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Resources » Paper

Ringstad, Niels et al. (2009) International Worm Meeting "Inward Rectifier Potassium Channels Inhibit C. elegans Egg Laying and Locomotion."

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  • Comments on Ringstad, Niels et al. (2009) International Worm Meeting "Inward Rectifier Potassium Channels Inhibit C. elegans Egg Laying and Locomotion." (0)

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    Status:
    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00034195

    Ringstad, Niels, & Horvitz, Bob (2009). Inward Rectifier Potassium Channels Inhibit C. elegans Egg Laying and Locomotion presented in International Worm Meeting. Unpublished information; cite only with author permission.

    Inward-rectifier K+ (IRK) channels function to regulate membrane excitability in neurons and neuroendocrine cells. Three C. elegans genes, irk-1, irk-2 and irk-3, are predicted to encode potassium channel subunits similar to mammalian Kir1-7, which form tetrameric inward-rectifier potassium channels that are activated by diverse intracellular signals, including G proteins, ATP and phosphoinositides. To study the function of C. elegans inward rectifier K+ channels, we isolated deletion alleles of irk-1, irk-2 and irk-3. irk-1 mutants move faster than the wild type and lay early-stage eggs. irk-1 deletion also suppresses the egg-laying defect caused by a gain-of-function mutation in the EGL-6 G protein-coupled receptor for FMRFamides that activate inhibitory G protein signaling in the HSN egg-laying motor neurons. We did not observe gross behavioral defects of irk-2 and irk-3 mutants. An irk-1::gfp reporter transgene was expressed in a small number of neurons, including the HSNs. Expression of ChannelRhodopsin using the irk-1 promoter caused animals to lay eggs and accelerate in response to a blue-light stimulus, indicating that irk-1 functions to inhibit neurons that promote egg laying and locomotion. Xenopus laevis oocytes expressing irk-1 showed inward-rectifying currents in high-potassium saline. We are currently testing whether signaling pathways known to modulate IRK channels in other organisms function to modulate IRK-1 in vitro and in vivo.


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