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A glial DEG/ENaC channel functions with neuronal channel DEG‐1 to mediate specific sensory functions in C. elegans
Author(s) -
Wang Ying,
Apicella Alfonso,
Lee SunKyung,
Ezcurra Marina,
Slone Robert D,
Goldmit Maya,
Schafer William R,
Shaham Shai,
Driscoll Monica,
Bianchi Laura
Publication year - 2008
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.1038/emboj.2008.161
Subject(s) - miami , experimental biology , biology , library science , computational biology , computer science , environmental science , soil science
Mammalian neuronal DEG/ENaC channels known as ASICs ( a cid‐ s ensing i on c hannels) mediate sensory perception and memory formation. ASICS are closed at rest and are gated by protons. Members of the DEG/ENaC family expressed in epithelial tissues are called ENaCs and mediate Na + transport across epithelia. ENaCs exhibit constitutive activity and strict Na + selectivity. We report here the analysis of the first DEG/ENaC in Caenorhabditis elegans with functional features of ENaCs that is involved in sensory perception. ACD‐1 ( a cid‐sensitive c hannel, d egenerin‐like) is constitutively open and impermeable to Ca 2+ , yet it is required with neuronal DEG/ENaC channel DEG‐1 for acid avoidance and chemotaxis to the amino acid lysine. Surprisingly, we document that ACD‐1 is required in glia rather than neurons to orchestrate sensory perception. We also report that ACD‐1 is inhibited by extracellular and intracellular acidification and, based on the analysis of an acid‐hypersensitive ACD‐1 mutant, we propose a mechanism of action of ACD‐1 in sensory responses based on its sensitivity to protons. Our findings suggest that channels with ACD‐1 features may be expressed in mammalian glia and have important functions in controlling neuronal function.