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Public metabolites such as vitamins play critical roles in maintaining the ecological functions of microbial community. However, the biochemical and physiological bases for fine-tuning of public metabolites in the microbiome remain poorly understood. Here, we examine the interactions between myxobacteria and Phytophthora sojae , an oomycete pathogen of soybean. We find that host plant and soil microbes complement P. sojae’ s auxotrophy for thiamine. Whereas, myxobacteria inhibits Phytophthora growth by a thiaminase I CcThi1 secreted into extracellular environment via outer membrane vesicles (OMVs). CcThi1 scavenges the required thiamine and thus arrests the thiamine sharing behavior of P. sojae from the supplier, which interferes with amino acid metabolism and expression of pathogenic effectors, probably leading to impairment of P. sojae growth and pathogenicity. Moreover, myxobacteria and CcThi1 are highly effective in regulating the thiamine levels in soil, which is correlated with the incidence of soybean Phytophthora root rot. Our findings unravel a novel ecological tactic employed by myxobacteria to maintain the interspecific equilibrium in soil microbial community. The plant pathogen Phytophthora sojae requires exogenous thiamine for growth. Here, Li et al. show that soil myxobacteria inhibit Phytophthora ’s growth by scavenging thiamine through the secretion a thiaminase via outer membrane vesicles.

Thiamine deficiency complex (TDC) is a disorder resulting from the inability to acquire or retain thiamine (vitamin B1) and has been documented in organisms in aquatic ecosystems ranging from the Baltic Sea to the Laurentian Great Lakes. The biological mechanisms leading to TDC emergence may vary among systems, but in fishes, one common outcome is high mortality among early life stages. Here, we review the causes and consequences of thiamine deficiency in fishes and identify potential solutions. First, we examine the biochemical and physiological roles of thiamine in vertebrates and find that thiamine deficiency consistently results in impaired neurological function across diverse taxa. Next, we review natural producers of thiamine, which include bacteria, fungi, and plants, and suggest that thiamine is not currently limiting for most animal species inhabiting natural aquatic environments. A survey of historic occurrences of thiamine deficiency identifies consumption of a thiamine-degrading enzyme, thiaminase, as the primary explanation for low levels of thiamine in individuals and subsequent onset of TDC. Lastly, we review conservation and management strategies for TDC mitigation ranging from evolutionary rescue to managing for a diverse forage base. As recent evidence suggests occurrences of thiamine deficiency may be increasing in frequency, increased awareness and a better mechanistic understanding of the underlying causes associated with thiamine deficiency may help prevent further population declines.

Thiamine (vitamin B 1 ) is required by all living organisms in multiple metabolic pathways. It is scarce in natural systems, and deficiency can lead to reproductive failure, neurological issues, and death. One major cause of thiamine deficiency is an overreliance on diet items containing the enzyme thiaminase. Thiaminase activity has been noted in many prey fishes and linked to cohort failure in salmonid predators that eat prey fish with thiaminase activity, yet it is generally unknown whether evolutionary history, fish traits, and/or environmental conditions lead to production of thiaminase. We conducted literature and GenBank BLAST sequence searches to collect thiaminase activity data and sequence homology data in expressed protein sequences for 300 freshwater and marine fishes. We then tested whether presence or absence of thiaminase could be predicted by evolutionary relationships, trophic level, omega-3 fatty acid concentrations, habitat, climate, invasive potential, and body size. There was no evolutionary relationship with thiaminase activity. It first appears in Class Actinoptergyii (bony ray-finned fishes) and is present across the entire Actinoptergyii phylogeny in both primitive and derived fish orders. Instead, ecological factors explained the most variation in thiaminase: fishes were more likely to express thiaminase if they fed closer to the base of the food web, were high in polyunsaturated fatty acids, lived in freshwater, and were from tropical climates. These data provide a foundation for understanding sources of thiaminase leading to thiamine deficiency in fisheries and other organisms, including humans that eat uncooked fish.

