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Bacterial vitamin B6 is required for post-embryonic development in C. elegans

ABSTRACT: Bacterial vitamin B6 is required for post-embryonic development in C. elegans

PROVIDER: PRJNA1069772 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27747450_1.fastq.gz	Fastqsanger.gz
	SRR27747450_2.fastq.gz	Fastqsanger.gz
	SRR27747451_1.fastq.gz	Fastqsanger.gz
	SRR27747451_2.fastq.gz	Fastqsanger.gz

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Bacterial vitamin B6 is required for post-embryonic development in C. elegans

Project description:Nutritional intake influences animal growth, reproductive capacity, and survival of animals. Under nutrition deficiency, animal developmental arrest occurs as an adaptive strategy to survive. However, the nutritional basis and the underlying nutrient sensing mechanism essential for animal regrowth after developmental arrest remain to be explored. In Caenorhabditis elegans, larvae undergo early developmental arrest are stress resistant, and they require certain nutrients to recover postembryonic development. Here, we investigated the developmental arrest in C. elegans feeding on Lactiplantibacillus plantarum, and the rescue of the diapause state with trace supplementation of Escherichia coli. We performed a genome-wide screen using 3983 individual gene deletion E. coli mutants and identified E. coli genes that are indispensable for C. elegans larval growth on originally not nutritionally sufficient bacteria L. plantarum. Among these crucial genes, we confirmed E. coli pdxH, and the downstream metabolite pyridoxal 5-P (PLP, Vitamin B6) as important nutritional factors for C. elegans postembryonic development. Transcriptome results suggest that bacterial pdxH affects host development by coordinating host metabolic processes and PLP binding. Additionally, the developmental arrest induced by the L. plantarum diet in worm does not depend on the activation of FoxO/DAF-16. Altogether, these results highlight the role of microbial metabolite PLP as a crucial cofactor to restore postembryonic development in C. elegans.

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Vitamin B6 metabolism determines T cell anti-tumor responses

Project description:Targeting T cell metabolism is an established method of immunomodulation. Following activation, T cells engage distinct metabolic programs leading to the uptake and processing of nutrients that determine cell proliferation and differentiation. Redirection of T cell fate by modulation of these metabolic programs has been shown to boost or suppress immune responses in vitro and in vivo. Using publicly available T cell transcriptomic and proteomic datasets we identified vitamin B6-dependent transaminases as key metabolic enzymes driving T cell activation and differentiation. Inhibition of vitamin B6 metabolism using the pyridoxal 5’-phosphate (PLP) inhibitor, aminoxyacetic acid (AOA), suppresses CD8+ T cell proliferation and effector differentiation in a dose-dependent manner. We show that pyridoxal phosphate phosphatase (PDXP), a negative regulator of intracellular vitamin B6 levels, is under the control of the hypoxia-inducible transcription factor (HIF1), a central driver of T cell metabolism. Furthermore, by adoptive transfer of CD8 T cells into a C57BL/6 mouse melanoma model, we demonstrate the requirement for vitamin B6-dependent enzyme activity in mediating effective anti-tumor responses. Our findings show that vitamin B6 metabolism is required for CD8+ T cell proliferation and effector differentiation in vitro and in vivo. Targeting vitamin B6 metabolism may therefore serve as an immunodulatory strategy to improve anti-tumor immunotherapy.

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Vitamin B6 reduces hippocampal apoptosis in experimental pneumococcal meningitis

Project description:Hippocampal apoptosis is a characteristic feature of penumococcal meningitis associated with learning and memory deficitis as a sequel of the disease. We investigated the effect of vitamin B6 using an established infant rat model of experimental pneumococcal meningitis by histomorphology, transcriptomics and measurement of cellular nicotine amide adenine dinucleotide content. The data provides evidence that vitamin B6 is neuroprotecitve in terms of reduced hippocampal apoptosis involving reduction of the inflammatory response, preservation of cellular energy stores and up-regulated brain-derived neurotrophic factor levels.

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Effect of dietary vitamin B6 on white adipose tissue

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Project description:Vitamin B6 metabolism determines T cell anti-tumor responses

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Project description:Vitamin B6 supplementation with 10 mg/d pyridoxine-HCl for 28-d was given to oral contraceptive (OC) users who initially had vitamin B6 deficiency (PLP < 30 nmol/L). Samples are analyzed before and after supplementation. In addition samples from OC users with low (PLP < 30 nmol/L) , middle (PLP 31-99 nmol/L) and high (PLP > 100 nmol/L) vitamin B6 concentration are compared.

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