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Resources » Paper

Yingchuan Qi et al. (2008) C.elegans Neuronal Development Meeting "Neuronal acetylcholine receptors ACR-2 and ACR-12 subunits are required in motor neurons for coordinated locomotion"

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    Publication type:
    Meeting_abstract
    WormBase ID:
    WBPaper00032691

    Yingchuan Qi, Tamara Stawicki, H Horvitz, & Yishi Jin (2008). Neuronal acetylcholine receptors ACR-2 and ACR-12 subunits are required in motor neurons for coordinated locomotion presented in C.elegans Neuronal Development Meeting. Unpublished information; cite only with author permission.

    Ventral cord motor neurons regulate the sinusoidal movement of the worm by generating sequential contraction and relaxation of longitudinal muscles. When muscles on one side are activated by cholinergic A- and B-type motor neurons, the muscles on the opposite side are reciprocally inhibited by GABAergic D-type motor neurons. A and B type motor neurons form dyadic synapses with muscles as one post-synaptic partner and the D-type motor neurons as the other. We are interested in understanding the cellular basis of neuronal signaling within the motor neuron circuit and have examined the roles of the acetylcholine receptor non-alpha subunit ACR-2. acr-2 is expressed in A- and B-type motor neurons. We have characterized an unusual mutation, acr-2(n2420gf), which causes hypercontraction in response to gentle touch, a ''shrinker'' phenotype resembling that of classical GABA-defective mutants such as unc-25 or unc-49. Interestingly, acr-2(n2420gf) animals also shrink spontaneously. acr-2(n2420) is predicted to produce a slow-desensitizing acetylcholine receptor that may lead to elevated presynaptic activity in A-/B- motor neurons (see abstract by Stawicki et al.). To determine the signaling components required for acr-2 function, we screened for genetic suppressors of acr-2(n2420gf). About ten suppressor mutations were found to be loss-of-function mutations of the acr-12 gene. acr-12 encodes an alpha-type acetylcholine receptor subunit that it is expressed in many neurons, including the ventral cord A-/B- and D-type motor neurons (Gottschalk et al., 2006, Cinar et al., 2005). Using cell-type specific transgene expression, we find that restoration of acr-12 expression in either A/B or D-type motor neurons is sufficient to revert the acr-12(0); acr-2(n2420gf) from the wild-type to the shrinking phenotype. These preliminary results suggest that although the acr-2(n2420gf) shrinker phenotype requires ACR-2 in A and B type neurons, its effect on locomotion may depend on the action of ACR-12 in GABAergic postsynaptic partners. Our data reveal neuronal AChRs function in cholinergic and GABAergic motorneurons to ensure correct coordination of the locomotion circuit.


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