
- American Journal of Physiology: Cell Physiology, Vol.303(8), pp.C883-C894
- DOI
- 10.1152/ajpcell.00201.2012
- PMID
- 22914641
- PMCID
- PMC3774093
- NLM abbreviation
- Am J Physiol Cell Physiol
- ISSN
- 0363-6143
- eISSN
- 1522-1563
- Publisher
- Amer Physiological Soc
- Number of pages
- 12
- Grant note
- DK-091316; DK-007257; DK-59530; DK-41612; DK-078596; DK-079328 / National Institute of Diabetes and Digestive and Kidney Diseases; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK) T32DK007257 / NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES; United States Department of Health & Human Services; National Institutes of Health (NIH) - USA; NIH National Institute of Diabetes & Digestive & Kidney Diseases (NIDDK)
- Language
- English
- Date published
- 10/01/2012
- Academic Unit
- Nephrology; Internal Medicine
- Record Identifier
- 9984360041402771
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