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Expression data from WT Col-0 and the pdx1.3 ko mutant of Arabidopsis

ABSTRACT: We performed a microarray experiment to assess the global changes in transcription occurring in leaves and roots of the vitamin B6 deficient pdx1.3 knockout mutant in comparison to WT. Vitamin B6 (pyridoxal 5′-phosphate) is an essential cofactor of many metabolic enzymes. Plants biosynthesize the vitamin de novo employing two enzymes, pyridoxine synthase1 (PDX1) and PDX2. In Arabidopsis (Arabidopsis thaliana), there are two catalytically active paralogs of PDX1 (PDX1.1 and PDX1.3) producing the vitamin at comparable rates. Since single mutants are viable but the pdx1.1 pdx1.3 double mutant is lethal, the corresponding enzymes seem redundant. However, the single mutants exhibit substantial phenotypic differences, particularly at the level of root development, with pdx1.3 being more impaired than pdx1.1. Here, we investigate the impact of possible global changes in gene expression in the pdx1.3 mutant compared to WT on the phenotype.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE71312 | GEO | 2015/07/25

SECONDARY ACCESSION(S): PRJNA290882

REPOSITORIES: GEO

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Expression data from WT Col-0 and the pdx1.3 ko mutant of Arabidopsis

Project description:We performed a microarray experiment to assess the global changes in transcription occurring in leaves and roots of the vitamin B6 deficient pdx1.3 knockout mutant in comparison to WT. Vitamin B6 (pyridoxal 5′-phosphate) is an essential cofactor of many metabolic enzymes. Plants biosynthesize the vitamin de novo employing two enzymes, pyridoxine synthase1 (PDX1) and PDX2. In Arabidopsis (Arabidopsis thaliana), there are two catalytically active paralogs of PDX1 (PDX1.1 and PDX1.3) producing the vitamin at comparable rates. Since single mutants are viable but the pdx1.1 pdx1.3 double mutant is lethal, the corresponding enzymes seem redundant. However, the single mutants exhibit substantial phenotypic differences, particularly at the level of root development, with pdx1.3 being more impaired than pdx1.1. Here, we investigate the impact of possible global changes in gene expression in the pdx1.3 mutant compared to WT on the phenotype. Four different types of samples (conditions) were analyzed, namely pdx1.3 leaves, pdx1.3 roots, WT leaves and WT roots with three biological replicates per condition (12 samples altogether). WT samples served as reference (control) for the respective pdx1.3 samples.

2015-07-25 | E-GEOD-71312 | biostudies-arrayexpress

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.

2021-08-31 | GSE182999 | GEO

Customizing functionalized cofactor mimics to study the human pyridoxal 5'-phosphate-binding proteome

Project description:Here we apply functionalized cofactor derivatives to study vitamin B6-dependent enzymes in human cells. We are able to cover for a large fraction of the pyridoxal 5'-phosphate-binding proteome (PLP-ome) and validate our results exemplarily for two PLP-DEs. One of those, named pyridoxal 5'-phosphate binding protein (PLPBP) is characterized further including studies with chemical cross-linking combined with mass spectrometry. We proceed with an in situ PLP-DE target screen applying B6-targeting compounds revealing interesting insights into selectivity. Finally, we broaden our analysis to multiple human cell lines revealing an altered PLP-DE target profile.

2019-08-27 | PXD014771 | Pride

Evidence that COG0325 proteins are involved in PLP homeostasis

Project description:Pyridoxal 5'-phosphate (PLP) is an essential cofactor for nearly 60 Escherichia coli enzymes but is a highly reactive molecule that is toxic in its free form. How PLP levels are regulated and how PLP is delivered to target enzymes are still open questions. The COG0325 protein family belongs to the fold-type III class of PLP enzymes and binds PLP but has no known biochemical activity although it occurs in all kingdoms of life. Various pleiotropic phenotypes of the E. coli COG0325 (yggS) mutant have been reported, some of which were reproduced and extended in this study. Comparative genomic, genetic and metabolic analyses suggest that these phenotypes reflect an imbalance in PLP homeostasis. The E. coli yggS mutant accumulates the PLP precursor pyridoxine 5'-phosphate (PNP) and is sensitive to an excess of pyridoxine but not of pyridoxal. The pyridoxine toxicity phenotype is complemented by the expression of eukaryotic yggS orthologs. It is also suppressed by the presence of amino acids, specifically isoleucine, threonine and leucine, suggesting the PLP-dependent enzyme transaminase B (IlvE) is affected. These genetic results lay a foundation for future biochemical studies of the role of COG0325 proteins in PLP homeostasis.

