Abstract
During mating behavior the Caenorhabditis elegans male must regulate periodic and prolonged protractor muscle contractions to insert his copulatory spicules into his mate. The protractors undergo periodic contractions to allow the spicules to reattempt insertion if a previous thrust failed to breach the vulva. When the spicule tips penetrate the vulva, the protractors undergo prolonged contraction to keep the spicules inside the hermaphrodite until sperm transfer is complete. To understand how these contractions are regulated, we isolated EMS-induced mutations that cause males to execute prolonged contraction inappropriately. Loss-of-function mutations in the unc-103 ERG-like K(+) channel gene cause the protractor muscles to contract in the absence of mating stimulation. unc-103-induced spicule protraction can be suppressed by killing the SPC motor neurons and the anal depressor muscle: cells that directly contact the protractors. Also, reduction in acetylcholine suppresses unc-103-induced protraction, suggesting that UNC-103 keeps cholinergic neurons from stimulating the protractors before mating behavior. UNC-103 also regulates the timing of spicule protraction during mating behavior. unc-103 males that do not display mating-independent spicule protraction show abnormal spicule insertion behavior during sex. In contrast to wild-type males, unc-103 mutants execute prolonged contractions spontaneously within sequences of periodic protractor contractions. The premature prolonged contractions cause the spicules to extend from the male tail before the spicule tips penetrate the vulva. These observations demonstrate that unc-103 controls various aspects of spicule function.
Highlights
IntroductionAnalysis of Drosophila behavioral mutants led to the first in vivo correlation among K ϩ channel genes such as shaker (Kamb et al, 1987; Temple et al, 1987; Pongs et al, 1988), slowpoke (Atkinson et al, 1991), ether-a-go-go (Kaplan and Trout, 1969; Warmke et al, 1991), and seizure/erg (Titus et al, 1997; Wang et al, 1997) and their roles in specific motor outputs (Papazian et al, 1988)
We find that mutations in unc-103, the worm homolog of Drosophila seizure/erg-encoded and the human h-erg-encoded delayed inward rectifying voltage-gated K ϩ channel, affect the spicule insertion step
We find that in C. elegans males UNC-103 has a specific role in mating behavior, and it regulates sex muscle contractions before and during copulation
Summary
Analysis of Drosophila behavioral mutants led to the first in vivo correlation among K ϩ channel genes such as shaker (Kamb et al, 1987; Temple et al, 1987; Pongs et al, 1988), slowpoke (Atkinson et al, 1991), ether-a-go-go (Kaplan and Trout, 1969; Warmke et al, 1991), and seizure/erg (Titus et al, 1997; Wang et al, 1997) and their roles in specific motor outputs (Papazian et al, 1988). Personal communication), egl-36 (the homolog of shaw) (Elkes et al, 1997; Johnstone et al, 1997), egl-2 (the homolog of ether-a-go-go) (Weinshenker et al, 1999), twk-18 (two-P domain K ϩ channel)
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