Questions, Feedback & Help
Send us an email and we'll get back to you ASAP. Or you can read our Frequently Asked Questions.
  • page settings
  • hide sidebar
  • show empty fields
  • layout
  • (too narrow)
  • open all
  • close all
Resources » Paper

JP McKay et al. (1999) International C. elegans Meeting "EAT-2 is a beta subunit of a nicotinic acetylcholine receptor involved in neurotransmission from MC to pharyngeal muscle"

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on JP McKay et al. (1999) International C. elegans Meeting "EAT-2 is a beta subunit of a nicotinic acetylcholine receptor involved in neurotransmission from MC to pharyngeal muscle" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00023605

    JP McKay, DM Raizen, & L Avery (1999). EAT-2 is a beta subunit of a nicotinic acetylcholine receptor involved in neurotransmission from MC to pharyngeal muscle presented in International C. elegans Meeting. Unpublished information; cite only with author permission.

    Pharyngeal pumping speeds up in response to bacteria. This behavior requires pharyngeal motor neuron, MC (Neuron 3:473). Mutations in eat-2 prevent rapid pharyngeal pumping. Two results implicate eat-2 in MC neurotransmission. First, electrical recordings from the pharynx of an eat-2 mutant are similar to recordings from an MC - worm. Second, ablating MC has no effect on the pumping rate of eat-2 mutants. We have identified fourteen independent recessive mutations in eat-2 that result in a reduced pumping rate. There is complex intragenic complementation between some of the eat-2 alleles as well as allele-specific interactions between eat-2 and a semidominant allele of another slow pumping mutant, eat-18 (Genetics 141: 1365). eat-18 is MC - by the same criteria as eat-2 . A model consistent with these data is that EAT-2 and EAT-18 interact in a protein complex that is involved in acetylcholine neurotransmission from MC. We cloned eat-2 and it encodes a b -subunit of a nicotinic acetylcholine receptor. Expression of an eat-2::GFP fusion construct is restricted to pharyngeal muscle. Also, an eat-2 cDNA expressed under the control of the pharyngeal muscle specific myo-2 promoter rescues the slow pumping eat-2 mutant phenotype. These results indicate that EAT-2 functions in pharyngeal muscle. We sequenced the eat-2 alleles that demonstrate intragenic complementation or allele specific interaction with eat-18 and found that all are missense mutations. The amino acid changes in the eat-2 alleles that show intragenic complementation cluster in the amino-terminal extracellular region of the protein. This region has been shown previously to be important for receptor assembly and ligand binding. These mutations may identify specific amino acids that are important for these processes.


    Tip: Seeing your name marked red? Please help us identify you.