2017-09-14 | ST000884 | MetabolomicsWorkbench

Pyridoxine in Preventing Hand-Foot Syndrome in Patients Who Are Receiving Capecitabine for Advanced Colorectal Cancer or Breast Cancer

Project description:RATIONALE: Pyridoxine (vitamin B6) may prevent or lessen hand-foot syndrome caused by chemotherapy. It is not yet known whether pyridoxine is more effective than a placebo in preventing hand-foot syndrome. PURPOSE: This phase III randomized trial is studying pyridoxine to see how well it works compared to a placebo in preventing hand-foot syndrome in patients who are receiving capecitabine for advanced colorectal cancer or breast cancer.

| 2046490 | ecrin-mdr-crc

Evidence that the metabolite repair enzyme NAD(P)HX epimerase has a moonlighting function

Project description:NAD(P)H-hydrate epimerase (EC 5.1.99.6) is known to help repair NAD(P)H hydrates (NAD(P)HX), which are damage products existing as R and S epimers. The S epimer is reconverted to NAD(P)H by a dehydratase; the epimerase facilitates epimer interconversion. Epimerase deficiency in humans causes a lethal disorder attributed to NADHX accumulation. However, bioinformatic evidence suggests caution about this attribution by predicting that the epimerase has a second function connected to vitamin B6 (pyridoxal 5'-phosphate and related compounds). Specifically, (i) the epimerase is fused to a B6 salvage enzyme in plants, (ii) epimerase genes cluster on the chromosome with B6-related genes in bacteria, and (iii) epimerase and B6-related genes are coexpressed in yeast and Arabidopsis. The predicted second function was explored in Escherichia coli, whose epimerase and dehydratase are fused and encoded by the yjeF gene. The putative NAD(P)HX epimerase active site has a conserved lysine residue (K192 in E. coli YjeF). Changing this residue to alanine cut in-vitro epimerase activity by ≥95% but did not affect dehydratase activity. Mutant cells carrying the K192A mutation had essentially normal NAD(P)HX levels, showing that the mutation had very little or no effect on NAD(P)HX repair in vivo. However, these cells showed metabolome changes, particularly in amino acids, that exceeded those in cells lacking the entire yjeF gene. The K192A mutant cells also had lower levels of free pyridoxal 5'-phosphate than wild-type cells. These results provide strong circumstantial evidence that the epimerase has a metabolic function beyond NAD(P)HX repair and that this function involves vitamin B6.

2017-11-14 | ST000900 | MetabolomicsWorkbench

Vitamin B6 Effects on one-carbon metabolism

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.

2015-03-13 | ST000293 | MetabolomicsWorkbench

Transcription profiling of liver from wild type, Rev knock out and Rev-erb-alpha transcgenic mice to identify target genes of PAR bZip

Project description:Found PAR bZip target genes. The loss of circadian PAR bZip transcription factors results in epilepsy, DBP (albumin D-site-binding protein), HLF (hepatic leukemia factor), and TEF (thyrotroph embryonic factor) are the three members of the PAR bZip (proline and acidic amino acid-rich basic leucine zipper) transcription factor family. All three of these transcriptional regulatory proteins accumulate with robust circadian rhythms in tissues with high amplitudes of clock gene expression, such as the suprachiasmatic nucleus (SCN) and the liver. However, they are expressed at nearly invariable levels in most brain regions, in which clock gene expression only cycles with low amplitude. Here we show that mice deficient for all three PAR bZip proteins are highly susceptible to generalized spontaneous and audiogenic epilepsies that frequently are lethal. Transcriptome profiling revealed pyridoxal kinase (Pdxk) as a target gene of PAR bZip proteins in both liver and brain. Pyridoxal kinase converts vitamin B6 derivatives into pyridoxal phosphate (PLP), the coenzyme of many enzymes involved in amino acid and neurotransmitter metabolism. PAR bZip-deficient mice show decreased brain levels of PLP, serotonin, and dopamine, and such changes have previously been reported to cause epilepsies in other systems. Hence, the expression of some clock-controlled genes, such as Pdxk, may have to remain within narrow limits in the brain. This could explain why the circadian oscillator has evolved to generate only low-amplitude cycles in most brain regions.; find REV-ERB ALPHA target genes

2010-06-22 | E-TABM-726 | biostudies-arrayexpress

Effect of dietary vitamin B6 on white adipose tissue

Project description:Transcriptional profiling of mouse white adipose tissues The objective of this study is to explore the relationship between vitamin B6 activity and chronic inflammation of white adipose tissue in mice fed a high-fat diet. Twenty-four CD-1 mice were divided into two groups (n = 12) and fed either a 1 mg pyridoxine (PN) HCl /kg diet or a 35 mg PN HCl /kg diet for 8 weeks. We isolated total RNA from epididymal white adipose tissue of each group and compared gene expression profiles by DNA microarray data analysis. Noriyuki Yanaka

2013-01-12 | E-GEOD-43465 | biostudies-arrayexpress

Effect of dietary vitamin B6 on white adipose tissue

2013-01-12 | GSE43465 | GEO

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