4.8 Article

Hunting the eagle killer: A cyanobacterial neurotoxin causes vacuolar myelinopathy

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SCIENCE
卷 371, 期 6536, 页码 1335-+

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AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.aax9050

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资金

  1. Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) [NI 1152/3-1, INST 271/388-1]
  2. Czech Science Foundation (GACR) [19-21649J]
  3. U.S. Fish and Wildlife Service (UGA) [FWS-800-037-215, FWS-800-037-2016-UGA]
  4. Florida Fish and Wildlife Conservation Commission [FP00011365]
  5. Gulf States Marine Fisheries Commission [FWS8010372019]
  6. McIntire-Stennis Capacity Grant from the USDA National Institute of Food and Agriculture [GEOZ-0174-MS, 1022348]
  7. American Eagle Foundation (UGA) [RAEETRR272746CV]
  8. National Institute of Neurological Disorders and Stroke [R01NS090645]

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Vacuolar myelinopathy is a fatal neurological disease discovered during a mass mortality of bald eagles in Arkansas, USA, caused by a neurotoxin produced by an epiphytic cyanobacterial species growing on aquatic vegetation. Environmental factors, especially bromide availability, promote toxin production and spread of the disease.
Vacuolar myelinopathy is a fatal neurological disease that was initially discovered during a mysterious mass mortality of bald eagles in Arkansas in the United States. The cause of this wildlife disease has eluded scientists for decades while its occurrence has continued to spread throughout freshwater reservoirs in the southeastern United States. Recent studies have demonstrated that vacuolar myelinopathy is induced by consumption of the epiphytic cyanobacterial species Aetokthonos hydrillicola growing on aquatic vegetation, primarily the invasive Hydrilla verticillata. Here, we describe the identification, biosynthetic gene cluster, and biological activity of aetokthonotoxin, a pentabrominated biindole alkaloid that is produced by the cyanobacterium A. hydrillicola. We identify this cyanobacterial neurotoxin as the causal agent of vacuolar myelinopathy and discuss environmental factors-especially bromide availability-that promote toxin production.

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