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C. elegans methionine/S-adenosylmethionine cycle activity is sensed and adjusted by a nuclear hormone receptor: RNA-seq dataset 2

ABSTRACT: Vitamin B12 is an essential micronutrient that functions in two metabolic pathways: the canonical propionate breakdown pathway and the methionine/S-adenosylmethionine (Met/SAM) cycle. In Caenorhabditis elegans, low vitamin B12, or genetic perturbation of the canonical propionate breakdown pathway results in propionate accumulation and the transcriptional activation of a propionate shunt pathway. This propionate-dependent mechanism requires nhr-10 and is referred to as “B12-mechanism-I”. Here, we report that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanism we refer to as “B12-mechanism-II”. This mechanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin B12. B12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transporter, pmp-5, and adjust influx and efflux of the cycle by activating msra-1 and repressing cbs-1, respectively. Taken together, Met/SAM cycle activity is sensed and transcriptionally adjusted to be in a tight metabolic regime.

ORGANISM(S): Caenorhabditis elegans

PROVIDER: GSE151847 | GEO | 2020/06/05

REPOSITORIES: GEO

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C. elegans methionine/S-adenosylmethionine cycle activity is sensed and adjusted by a nuclear hormone receptor: RNA-seq dataset 1

Project description:Vitamin B12 is an essential micronutrient that functions in two metabolic pathways: the canonical propionate breakdown pathway and the methionine/S-adenosylmethionine (Met/SAM) cycle. In Caenorhabditis elegans, low vitamin B12, or genetic perturbation of the canonical propionate breakdown pathway results in propionate accumulation and the transcriptional activation of a propionate shunt pathway. This propionate-dependent mechanism requires nhr-10 and is referred to as “B12-mechanism-I”. Here, we report that vitamin B12 represses the expression of Met/SAM cycle genes by a propionate-independent mechanism we refer to as “B12-mechanism-II”. This mechanism is activated by perturbations in the Met/SAM cycle, genetically or due to low dietary vitamin B12. B12-mechanism-II requires nhr-114 to activate Met/SAM cycle gene expression, the vitamin B12 transporter, pmp-5, and adjust influx and efflux of the cycle by activating msra-1 and repressing cbs-1, respectively. Taken together, Met/SAM cycle activity is sensed and transcriptionally adjusted to be in a tight metabolic regime.

2020-06-05 | GSE151846 | GEO

A Persistence Detector for Metabolic Network Rewiring in an Animal

Project description:Biological systems must possess mechanisms that prevent inappropriate responses to spurious environmental inputs. Caenorhabditis elegans has two breakdown pathways for the short-chain fatty acid propionate: a canonical, vitamin B12-dependent pathway and a propionate-shunt that is used when vitamin B12 levels are low. The shunt pathway is kept off when there is sufficient flux through the canonical pathway, likely to avoid generating shunt-specific toxic intermediates. Here, we discover a transcriptional regulatory circuit that activates shunt gene expression upon propionate buildup. The nuclear hormone receptors NHR-10 and NHR-68 function together as a ‘persistence detector’ in a type 1, coherent feed-forward loop with an AND-logic gate to delay shunt activation upon propionate accumulation, and to avoid spurious shunt activation in response to a non-sustained pulse of propionate. Together, our findings identify the first persistence detector in an animal, which transcriptionally rewires propionate metabolism to maintain homeostasis.

2018-12-08 | GSE123507 | GEO

Transcriptomic changes associated with growth of Mycobacterium tuberculosis H37Rv wild-type strain and ∆prpR mutant in mineral medium supplemented with cholesterol as the sole carbon source or standard medium supplemented with vitamin B12.

Project description:RNA-Seq results accompanying submission of a manuscript: "Cholesterol-dependent transcriptome remodeling reveals new insight into the contribution of cholesterol to Mycobacterium tuberculosis pathogenesis" describing the role of cholesterol and vitamin B12 in shaping the transcriptome of the Mycobacterium tuberculosis H37Rv and M. tuberculosis ∆prpR - propionate regulator (PrpR) mutant. Next generation sequencing results are provided in three independent biological replicates for each strain growing in three different media - minimal medium with glycerol or cholesterol as the sole carbon source and standard 7H9/10% OADC medium. The influence of vitamin B12 on M. tuberculosis transcriptome was analysed on 7H9/10% OADC medium supplemented with B12. The study allowed us to re-establish the list of genes potentially involved in cholesterol metabolism. We further proposed a novel regulatory function of vitamin B12 and PrpR, a propionate regulator, in coordinated cholesterol breakdown metabolite dissipation and virulent phenotype induction. Finally, we demonstrated that a key role of cholesterol in Mtb metabolism is not only providing carbon and energy but also inducing a transcriptome remodeling program that helps in developing tolerance to the unfavorable host cell environment.

2021-05-31 | GSE175812 | GEO

Metabolic rescue of α-synuclein-induced neurodegeneration through propionate supplementation and intestine-neuron signaling in C. elegans

Project description:Vitamin B12 depletion or propionate supplementation can reverse the transcriptomic aberration in the C. elegans model of PD with neuronal overexpression of alpha-synuclein A53T

2023-04-28 | GSE230786 | GEO

Effect of depletion of NHR-114/HNF4, and maternal B12 treatment on gene expression of C. elegans in Larva 4 stage.

