线虫秀丽隐杆线虫的胆碱能受体突变体。
Cholinergic receptor mutants of the nematode Caenorhabditis elegans.
作者信息
Lewis J A, Elmer J S, Skimming J, McLafferty S, Fleming J, McGee T
机构信息
Department of Biological Sciences, University of Missouri, Columbia 65211.
出版信息
J Neurosci. 1987 Oct;7(10):3059-71. doi: 10.1523/JNEUROSCI.07-10-03059.1987.
Potential acetylcholine receptor (AChR) mutants of the nematode are selectable by resistance to the neurotoxic drug levamisole, a probable cholinergic agonist. To determine which mutants may have achieved resistance through loss of levamisole receptor function, we have assayed mutant extracts for specific 3H-meta-aminolevamisole binding activity in the presence and absence of mecamylamine. We find that mutants in 3 of the 7 genes associated with extreme levamisole resistance are obviously deficient in saturable specific 3H-meta-aminolevamisole binding activity. Mutants of the 4 other genes have abnormal binding activities that fail to undergo the apparent allosteric activation of saturable specific 3H-meta-aminolevamisole binding activity caused by mecamylamine. Thus, all 7 genes appear to be required to produce a fully functional levamisole receptor. Mutants of several other genes associated only with partial resistance to levamisole have at least grossly normal receptor binding activities.
线虫潜在的乙酰胆碱受体（AChR）突变体可通过对神经毒性药物左旋咪唑（一种可能的胆碱能激动剂）产生抗性来进行筛选。为了确定哪些突变体可能是通过丧失左旋咪唑受体功能而获得抗性的，我们在有和没有美加明的情况下，检测了突变体提取物中特定的3H-间氨基左旋咪唑结合活性。我们发现，与极高左旋咪唑抗性相关的7个基因中有3个基因的突变体，其可饱和的特异性3H-间氨基左旋咪唑结合活性明显不足。其他4个基因的突变体具有异常的结合活性，不会发生由美加明引起的可饱和特异性3H-间氨基左旋咪唑结合活性的明显变构激活。因此，似乎所有7个基因都是产生功能完全正常的左旋咪唑受体所必需的。其他几个仅与对左旋咪唑部分抗性相关的基因的突变体，其受体结合活性至少大体上是正常的。
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