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Fundamental shift in vitamin B12 eco-physiology of a model alga demonstrated by experimental evolution.

ABSTRACT: A widespread and complex distribution of vitamin requirements exists over the entire tree of life, with many species having evolved vitamin dependence, both within and between different lineages. Vitamin availability has been proposed to drive selection for vitamin dependence, in a process that links an organism's metabolism to the environment, but this has never been demonstrated directly. Moreover, understanding the physiological processes and evolutionary dynamics that influence metabolic demand for these important micronutrients has significant implications in terms of nutrient acquisition and, in microbial organisms, can affect community composition and metabolic exchange between coexisting species. Here we investigate the origins of vitamin dependence, using an experimental evolution approach with the vitamin B(12)-independent model green alga Chlamydomonas reinhardtii. In fewer than 500 generations of growth in the presence of vitamin B(12), we observe the evolution of a B(12)-dependent clone that rapidly displaces its ancestor. Genetic characterization of this line reveals a type-II Gulliver-related transposable element integrated into the B(12)-independent methionine synthase gene (METE), knocking out gene function and fundamentally altering the physiology of the alga.

SUBMITTER: Helliwell KE

PROVIDER: S-EPMC4430296 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Tissue distribution of oral vitamin B12 is influenced by B12 status and B12 form: an experimental study in rats.

Project description:PurposeHydroxocobalamin (HOCbl) is the dominating Cbl form in food, whereas cyanocobalamin (CNCbl) is common in vitamin pills and oral supplements. This study compares single-dose absorption and distribution of oral HO[57Co]Cbl and CN[57Co]Cbl in Cbl-deficient and normal rats.MethodsMale Wistar rats (7 weeks) were fed a 14-day diet with (n?=?15) or without (n?=?15) Cbl. We compared the uptakes of HO[57Co]Cbl (free or bound to bovine transcobalamin) and free CN[57Co]Cbl administered by gastric gavage (n?=?5 in each diet group). Rats were sacrificed after 24 h. Blood, liver, kidney, brain, heart, spleen, intestines, skeletal muscle, 24-h urine and faeces were collected, and the content of [57Co]Cbl was measured. Endogenous Cbl in tissues and plasma was analysed by routine methods.ResultsMean endogenous plasma-Cbl was sevenfold lower in deficient vs. normal rats (190 vs. 1330 pmol/L, p?<?0.0001). Cbl depletion increased endogenous Cbl ratios (tissue/plasma?=?k in/k out) in all organs except for the kidney, where the ratio decreased considerably. Twenty-four-hour accumulation of labelled Cbl showed that HOCbl?>?CNCbl (liver) and CNCbl?>?HOCbl (brain, muscle and plasma).ConclusionsThe Cbl status of rats and the administered Cbl form influence 24-h Cbl accumulation in tissues and plasma.

| S-EPMC5960002 | biostudies-literature

Direct exchange of vitamin B12 is demonstrated by modelling the growth dynamics of algal-bacterial cocultures.

Project description:The growth dynamics of populations of interacting species in the aquatic environment is of great importance, both for understanding natural ecosystems and in efforts to cultivate these organisms for industrial purposes. Here we consider a simple two-species system wherein the bacterium Mesorhizobium loti supplies vitamin B12 (cobalamin) to the freshwater green alga Lobomonas rostrata, which requires this organic micronutrient for growth. In return, the bacterium receives photosynthate from the alga. Mathematical models are developed that describe minimally the interdependence between the two organisms, and that fit the experimental observations of the consortium. These models enable us to distinguish between different mechanisms of nutrient exchange between the organisms, and provide strong evidence that, rather than undergoing simple lysis and release of nutrients into the medium, M. loti regulates the levels of cobalamin it produces, resulting in a true mutualism with L. rostrata. Over half of all microalgae are dependent on an exogenous source of cobalamin for growth, and this vitamin is synthesised only by bacteria; it is very likely that similar symbiotic interactions underpin algal productivity more generally.

| S-EPMC4069406 | biostudies-literature

Basal Gnathostomes provide unique insights into the evolution of vitamin B12 binders.

Project description:The uptake and transport of vitamin B12 (cobalamin; Cbl) in mammals involves a refined system with three evolutionarily related transporters: transcobalamin 1 (Tcn1), transcobalamin 2 (Tcn2), and the gastric intrinsic factor (Gif). Teleosts have a single documented binder with intermediate features to the human counterparts. Consequently, it has been proposed that the expansion of Cbl binders occurred after the separation of Actinopterygians. Here, we demonstrate that the diversification of this gene family took place earlier in gnathostome ancestry. Our data indicates the presence of single copy orthologs of the Sarcopterygii/Tetrapoda duplicates Tcn1 and Gif, and Tcn2, in Chondrichthyes. In addition, a highly divergent Cbl binder was found in the Elasmobranchii. We unveil a complex scenario forged by genome, tandem duplications and lineage-specific gene loss. Our findings suggest that from an ancestral transporter, exhibiting large spectrum and high affinity binding, highly specific Cbl transporters emerged through gene duplication and mutations at the binding pocket.

| S-EPMC4350170 | biostudies-literature

Plasma Vitamin B12 Levels, High-Dose Vitamin B12 Treatment, and Risk of Dementia.

