eat-2 and eat-18 are required for nicotinic neurotransmission in the Caenorhabditis elegans pharynx

被引:122
作者
McKay, JP
Raizen, DM
Gottschalk, A
Schafer, WR
Avery, L
机构
[1] Univ Texas, SW Med Ctr, Dept Mol Biol, Dallas, TX 75390 USA
[2] Hosp Univ Penn, Div Sleep, Philadelphia, PA 19104 USA
[3] Univ Calif San Diego, Div Biol Sci, La Jolla, CA 92093 USA
关键词
D O I
10.1534/genetics.166.1.161
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
Mutations in eat-2 and eat-18 cause the same defect in C. elegans feeding behaviour: the pharynx is unable to pump rapidly in the presence of food. EAT-2 is a nicotinic acetylcholine receptor subunit that functions in the pharyngeal muscle. It is localized to the synapse between pharyngeal muscle and the main pharyngeal excitatory motor neuron MC, and it is required for MC stimulation of pharyngeal muscle. eat-18 encodes a small protein that has no homology to previously characterized proteins. It has a single transmembrane domain and a short extracellular region. Allele-specific genetic interactions between eat-2 and eat-18 suggest that EAT-18 interacts physically with the EAT-2 receptor. While eat-2 appears to be required specifically for MC neurotransmission, eat-18 also appears to be required for the function of other nicotinic receptors in the pharynx. In eat-18 mutants, the gross localization of EAT-2 at the MC synapse is normal, suggesting that it is not required for trafficking. These data indicate that eat-18 could be a novel component of the pharyngeal nicotinic receptor.
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页码:161 / 169
页数:9
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