Ontology highlight
ABSTRACT:
PROVIDER: PRJNA577012 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR10273168_1.fastq.gz | Fastqsanger.gz | |||
| SRR10273168_2.fastq.gz | Fastqsanger.gz | |||
| SRR10273169_1.fastq.gz | Fastqsanger.gz | |||
| SRR10273169_2.fastq.gz | Fastqsanger.gz | |||
| SRR10273170.fastq.gz | Fastqsanger.gz |
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Project description:Propiogenic substrate catabolism and gut bacteria produce propionate, a post-translational protein modifier. Here, using a mouse model of propionic acidaemia (PA), we characterise how disturbances to propionate metabolism modify histones and affect cardiac gene expression and function. Plasma propionate was raised in PA mice, but male hearts accumulated a smaller propionyl-CoA excess, correlating with -alanine build-up. Raising -alanine experimentally in myocytes cultured under propionate-stress reduced propionyl-CoA and partially reversed the propionate-evoked metabolic disturbance. Female PA hearts manifested a moderate diastolic dysfunction phenotype, with raised diastolic [Ca2+], expanded end-systolic ventricular volume, and reduced stroke volume. Differentially-expressed genes included Pde9a and Mme that relate to contractile dysfunction through down-scaled cGMP signalling, consistent with phosphoproteome changes. Propionate was traced to histone H3 propionylation and increased acetylation genome-wide, including at Pde9a and Mme promoters, with more pronounced effects in female PA hearts. We link perturbed propionate metabolism to epigenetic changes that impact cardiac function.
2023-09-28 | GSE205837 | GEO
Project description:Propiogenic substrate catabolism and gut bacteria produce propionate, a post-translational protein modifier. Here, using a mouse model of propionic acidaemia (PA), we characterise how disturbances to propionate metabolism modify histones and affect cardiac gene expression and function. Plasma propionate was raised in PA mice, but male hearts accumulated a smaller propionyl-CoA excess, correlating with -alanine build-up. Raising -alanine experimentally in myocytes cultured under propionate-stress reduced propionyl-CoA and partially reversed the propionate-evoked metabolic disturbance. Female PA hearts manifested a moderate diastolic dysfunction phenotype, with raised diastolic [Ca2+], expanded end-systolic ventricular volume, and reduced stroke volume. Differentially-expressed genes included Pde9a and Mme that relate to contractile dysfunction through down-scaled cGMP signalling, consistent with phosphoproteome changes. Propionate was traced to histone H3 propionylation and increased acetylation genome-wide, including at Pde9a and Mme promoters, with more pronounced effects in female PA hearts. We link perturbed propionate metabolism to epigenetic changes that impact cardiac function.
2023-09-28 | GSE205836 | GEO
Project description:Xylanibacter ruminicola is an abundant rumen bacterium that produces propionate in a cobalamin-dependent manner. However, the effect of cobalamin supplementation on the expression of propionate pathway enzymes has yet to be investigated. To assess this, comparative transcriptomics and proteomics was carried out on X. ruminicola KHP1 cultures grown in defined media in the presence and absence of cobalamin. Cobalamin supplementation did not affect expression of most propionate pathway proteins, with the only differentially abundant pathway enzyme being the cobalamin-dependent methylmalonyl-CoA mutase, which showed a minor upregulation in the presence of cobalamin. Our results demonstrate expression of the propionate pathway regardless of cobalamin availability, suggesting that cobalamin-dependent induction of propionate production by X. ruminicola is controlled post-translationally.
2024-10-14 | PXD053273 | Pride
Project description:Propiogenic substrate catabolism and gut bacteria produce propionate, a post-translational protein modifier. Here, using a mouse model of propionic acidaemia (PA), we characterise how disturbances to propionate metabolism modify histones and affect cardiac gene expression and function. Plasma propionate was raised in PA mice, but male hearts accumulated a smaller propionyl-CoA excess, correlating with -alanine build-up. Raising -alanine experimentally in myocytes cultured under propionate-stress reduced propionyl-CoA and partially reversed the propionate-evoked metabolic disturbance. Female PA hearts manifested a moderate diastolic dysfunction phenotype, with raised diastolic [Ca2+], expanded end-systolic ventricular volume, and reduced stroke volume. Differentially-expressed genes included Pde9a and Mme that relate to contractile dysfunction through down-scaled cGMP signalling, consistent with phosphoproteome changes. Propionate was traced to histone H3 propionylation and increased acetylation genome-wide, including at Pde9a and Mme promoters, with more pronounced effects in female PA hearts. We link perturbed propionate metabolism to epigenetic changes that impact cardiac function.