Project description:BackgroundIt is controversial whether B12 deficiency causes dementia or B12 treatment can prevent dementia.ObjectiveTo assess associations between low plasma (P-)B12 levels, B12 treatment, and risk of Alzheimer's disease (AD; primary outcome) and all-cause or vascular dementia (secondary outcomes).MethodsWe conducted a population-based cohort study using Danish registry data to assess associations between low P-B12 levels, high-dose injection or oral B12 treatment, and risk of dementia (study period 2000-2013). The primary P-B12 cohort included patients with a first-time P-B12 measurement whose subsequent B12 treatment was recorded. The secondary B12 treatment cohort included patients with a first-time B12 prescription and P-B12 measurement within one year before this prescription. For both cohorts, patients with low P-B12 levels (<200 pmol/L) were propensity score-matched 1:1 with patients with normal levels (200-600 pmol/L). We used multivariable Cox regression to compute 0-15-year hazard ratios for dementia.ResultsFor low P-B12 and normal P-B12 level groups, we included 53,089 patients in the primary P-B12 cohort and 13,656 patients in the secondary B12 treatment cohort. In the P-B12 cohort, hazard ratios for AD centered around one, regardless of follow-up period or treatment during follow-up. In the B12 treatment cohort, risk of AD was unaffected by low pre-treatment P-B12 levels, follow-up period and type of B12 treatment. Findings were similar for all-cause and vascular dementia.ConclusionWe found no associatio1n between low P-B12 levels and dementia. Associations were unaffected by B12 treatment. Results do not support routine screening for B12 deficiency in patients with suspected dementia.

| S-EPMC7990402 | biostudies-literature

Vitamin B12 is neuroprotective in experimental pneumococcal meningitis through modulation of hippocampal DNA methylation.

Project description:Bacterial meningitis (BM) causes apoptotic damage to the hippocampus and homocysteine (Hcy) accumulation to neurotoxic levels in the cerebrospinal fluid of children. The Hcy pathway controls bioavailability of methyl, and its homeostasis can be modulated by vitamin B12, a cofactor of the methionine synthase enzyme. Herein, the neuroprotective potential and the underlying mode of action of vitamin B12 adjuvant therapy were assessed in an infant rat model of BM. Eleven-day old rats were intracysternally infected with Streptococcus pneumoniae serotype 3, or saline, treated with B12 or placebo, and, 24?h after infection, their hippocampi were analyzed for apoptosis in the dentate gyrus, sulfur amino acids content, global DNA methylation, transcription, and proximal promoter methylation of candidate genes. Differences between groups were compared using 2-way ANOVA followed by Bonferroni post hoc test. Correlations were tested with Spearman's test. B12 attenuated BM-induced hippocampal apoptosis in a Hcy-dependent manner (r =?0.80, P <?0.05). BM caused global DNA hypomethylation; however, B12 restored this parameter. Accordingly, B12 increased the methylation capacity of hippocampal cells from infected animals, as inferred from the ratio S-adenosylmethionine (SAM):S-adenosylhomocysteine (SAH) in infected animals. BM upregulated selected pro-inflammatory genes, and this effect was counteracted by B12, which also increased methylation of CpGs at the promoter of Ccl3 of infected animals. Hcy is likely to play a central role in hippocampal damage in the infant rat model of BM, and B12 shows an anti-inflammatory and neuroprotective action through methyl-dependent epigenetic mechanisms.

| S-EPMC7115084 | biostudies-literature

Cobalamin (Vitamin B12) Induced a Shift in Microbial Composition and Metabolic Activity in an in vitro Colon Simulation.

Project description:Cobalamin deficiency is believed to be related to disturbances in cell division, neuropathy, nervous system disease and pernicious anemia. Elderly people are usually advised to supplement their diets with cobalamin. As cobalamin has several forms, the effects of different forms of cobalamin on gut microbiota were investigated in this study. After 7 days of supplementation, methylcobalamin had reduced the diversity of gut microbiota compared to that in the control and cyanocobalamin groups. After supplementation with methylcobalamin, the percentage of Acinetobacter spp. had increased to 45.54%, while the percentages of Bacteroides spp., Enterobacteriaceae spp. and Ruminococcaceae spp. had declined to 11.15, 9.34, and 2.69%, respectively. However, cyanocobalamin had different influences on these bacteria. Both cobalamins increased the amount of short-chain fatty acids, particularly butyrate and propionic acid. The cyanocobalamin group showed increased activity of cellulase compared with that in the other two groups. According to CCA and PICRUSt analysis, methylcobalamin had a positive correlation with Pseudomonas bacteria, propionic acid, and butyrate. Methylcobalamin promoted lipid, terpenoid, and polyketide metabolism by gut bacteria, promoted the degradation of exogenous substances, and inhibited the synthesis of transcription factors and secondary metabolites. Our results indicate that the various forms of cobalamin in the food industry should be monitored and regulated, because the two types of cobalamin had different effects on the gut microbiome and on microbial metabolism, although they have equal bio-activity in humans. Given the effects of methylcobalamin on gut microbiota and microbial metabolism, methylcobalamin supplementation should be suggested as the first option.

| S-EPMC6250798 | biostudies-literature

Vitamin B12 Deficiency Is Prevalent Among Czech Vegans Who Do Not Use Vitamin B12 Supplements.

