Linked Life Data

21125654

Source:http://linkedlifedata.com/resource/pubmed/id/21125654

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2010-12-20
pubmed:abstractText
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.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1098-1136
pubmed:author
pubmed:copyrightInfo
© 2010 Wiley-Liss, Inc.
pubmed:issnType
Electronic
pubmed:volume
59
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
320-32
pubmed:dateRevised
2011-8-1
pubmed:meshHeading
pubmed-meshheading:21125654-Action Potentials, pubmed-meshheading:21125654-Animals, pubmed-meshheading:21125654-Animals, Genetically Modified, pubmed-meshheading:21125654-Blood-Nerve Barrier, pubmed-meshheading:21125654-Cells, Cultured, pubmed-meshheading:21125654-Drosophila, pubmed-meshheading:21125654-Drosophila Proteins, pubmed-meshheading:21125654-Extracellular Space, pubmed-meshheading:21125654-Humans, pubmed-meshheading:21125654-Larva, pubmed-meshheading:21125654-Microscopy, Electron, Transmission, pubmed-meshheading:21125654-Models, Biological, pubmed-meshheading:21125654-Mutation, pubmed-meshheading:21125654-Neural Conduction, pubmed-meshheading:21125654-Neuroglia, pubmed-meshheading:21125654-Neurons, pubmed-meshheading:21125654-Peripheral Nerves, pubmed-meshheading:21125654-Protein-Serine-Threonine Kinases, pubmed-meshheading:21125654-Symporters, pubmed-meshheading:21125654-Two-Hybrid System Techniques
pubmed:year
2011
pubmed:articleTitle
Drosophila glia use a conserved cotransporter mechanism to regulate extracellular volume.
pubmed:affiliation
Molecular, Cellular, and Developmental Biology Department, Yale University, New Haven, Connecticut 06520-8103, USA. william.leiserson@yale.edu
pubmed:publicationType
Journal Article, In Vitro, Research Support, U.S. Gov't, Non-P.H.S., Research Support, N.I.H., Extramural