Knowledge of the dietary components of fish species is important for understanding their growth, survival, and recruitment. Deficiency in thiamine (vitamin B1) leading to reproductive failure and physiological illness among freshwater fishes has been attributed to thiaminase activity in fish in the Great Lakes and the New York Finger Lakes, but the causes of variation in thiaminase activity among freshwater fishes is unclear. We characterized thiaminase activity in 29 species of freshwater fishes across 7 ray-finned and 1 jawless family. All fish were further categorized by phylogeny, trophic category (trophic level and feeding mode), and native or non-native status to evaluate how ecological processes correspond with thiaminase activity. Thiaminase activity varied significantly across species, families, trophic factors, phylogenetic groups, and sites. Teleosts that were more recently derived had higher thiaminase activity than more basal species. Thiaminase activity was also higher among herbivores than omnivores or carnivores. This trend was clearest in the Cyprinidae family, which had the greatest range in thiaminase activity and a wide range in trophic-level position and trophic categories (herbivores, omnivores, and carnivores). Variation in average thiaminase activity of Spotfin Shiners (Cyprinella spiloptera) among sites within a watershed was correlated with anthropogenic and natural components of land cover. Our study contributes much-needed quantitative ecological information related to thiaminase activity in a suite of fish species that vary in evolutionary history, trophic level, and foraging modes. However, more studies are needed to identify interacting causes of thiaminase variation and examine the implications of these findings on the overall health of aquatic populations and freshwater ecosystems.

Thiamine (vitamin B 1 ) 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.

Fish population declines from thiamine (vitamin B1) deficiency have been widespread in ecologically and economically valuable organisms, ranging from the Great Lakes to the Baltic Sea and, most recently, the California coast. Thiamine deficiencies in predatory fishes are often attributed to a diet of prey fishes with high levels of thiamine-degrading (e.g., thiaminase) enzymes, such as alewives, rainbow smelt, and anchovies. Since their discovery, thiaminase I enzymes have been recognized for breaking down thiamine into its pyrimidine and thiazole moieties using various nucleophilic co-substrates to afford cleavage, but these studies have not thoroughly considered other factors that could modify enzyme activity. We found the thiaminase I enzyme from Clostridium botulinum efficiently degrades thiamine in the presence of pyridoxine (vitamin B6) as a co-substrate but has relatively limited activity in the presence of nicotinic acid (vitamin B3). Using fluorescence measurements, thiamine degradation in an over-the-counter complete multivitamin formulation was inhibited, and a B-complex formulation required co-substrate supplementation for maximal thiamine depletion. These studies prompted the evaluation of specific constituents contributing to thiaminase I inhibition by both chromatography and fluorescence assays: Cu 2+ potently and irreversibly inhibited thiamine degradation; ascorbic acid was a strong but reversible inhibitor; Fe 2+ , Mn 2+ and Fe 3+ modulated thiamine degradation to a lesser degree. The enhancement by pyridoxine and inhibition by Cu 2+ extended to thiaminase-mediated degradation from Burkholderia thailandensis , Paenibacillus thiaminolyticus , and Paenibacillus apiarius in tryptic soy broth supernatants. These co-substrate limitations and the common presence of inhibitory dietary factors complement recent studies reporting that the intended function of thiaminase enzymes is to recycle thiamine breakdown products for thiamine synthesis, not thiamine degradation.

Thiamine (vitamin B1) is a precursor of the well-known coenzyme of central metabolic pathways thiamine diphosphate (ThDP). Highly intense glucose oxidation in the brain requires ThDP-dependent enzymes, which determines the critical significance of thiamine for neuronal functions. However, thiamine can also act through the non-coenzyme mechanisms. The well-known facilitation of acetylcholinergic neurotransmission upon the thiamine and acetylcholine co-release into the synaptic cleft has been supported by the discovery of thiamine triphosphate (ThTP)-dependent phosphorylation of the acetylcholine receptor-associated protein rapsyn, and thiamine interaction with the TAS2R1 receptor, resulting in the activation of synaptic ion currents. The non-coenzyme regulatory binding of thiamine compounds has been demonstrated for the transcriptional regulator p53, poly(ADP-ribose) polymerase, prion protein PRNP, and a number of key metabolic enzymes that do not use ThDP as a coenzyme. The accumulated data indicate that the molecular mechanisms of the neurotropic action of thiamine are far broader than it has been originally believed, and closely linked to the metabolism of thiamine and its derivatives in animals. The significance of this topic has been illustrated by the recently established competition between thiamine and the antidiabetic drug metformin for common transporters, which can be the reason for the thiamine deficiency underlying metformin side effects. Here, we also discuss the medical implications of the research on thiamine, including the role of thiaminases in thiamine reutilization and biosynthesis of thiamine antagonists; molecular mechanisms of action of natural and synthetic thiamine antagonists, and biotransformation of pharmacological forms of thiamine. Given the wide medical application of thiamine and its synthetic forms, these aspects are of high importance for medicine and pharmacology, including the therapy of neurodegenerative diseases.

