TY - JOUR
T1 - Behavioral defects in C. elegans egl-36 mutants result from potassium channels shifted in voltage-dependence of activation
AU - Johnstone, Duncan B.
AU - Wei, Aguan
AU - Butler, Alice
AU - Salkoff, Lawrence
AU - Thomas, James H.
N1 - Funding Information:
We thank David Weinshenker, Betsy Malone, Bertil Hille, and Sharona Gordon for their comments on sections of this manuscript; Jane Mendel for advice on protocols; Andrew Link for computer assistance; and Anatoli Lopatin, Jim Huettner, Mike Nonet, Colin Nichols, Chris Lingle, and Matt Schreiber for discussion of ideas in this manuscript. We thank Carol Trent for identifying n728 and Erik Jorgensen for identifying n2332 and for discussing with us his favorite topic, retrovesicular ganglion anatomy. This work was supported by Public Health Service Grant R01NS30187 to J. H. T., and by Public Health Service Grant R01NS24785 and a grant from the Muscular Dystrophy Association to L. S. Some strains were obtained from the Caenorhabditis Genetics Research Center, which is funded by the National Institutes of Health National Center for Research Resources.
PY - 1997/7
Y1 - 1997/7
N2 - Mutations in the C. elegans egl-36 gene result in defective excitation of egg-laying and enteric muscles. Dominant gain-of-function alleles inhibit enteric and egg-laying muscle contraction, whereas a putative null mutation has no observed phenotype. egl-36 encodes a Shaw-type (Kv3) voltage-dependent potassium channel subunit. In Xenopus oocytes, wild-type egl-36 expresses noninactivating channels with slow activation kinetics. One gain-of-function mutation causes a single amino acid substitution in S6, and the other causes a substitution in the cytoplasmic amino terminal domain. Both mutant alleles produce channels dramatically shifted in their midpoints of activation toward hyperpolarized voltages. An egl-36::gfp fusion is expressed in egg-laying muscles and in a pair of enteric muscle motor neurons. The mutant egl-36 phenotypes can thus be explained by expression in these cells of potassium channels that are inappropriately opened at hyperpolarized potentials, causing decreased excitability due to increased potassium conductance.
AB - Mutations in the C. elegans egl-36 gene result in defective excitation of egg-laying and enteric muscles. Dominant gain-of-function alleles inhibit enteric and egg-laying muscle contraction, whereas a putative null mutation has no observed phenotype. egl-36 encodes a Shaw-type (Kv3) voltage-dependent potassium channel subunit. In Xenopus oocytes, wild-type egl-36 expresses noninactivating channels with slow activation kinetics. One gain-of-function mutation causes a single amino acid substitution in S6, and the other causes a substitution in the cytoplasmic amino terminal domain. Both mutant alleles produce channels dramatically shifted in their midpoints of activation toward hyperpolarized voltages. An egl-36::gfp fusion is expressed in egg-laying muscles and in a pair of enteric muscle motor neurons. The mutant egl-36 phenotypes can thus be explained by expression in these cells of potassium channels that are inappropriately opened at hyperpolarized potentials, causing decreased excitability due to increased potassium conductance.
UR - http://www.scopus.com/inward/record.url?scp=0030762007&partnerID=8YFLogxK
U2 - 10.1016/S0896-6273(00)80355-4
DO - 10.1016/S0896-6273(00)80355-4
M3 - Article
C2 - 9247271
AN - SCOPUS:0030762007
VL - 19
SP - 151
EP - 164
JO - Neuron
JF - Neuron
SN - 0896-6273
IS - 1
ER -