Project description:As not much is known about the prevalence and predictors of nutritional deficiencies among vegans in the Czech Republic, we evaluated whether supplement use and duration of adherence to the vegan diet are associated with the risk of cobalamin and iron deficiencies. Associations between self-reported supplementation and duration of vegan diet with biomarkers of cobalamin (serum cobalamin, holotranscobalamin, homocysteine, folate) and iron status (serum ferritin, iron binding capacity, transferrin and saturation of transferrin) were assessed by cross-sectional analyses of medical data from a clinical nutrition center. Data from 151 (72 females) adult vegans (age 18-67 years), who were free of major chronic diseases and 85 (40 females) healthy non-vegans (age 21-47 years) were analyzed. Overall, vegans had significantly lower cobalamin, hemoglobin and ferritin levels, but higher folate and MCV values compared to non-vegans. Vegans not using cobalamin supplements were at higher risk of low plasma cobalamin than regularly supplementing vegans (OR: 4.41, 95% CI 1.2-16.16 for cobalamin, OR: 19.18, 95% CI 1.02-359.42 for holotranscobalamin), whereas no significant differences in cobalamin status related to duration of the vegan diet were observed. Regularly supplementing vegans had similar levels of cobalamin/holotranscobalamin as non-vegans. Despite lower ferritin and hemoglobin levels, there was no indication of a higher risk of iron-deficiency among vegans. To conclude cobalamin deficiency risk depends on supplementation status and not on the duration of an exclusive vegan diet, which underlines the need to integrate cobalamin status monitoring and counselling on supplement use in routine clinical care in the Czech Republic.

| S-EPMC6950550 | biostudies-literature

Clinical relevance of vitamin B12 level and vitamin B12 metabolic gene variation in pulmonary tuberculosis.

Project description:The aim of this study was to assess the association of vitamin B12 level and single nucleotide polymorphisms (SNPs) in vitamin B12 metabolic genes with pulmonary tuberculosis (PTB) in Chinese Han population. The plasma vitamin B12 expression level was detected using ELISA. Ten SNPs in six key genes (TCN1, TCN2, CUBN, MMACHC, FUT6, and MUT) of vitamin B12 metabolic pathway were included for genotyping by the SNPscan technique among 454 PTB patients and 467 controls. Our results found that vitamin B12 level was significantly reduced in PTB patients when compared with controls. There was no significant association between TCN1 rs526934, TCN2 rs1801198, CUBN rs7906242, rs10904861, rs1801222, MMACHC rs10789465, FUT6 rs3760776, rs3760775, MUT rs9473555, rs9381784 variants, and PTB susceptibility. TCN2 rs1801198 CC genotype, C allele was significantly associated with hypoproteinemia in PTB patients. In CUBN, rs7906242 GG genotype, G allele, rs10904861 TT genotype, and T allele were significantly related to the decreased frequency of sputum smear-positive, and rs10904861 variant affected the occurrence of drug resistance in PTB patients. In addition, the increased frequency of CUBN rs1801222 AA genotype was significantly associated with leukopenia. The decreased frequency of MUT rs9473555 CC genotype was found in the PTB patients with hypoproteinemia. However, vitamin B12 expression was not associated with the genotype distribution of above SNPs. In conclusion, vitamin B12 level was significantly decreased in PTB patients and genetic variants in vitamin B12 metabolic genes were not contributed to PTB susceptibility. Several SNPs in TCN2, CUBN, and MUT gene might associate with multiple clinical manifestations in PTB.

| S-EPMC9583150 | biostudies-literature

Transcobalamin deficiency: vitamin B12 deficiency with normal serum B12 levels.

Project description:Transcobalamin (TC) deficiency is a rare autosomal recessive inborn error of cobalamin transport which clinically manifests in early infancy. We describe a child with TC deficiency who presented with classical clinical and lab stigmata of inborn error of vitamin B12 metabolism except normal serum B12 levels. He was started on empirical parenteral cobalamin supplements at 2 months of age; however, the definitive diagnosis could only be established at 6 years of age when a genetic evaluation revealed homozygous nonsense variation in exon 8 of the TCN2 gene (chr22:g.31019043C>T).

| S-EPMC6827761 | biostudies-literature