Author:
Richter Catherine A.,Evans Allison N.,Heppell Scott A.,Zajicek James L.,Tillitt Donald E.
Abstract
AbstractThiamine (vitamin B1) metabolism is an important driver of human and animal health and ecological functioning. Some organisms, including species of ferns, mollusks, and fish, contain thiamine-degrading enzymes known as thiaminases, and consumption of these organisms can lead to thiamine deficiency in the consumer. Consumption of fish containing thiaminase has led to elevated mortality and recruitment failure in farmed animals and wild salmonine populations around the world. In the North American Great Lakes, consumption of the non-native prey fish alewife (Alosa pseudoharengus) by native lake trout (Salvelinus namaycush) led to thiamine deficiency in the trout, contributed to elevated fry mortality, and impeded natural population recruitment. Several thiaminases have been genetically characterized in bacteria and unicellular eukaryotes, and the source of thiaminase in multicellular organisms has been hypothesized to be gut microflora. In an unexpected discovery, we identified thiaminase I genes in zebrafish (Danio rerio) with homology to bacterial tenA thiaminase II. The biochemical activity of zebrafish thiaminase I (GenBank NP_001314821.1) was confirmed in a recombinant system. Genes homologous to the zebrafish tenA-like thiaminase I were identified in many animals, including common carp (Cyprinus carpio), zebra mussel (Dreissena polymorpha) and alewife. Thus, the source of thiaminase I in alewife impacting lake trout populations is likely to be de novo synthesis.
Funder
Great Lakes Fishery Trust
U.S. Geological Survey Ecosystems Mission Area
Publisher
Springer Science and Business Media LLC
Cited by
8 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献