Project description:Vitamin B12 (B12) deficiency is a critical problem worldwide. Such deficiency in infants has long been known to increase the propensity to develop obesity and diabetes later in life through unclear mechanisms. Here, we establish a ∆nhr-114 animal as a Caenorhabditis elegans model to study how early-life B12 impacts adult health. We find that early-life B12 deficiency causes increased lipogenesis and lipid peroxidation in adult worms, which in turn induces germline defects through ferroptosis. In order to further identify genes that respond to early-life B12, we carried out an RNA sequencing (RNA-seq) assay to analyze the gene expression profiles of WT and ∆nhr-114 animals maternally supplied with 8 μM B12 or not.

2022-09-20 | GSE211747 | GEO

Propionate stimulates MUC2 expression through metabolism of β-oxidation-like pathway that boosts mitochondrial respiration and resultant induction of HIF-2α activation

Project description:Microbiota-derived short chain fatty acids (SCFAs) are one of the hottest issues for its various bioactivities in the gut, immune system extending to brain or other organs through several axises. Though many intensive studies have been implementing til recent, some parts among a plenty of actions occurred in the gut solely are unrevealed so as their mechanism. Propionate, one of the representative SCFAs with butyrate is basically known for its inhibiting activity of histone deacetylation (HDAC) and stimulation of mucin expression in mucosae. However, the mechanism of the stimulating action needs to be elucidated in more detail and understandable way. Here, we firstly investigated the effect of propionate on expression of MUC2, one of the main subtype mucin, in goblet cell line LS 174T and suggest a mechanism of the action along the order of events, linked to metabolic shift. Propionate at the concentration of 1 mM to 4 mM induced the expression of MUC2 gradually in the transcriptional- and protein level at 24 h. At the initial parts of treatment of propionate, the odd SCFA was metabolized along vitamin B12-independent β-oxidation-like pathway and the metabolism led cells to boost mitochondrial respiration until 18 h after treatment. However, another possible metabolism pathway, vitamin B12-dependent carboxylation pathway was not involved to the resulted action. At the latter parts, the master regulator of hypoxia, Hypoxia-induced factors (HIFs) were fluctuated respectively and among them, activated HIF-2α was identified to regulate the expression level of MUC2. In summary, propionate might induce β-oxidation-like pathway at the initial part so that mitochondrial respiration is upregulated. In an effort of LS 174T to adapt to naturally formed hypoxia by response to propionate, each activity of HIF subtypes was regulated in a way of entangled to each other and activated HIF-2α stimulated MUC2 expression.

2024-04-08 | GSE157016 | GEO

Effects of vitamin B12 on the gene expression of PAO1 under anaerobic growth conditions

Project description:Pseudomonas aeruginosa undergoes cell elongation and forms robust biofilms during anaerobic respiratory growth using nitrate (NO3-) as an alternative electron acceptor. Understanding the mechanism of cell shape change induced upon anaerobiosis is crucial to the development of effective treatments against P. aeruginosa biofilm infection. Anaerobic growth of PAO1 reached higher cell density in the presence of vitamin B12, an essential coenzyme of class II ribonucleotide reductase. In addition, cell morphology returned to a normal rod shape. These results suggest that vitamin B12, the production of which was suppressed during anaerobic growth, can restore cellular machineries for DNA replication and therefore facilitate better anaerobic growth of P. aeruginosa with normal cell division. We used microarray to elucidate the global gene expression profiles underlying vitamin B12-induced changes in bacterial cell shape and growth-associated properties. Gene expression profiles of PAO1 grown in LBN (LB+NO3-) or LBN supplemented with 1 microM vitamin B12 are compared.

2012-06-17 | E-GEOD-34836 | biostudies-arrayexpress

Mycobacterium smegmatis secreting methionine sulfoxide reductase A (MsrA) modulates cellular processes in mouse macrophages

Project description:Methionine sulfoxide reductase A (MsrA) is an antioxidant repair enzyme that reduces the oxidized methionine (Met-O) in proteins to methionine (Met). It plays a pivotal role in the cellular processes has been well established by overexpressing, silencing and knocking down of MsrA or by deleting the gene encoding MsrA in several species. We are specifically interested in understanding the role of secreted MsrA of bacterial pathogens. To elucidate this, we infected mouse bone marrow derived macrophages (BMDMs) with recombinant Mycobacterium smegmatis strain (MSM) secreting a bacterial MsrA or M. smegmatis strain (MSC) carrying only the control vector. BMDMs infected with MSM induced higher levels of ROS and TNF-α than BMDMs infected with MSC. The increased ROS and TNF-α in BMDMs infected with MSM correlated with elevated necrotic cell death. Further, RNA-Seq transcriptome analysis of BMDMs infected with MSC and MSM revealed differential expression of protein and RNA coding genes, suggesting that bacterial delivered MsrA could modulate the host cellular processes. Finally, KEGG pathway enrichment analysis identified down-regulation of cancer related signaling genes in MSM infected cells, indicating that MsrA has the potential to regulate the development and progression of cancer.

2023-08-28 | GSE212228 | GEO

Effects of vitamin B12 on the gene expression of PAO1 under anaerobic growth conditions

2012-06-18 | GSE34836 | GEO

Mutations of the selected strain growing in low levels of Vitamin B12 in Mycobacterium marinum

Project description:Vitamin B12 (B12) is an important cofactor in mycobacterial metabolism, and some pathogenic mycobacteria need to obtain it from the host. In this study, we investigated the transport of vitamin B12 in Mycobacterium marinum. We identified a transcriptor regulator that could be potentially involved in the uptake process. RNA sequencing analysis were performed in order to elucidate the regulon of this new transcriptor.

2023-08-14 | GSE240448 | GEO

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