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

Robert O'Hagan et al. (2004) West Coast Worm Meeting "DEG/ENaCs Form a Sensory Mechanotransduction Channel Complex in C. elegans Touch Receptor Neurons"

  • History

  • Referenced

  • Tree Display

  • My Favorites

  • My Library

  • Comments on Robert O'Hagan et al. (2004) West Coast Worm Meeting "DEG/ENaCs Form a Sensory Mechanotransduction Channel Complex in C. elegans Touch Receptor Neurons" (0)

  • Overview

    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00023963

    Robert O'Hagan, Martin Chalfie, & Miriam B Goodman (2004). DEG/ENaCs Form a Sensory Mechanotransduction Channel Complex in C. elegans Touch Receptor Neurons presented in West Coast Worm Meeting. Unpublished information; cite only with author permission.

    Transformation of mechanical energy into ionic currents is essential for touch, hearing, and nociception, as well as for control of bodily homeostasis. Members of two ion channel superfamilies (DEG/ENaCs and TRPs) are believed to be sensory mechanotransduction channels; evidence for this, however, remains indirect. In C. elegans , behavioral responses to touch require a set of six touch receptor neurons and at least twelve genes. We have recently shown that four of these genes form an ion channel complex in heterologous cells (1,2). To determine if such channels are directly activated by external force, we recorded from C. elegans touch neurons in vivo . We found that external force evokes rapidly activating mechanoreceptor currents (MRCs) carried mostly by Na + and blocked by amiloride—characteristics consistent with direct mechanical gating of a DEG/ENaC channel. Like mammalian Pacinian corpuscles, C. elegans touch neurons depolarize with both positive and negative changes in external force but not sustained force. Null mutations in the DEG/ENaC gene mec-4 and genes encoding the accessory ion channel subunits MEC-2 and MEC-6 eliminate MRCs. Elimination of touch neuron-specific, large-diameter microtubules by a null mutation in the mec-7 beta-tubulin gene reduces, but does not abolish, MRCs. Our findings provide the first direct evidence linking application of external force to activation of a molecularly-defined metazoan sensory transduction channel. 1. Chelur, D. S., et al. (2002). Nature 420(6916): 669-73. 2. Goodman, M. B., et al. (2002). Nature 415(6875): 1039-42. Supported by an HHMI predoctoral fellowship to RO; an NIGMS grant to MC; and Baxter Foundation, Sloan Foundation, and Terman Faculty Scholarships to MBG.


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