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The Journal of Neuroscience, January 1, 1999, 19(1):159-167
EAT-4, a Homolog of a Mammalian Sodium-Dependent Inorganic Phosphate Cotransporter, Is Necessary for Glutamatergic Neurotransmission in Caenorhabditis elegans
Raymond Y. N. Lee1, Elizabeth R. Sawin2, Martin Chalfie3, H. Robert Horvitz2, and Leon Avery1 1 Department of Molecular Biology and Oncology, University of Texas Southwestern Medical Center, Dallas, Texas 75235-9148, 2 Howard Hughes Medical Institute, Department of Biology, Massachusetts Institute of Technology, Cambridge, Massachusetts 02139, and 3 Department of Biological Sciences, Columbia University, New York, New York 10027
The Caenorhabditis elegans gene eat-4 affects multiple glutamatergic neurotransmission pathways. We find that eat-4 encodes a protein similar in sequence to a mammalian brain-specific sodium-dependent inorganic phosphate cotransporter I (BNPI). Like BNPI in the rat CNS, eat-4 is expressed predominantly in a specific subset of neurons, including several proposed to be glutamatergic. Loss-of-function mutations in eat-4 cause defective glutamatergic chemical transmission but appear to have little effect on other functions of neurons. Our data suggest that phosphate ions imported into glutamatergic neurons through transporters such as EAT-4 and BNPI are required specifically for glutamatergic neurotransmission.
Key words: C. elegans; behavior; genetics; glutamate; synaptic neurotransmission; sodium-dependent inorganic phosphate cotransporter
Copyright © 1999 Society for Neuroscience 0270-6474/99/191159-09$05.00/0
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