ArticleGlia2011
Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume.
Article in Glia, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 66 citations in OpenAlex.
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- Unanticipated domain requirements for Drosophila Wnk kinase in vivo.PLoS genetics · 2023Article
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- SIK3 and Wnk converge on Fray to regulate glial K+ buffering and seizure susceptibility.PLoS genetics · 2023Article
- Sequence analysis and function of mosquito aeCCC2 and Drosophila Ncc83 orthologs.Insect biochemistry and molecular biology · 2022Article
- Chloride oscillation in pacemaker neurons regulates circadian rhythms through a chloride-sensing WNK kinase signaling cascade.Current biology : CB · 2022Article
- Inter-Species Rescue of Mutant Phenotype-The Standard for Genetic Analysis of Human Genetic Disorders inInternational journal of molecular sciences · 2022Review
- Bidirectional regulation of glial potassium buffering - glioprotection versus neuroprotection.eLife · 2021Article
- AeLife · 2020Article
- Wrapping glia regulates neuronal signaling speed and precision in the peripheral nervous system of Drosophila.Nature communications · 2020Article
- Neuronal activity disrupts myelinated axon integrity in the absence of NKCC1b.The Journal of cell biology · 2020Article
- More Than Mortar: Glia as Architects of Nervous System Development and Disease.Frontiers in cell and developmental biology · 2020Review
- SIK3 suppresses neuronal hyperexcitability by regulating the glial capacity to buffer KThe Journal of cell biology · 2019Article
- The Drosophila Malpighian tubule as a model for mammalian tubule function.Current opinion in nephrology and hypertension · 2019Review
- Heterologous Expression ofInsects · 2019Article
- The glial sodium-potassium-2-chloride cotransporter is required for synaptic transmission in the Drosophila visual system.Scientific reports · 2019Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
The nervous system is protected by blood barriers that use multiple systems to control extracellular solute composition, osmotic pressure, and fluid volume. In the human nervous system, misregulation of the extracellular volume poses serious health threats. Here, we show that the glial cells that form the Drosophila blood-nerve barrier have a conserved molecular mechanism that regulates extracellular volume: the Serine/Threonine kinase Fray, which we previously showed is an ortholog of mammalian PASK/SPAK; and the Na-K-Cl cotransporter Ncc69, which we show is an ortholog of human NKCC1. In mammals, PASK/SPAK binds to NKCC1 and regulates its activity. In Drosophila, larvae mutant for Ncc69 develop a peripheral neuropathy, where fluid accumulates between glia and axons. The accumulation of fluid has no detectable impact on action potential conduction, suggesting that the role of Ncc69 is to maintain volume or osmotic homeostasis. Drosophila Ncc69 has kinetics similar to human NKCC1, and NKCC1 can rescue Ncc69, suggesting that they function in a conserved physiological mechanism. We show that fray and Ncc69 are coexpressed in nerve glia, interact in a yeast-two-hybrid assay, and have an essentially identical bulging nerve phenotype. We propose that normally functioning nerves generate extracellular solutes that are removed by Ncc69 under the control of Fray. This mechanism may perform a similar role in humans, given that NKCC1 is expressed at the blood-brain barrier.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.