相互作用的氨基酸替代物使毒青能够发展出抗胺的抵抗力
Rebecca D Tarvin1, Cecilia M Borghese2, Wiebke Sachs2,3
1Department of Integrative Biology, University of Texas at Austin, Austin, TX 78712, USA. rdtarvin@gmail.com.
Science (New York, N.Y.)
|September 23, 2017
概括
毒青通过改变尼古丁乙胆受体 (nAChRs) 进化了对自身有毒的表皮素的耐药性. 这种适应维持了受体功能,展示了动物的化学防御进化.
科学领域:
- 进化生物学
- 神经科学
- 生物化学
背景情况:
- 产生毒素的动物有自我中毒的风险, 需要进化的抵抗机制.
- 毒青使用强效的类化合物,如尼古丁乙胆受体 (nAChR) 激活剂,在低剂量时具有致命作用.
- 在不损害基本受体功能的情况下,Epibatidine的目标部位与乙胆重叠使得耐药性的发展具有挑战性.
研究的目的:
- 研究毒青对强有力的化物epibatidine产生耐药性的分子机制.
- 了解如何保持nAChR功能,尽管对epibatidine具有抗药性.
- 了解毒青的化学防御机制的演化过程.
主要方法:
- 对人类和青的尼古丁乙胆受体 (nAChR) 进行了电生理学测试.
- 分析了nAChR中特定的氨基酸替代物对酸丁和乙胆敏感性的影响.
- 对不同毒青血统的进化突变进行比较分析.
主要成果:
- 一种单一的氨基酸替代物,在毒青中独立进化了三次,降低了epibatidine的敏感性.
- 这种抗药性突变的代价是降低了对乙胆的敏感性.
- 随后,基因特异性氨基酸变化恢复了nAChR功能,恢复了受体的效率.
- 这些发现突显了抵抗机制的趋同演变.
结论:
- 毒青通过特定的nAChR修改对自己的毒素产生抵抗力.
- 抵抗机制的融合进化允许维持基本的生理功能.
- 在nAChRs中的基因适应使毒能够达到高水平的化学防御.
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