期刊
SCIENCE
卷 357, 期 6357, 页码 1261-1265出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aan5061
关键词
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资金
- American Society of Ichthyologists and Herpetologists
- Herpetologists' League
- Texas Herpetological Society
- Minnesota Herpetological Society
- Society for the Study of Amphibians and Reptiles
- Chicago Herpetological Society
- North Carolina Herpetological Society
- National Geographic Society [9468-14]
- Society for the Study of Evolution
- Society of Systematic Biologists
- NSF [DEB-1404409, DEB-1556967, IOS-1557857, PLR-1443637]
- Graduate School Continuing Fellowship at University of Texas at Austin
- NSF
- St. John's University
- National Science and Engineering Research Council Collaborative Research and Training Experience Training Program in Biodiversity Research at University of British Columbia
- Bauer Fellowship at Harvard University
- William F. Milton grant from Harvard Medical School
- L'Oreal For Women in Science Fellowship
- University of Texas at Austin Waggoner Center for Alcohol and Addiction Research
- NIH [R01-AA006399]
- [NSF EF-1241885]
- [EF-1241848]
- Direct For Biological Sciences
- Division Of Environmental Biology [1404409] Funding Source: National Science Foundation
- Direct For Biological Sciences
- Div Of Biological Infrastructure [1556967] Funding Source: National Science Foundation
Animals that wield toxins face self-intoxication. Poison frogs have a diverse arsenal of defensive alkaloids that target the nervous system. Among them is epibatidine, a nicotinic acetylcholine receptor (nAChR) agonist that is lethal at microgram doses. Epibatidine shares a highly conserved binding site with acetylcholine, making it difficult to evolve resistance yet maintain nAChR function. Electrophysiological assays of human and frog nAChR revealed that one amino acid replacement, which evolved three times in poison frogs, decreased epibatidine sensitivity but at a cost of acetylcholine sensitivity. However, receptor functionality was rescued by additional amino acid replacements that differed among poison frog lineages. Our results demonstrate how resistance to agonist toxins can evolve and that such genetic changes propel organisms toward an adaptive peak of chemical defense.
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