Garcia L Rene, Sternberg Paul W
Department of Biology, Texas A&M University, College Station, Texas 77843-3258, USA.
J Neurosci. 2003 Apr 1;23(7):2696-705. doi: 10.1523/JNEUROSCI.23-07-02696.2003.
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.
在交配行为过程中，秀丽隐杆线虫雄性必须调节周期性且持续时间较长的伸肌收缩，以便将其交配刺针插入配偶体内。如果前一次刺入未能穿透阴门，伸肌会进行周期性收缩，使刺针重新尝试插入。当刺针尖端穿透阴门时，伸肌会进行持续较长时间的收缩，以将刺针保持在雌雄同体体内，直到精子转移完成。为了了解这些收缩是如何调节的，我们分离出了由EMS诱导的突变，这些突变导致雄性不恰当地进行持续较长时间的收缩。unc-103内质网相关钾离子通道基因的功能丧失突变会导致伸肌在没有交配刺激的情况下收缩。通过杀死SPC运动神经元和肛门降肌（即直接与伸肌接触的细胞），可以抑制unc-103诱导的刺针伸出。此外，乙酰胆碱的减少会抑制unc-103诱导的伸出，这表明UNC-103在交配行为之前阻止胆碱能神经元刺激伸肌。UNC-103还调节交配行为过程中刺针伸出的时间。不表现出非交配依赖性刺针伸出的unc-103雄性在性行为中表现出异常的刺针插入行为。与野生型雄性不同，unc-103突变体在周期性伸肌收缩序列中会自发地进行持续较长时间的收缩。过早的持续较长时间的收缩会导致刺针在尖端穿透阴门之前就从雄性尾部伸出。这些观察结果表明，unc-103控制着刺针功能的各个方面。