2023-09-28 | GSE205835 | GEO
Project description:Propiogenic substrate catabolism and gut bacteria produce propionate, a post-translational protein modifier. Here, using a mouse model of propionic acidaemia (PA), we characterise how disturbances to propionate metabolism modify histones and affect cardiac gene expression and function. Plasma propionate was raised in PA mice, but male hearts accumulated a smaller propionyl-CoA excess, correlating with -alanine build-up. Raising -alanine experimentally in myocytes cultured under propionate-stress reduced propionyl-CoA and partially reversed the propionate-evoked metabolic disturbance. Female PA hearts manifested a moderate diastolic dysfunction phenotype, with raised diastolic [Ca2+], expanded end-systolic ventricular volume, and reduced stroke volume. Differentially-expressed genes included Pde9a and Mme that relate to contractile dysfunction through down-scaled cGMP signalling, consistent with phosphoproteome changes. Propionate was traced to histone H3 propionylation and increased acetylation genome-wide, including at Pde9a and Mme promoters, with more pronounced effects in female PA hearts. We link perturbed propionate metabolism to epigenetic changes that impact cardiac function.
2023-09-28 | GSE205834 | GEO
Project description:Mycobacterium tuberculosis (Mtb) is evolutionarily equipped to resist exogenous reactive oxygen species but shows vulnerability to an increase in endogenous ROS (eROS). Since eROS is an unavoidable consequence of aerobic metabolism, understanding how Mtb manages eROS levels is essential yet needs to be characterized. By combining the Mrx1-roGFP2 redox biosensor with transposon mutagenesis, we identified 368 genes (redoxosome) responsible for maintaining homeostatic levels of eROS in Mtb. Integrating redoxosome with a global network of transcriptional regulators revealed a hypothetical protein (Rv0158) as a critical node managing eROS in Mtb. Disruption of rv0158 (rv0158 KO) impaired growth, redox balance, respiration, and metabolism of Mtb on glucose but not on fatty acids. Importantly, rv0158 KO exhibited enhanced growth on propionate, and the Rv0158 protein directly binds to methylmalonyl-CoA, a key intermediate in propionate catabolism. Metabolite profiling, ChIP-Seq, and gene-expression analyses indicate that Rv0158 manages metabolic neutralization of propionate toxicity by regulating the methylcitrate cycle. Disruption of rv0158 enhanced the sensitivity of Mtb to oxidative stress, nitric oxide, and anti-TB drugs. Lastly, rv0158 KO showed poor survival in macrophages and persistence defect in mice. Our results suggest that Rv0158 is a metabolic integrator for carbon metabolism and redox balance in Mtb.
2023-09-05 | GSE242285 | GEO
Project description:Propionate is an abundant carboxylic acid in nature. Microorganisms metabolize propionate aerobically via the 2-methylcitrate pathway. This pathway depends on a series of three reactions in the citric acid cycle that leads to the conversion of succinate to oxaloacetate. Interestingly, the gamma-proteobacterium Escherichia coli can use propionate as a carbon and electron source under oxic but not under anoxic conditions. The typical downregulation of the citric acid cycle under anoxic conditions is only partially responsible for the inability to use propionate under anoxic conditions since an arcA mutant shows very limited growth on propionate. RT-PCR and transcriptomic analysis revealed a post-transcriptional regulation of the prp-genecluster encoding the necessary enzymes for propionate metabolism. The polycistronic mRNA was hydrolyzed in the 3`-5` direction under anoxic conditions. This regulatory strategy is highly constructive because the last gene of the operon encodes the first enzyme of the propionate metabolism. Further analysis revealed that RNase R catalyzes the hydrolysis of the prp transcripts. Consequently, an rnr-deletion strain could metabolize propionate under anoxic conditions. To the best of our knowledge, this is the first study describing the influence of RNase R on the anaerobic metabolism of E. coli.
2017-12-14 | GSE78814 | GEO
Project description:Acetate, propionate and butyrate are the main short-chain fatty acids (SCFAs) that arise from the fermentation of fibers by the colonic microbiota. While many studies focus on the regulatory role of SCFAs, their quantitative role as a catabolic or anabolic substrate for the host has received relatively little attention. To investigate this aspect, we infused conscious mice with physiological quantities of stable isotopes [1-13C]acetate, [2-13C]propionate or [2,4-13C2]butyrate directly into the cecum, which is the natural production site in mice, and analyzed their interconversion by the microbiota as well as their metabolism by the host. Cecal interconversion - pointing to microbial cross-feeding - was high between acetate and butyrate, low between butyrate and propionate and almost absent between acetate and propionate. As much as 62% of infused propionate was used in whole-body glucose production, in line with its role as gluconeogenic substrate. Conversely, glucose synthesis from propionate accounted for 69% of total glucose production. The synthesis of palmitate and cholesterol in the liver was high from cecal acetate (2.8% and 0.7%, respectively) and butyrate (2.7% and 0.9%, respectively) as substrates, but low or absent from propionate (0.6% and 0.0%, respectively). Label incorporation due to chain elongation of stearate was approximately 8-fold higher than de novo synthesis of stearate. Microarray data suggested that SCFAs exert only a mild regulatory effect on the expression of genes involved in hepatic metabolic pathways during the 6h infusion period. Altogether, gut-derived acetate, propionate and butyrate play important roles as substrates for glucose, cholesterol and lipid metabolism. Mice were infused in cecum with stably-labelled isotopes of the three main short chain fatty acids or control solution. After 6 hrs, livers were removed and pooled RNA samples were subjected to gene expression profiling.
2013-10-21 | E-GEOD-45926 | biostudies-arrayexpress
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 | GSE151847 | GEO
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