TenA thiamin-degrading enzymes are commonly found in prokaryotes, plants, fungi and algae and are involved in the thiamin salvage pathway. The gut symbiont Bacteroides thetaiotaomicron (Bt) produces a TenA protein (BtTenA) which is packaged into its extracellular vesicles. An alignment of BtTenA protein sequence with proteins from different databases using the basic local alignment search tool (BLAST) and the generation of a phylogenetic tree revealed that BtTenA is related to TenA-like proteins not only found in a small number of intestinal bacterial species but also in some aquatic bacteria, aquatic invertebrates, and freshwater fish. This is, to our knowledge, the first report describing the presence of TenA-encoding genes in the genome of members of the animal kingdom. By searching metagenomic databases of diverse host-associated microbial communities, we found that BtTenA homologues were mostly represented in biofilms present on the surface of macroalgae found in Australian coral reefs. We also confirmed the ability of a recombinant BtTenA to degrade thiamin. Our study shows that BttenA-like genes which encode a novel sub-class of TenA proteins are sparingly distributed across two kingdoms of life, a feature of accessory genes known for their ability to spread between species through horizontal gene transfer.

The lack of a fitness‐based theory of micronutrient allocation to specific tissues hinders understanding of the ultimate causes of mass juvenile mortality due to thiamine (vitamin B1) deficiency, which is an emerging threat to marine and coastal ecosystems worldwide. We modeled the optimal allocation of thiamine in salmon to somatic and reproductive tissues to investigate correlations between tissue thiamine levels, adult mortality, juvenile recruitment, and excretion rates that change with thiamine concentration. The model showed a positive correlation between thiamine levels in gonads and muscles, with a slope that increased with time. This was driven by a constrained thiamine input in salmon, but a negative or no correlation was found in scenarios with high thiamine input. These predictions were confirmed by analysis of empirical data from Atlantic salmon (Salmo salar) populations that differ in the occurrence of episodic thiamine deficiency. A positive correlation was indicative of low thiamine input, regardless of how juvenile recruitment and adult survival increased with thiamine concentration. The model output suggests that renal (i.e., kidney) reuptake is fundamental to understanding micronutrient allocation strategies. Measuring correlations between micronutrient concentrations in reproductive and somatic tissues of adults may help to detect early signs of thiamine deficiency before mass mortality of juveniles occurs. This can complement the previously suggested tissue concentrations and food web indicators. Future studies should try to distinguish and quantify the factors that alter the net thiamine input in salmonids and the subsequent allocation to offspring. Particular attention should be given to changes in thiamine uptake from the diet, including intestinal uptake mechanisms and effects of thiaminase activity. Additionally, more information is needed on internal factors that reduce thiamine availability, such as thiamine degradation as an antioxidant during lipid metabolism, and other physiological factors that can potentially increase thiamine loss, including allocation mechanisms and renal processes. The lack of a fitness‐based theory for micronutrient allocation hinders understanding of juvenile mortality due to thiamine deficiency, a threat to organisms in aquatic ecosystems. Our model showed that thiamine levels in gonads and muscles correlate positively, indicating low thiamine input, and this was confirmed by empirical data from Atlantic salmon. Renal reuptake is crucial for understanding micronutrient strategies, and measuring tissue correlations can detect early thiamine deficiency signs.

Ferns have been exposed to herbivorous insects since the latter evolved in the Devonian. Currently, ferns suffer similar percentages of leaf herbivory as angiosperms. Therefore, they often use a combination of chemical defenses as protection against herbivores. In this review, we summarize the distribution of five groups of biomolecules that may act as chemical defenses of ferns: phytoecdysteroids, flavonoids, thiaminase, cyanogenic glycosides, and alkaloids. For each of these biomolecules, we briefly discuss their biosynthesis, mode of action, and currently known taxonomic distribution in ferns, and include examples to illustrate their observed concentrations in different fern tissues. We conclude with a discussion of ferns that accumulate heavy metals, which may also serve in their defense against herbivores. Finally, we discuss research gaps to encourage future research in this widely understudied and ecologically important field of investigation.