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Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence

ABSTRACT: Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence

PROVIDER: PRJNA657876 | ENA |

REPOSITORIES: ENA

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Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence

Project description:Here, we identified a long-chain acyl-CoA-responsive transcriptional repressor, FdmR, as the key regulator of mycobacterial fatty acid catabolism. We employed ChIP-Seq to identify the genomic binding regions for FdmR. FdmR was found to bind upstream of fadA2, fabG4, fadE24, fixA, MMAR_1683, fadE5, icl, desA3, desA3_1, and MMAR_2730.We then demonstrated that FdmR acts as a valve to direct the fatty acid flux from β-oxidation towards lipid biosynthesis, thereby avoiding the overactive catabolism and accumulation of biologically toxic intermediates. This regulatory mechanism enables a high rate of cell growth with modest consumption of fatty acid substrates.

2021-03-01 | GSE156432 | GEO

Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence.

Project description: Not available

| S-EPMC8072231 | biostudies-literature

Project description:Mycobacterial fatty acid catabolism is repressed by FdmR to sustain lipogenesis and virulence

| PRJNA657493 | ENA

Amino acid catabolism fuels microalgal lipogenesis

Project description:Microalgal lipid, a feasible substrate for biofuel, is typically accumulated during the stationary growth phase. Generating strains which trigger lipogenesis from the exponential growth phase will enhance lipid productivity, reduce cost of biofuel production. We characterized a lipid-rich microalgal mutant, Dunaliella tertiolecta, which exhibited a six-fold enhancement of neutral lipids production in the exponential growth phase with marginal compromise on growth (4%). Using transcriptomics and metabolomics, regulatory mechanisms of the mutant were uncovered.

2016-10-24 | GSE82121 | GEO

Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity

Project description:Background: Lung function is dependent upon the precise regulation of the synthesis, storage, and catabolism of tissue and alveolar lipids. Results: Activation of SREBP (Sterol Response Element Binding Protein) induced lipogenesis in alveolar epithelial cells, causing neutral lipid accumulation, lung inflammation, and tissue remodeling. Conclusions: The accumulation of neutral lipids in type II epithelial cells and alveolar macrophages caused lung inflammation, consistent with findings in lipid storage disorders. Significance: Pulmonary lipotoxicity may contribute to the pathogenesis of lung dysfunction associated with diabetes, obesity, and other metabolic disorders. Genome-wide transcription profiling comparison between doxycycline-exposed SFTPC-rtTAWT/Tg/(tetO)7CMV-CreWT/Tg/Insig1flox/flox/Insig2-/- mice (i.e., Insig1/2∆/∆ ) and Insig1flox/flox/Insig2-/- . Three independent pooled RNA from isolated lung type 2 cells of each genotype were used.

2012-03-01 | E-GEOD-31797 | biostudies-arrayexpress

Activation of SREBP in Alveolar Type II Cells Enhances Lipogenesis Causing Pulmonary Lipotoxicity

2012-03-01 | GSE31797 | GEO

Mycobacterial communities in pulmonary NTM

Project description:Profiling Mycobacterial Communities in Pulmonary Nontuberculous Mycobacterial Disease

| PRJEB22153 | ENA

Intestinal FGF15/19 physiologically represses hepatic lipogenesis in the late fed-state by activating SHP and DNMT3A

Project description:Hepatic lipogenesis is normally tightly regulated but is aberrantly elevated in obesity. Fibroblast Growth Factor-19 (FGF19, mouse FGF15) is a late fed-state gut hormone that decreases hepatic lipid levels by unclear mechanisms. We examined whether FGF15/19 and FGF15/19-activated Small Heterodimer Partner (SHP/NR0B2) have a role in transcriptional repression of lipogenesis. Comparative genomic analyses reveal that most of the SHP cistrome, including lipogenic genes repressed by FGF19, have overlapping CpG islands. FGF19 treatment or SHP overexpression in mice inhibits lipogenesis in a DNA methyltransferase-3a (DNMT3A)-dependent manner. FGF19-mediated activation of SHP via phosphorylation recruits DNMT3A to lipogenic genes, leading to DNA methylation and gene repression. In non-alcoholic fatty liver disease (NAFLD) patients and obese mice, occupancy of SHP and DNMT3A and DNA methylation at lipogenic genes are low, with elevated gene expression. These results demonstrate that FGF15/19 represses hepatic lipogenesis by activating SHP and DNMT3A physiologically, which is likely dysregulated in NAFLD.

2020-09-23 | GSE158359 | GEO

Dunaliella tertiolecta UTEX 'LB 999'

Project description:Amino acid catabolism fuels microalgal lipogenesis

| PRJNA324164 | ENA

Sensing of mycobacterial arabinogalactan by galectin-9 exacerbates mycobacterial infection by inducing matrix metalloproteinases

Project description:Mycobacterial arabinogalactan (AG) is an essential cell wall component of Mycobacteria and a frequent structural and bio-synthetical target for anti-tuberculosis (TB) drug development. Yet, it is unclear whether mycobacterial AG is a pathogen-associated molecular pattern (PAMP) with an elusive pattern recognition receptor (PRR). Here, we report that mycobacterial AG is recognized by galectin-9 and exacerbates mycobacterial infection. Administration of AG-specific aptamers inhibited cellular infiltration caused by Mycobacterium tuberculosis (Mtb) or Mycobacterium bovis BCG, and moderately increased survival of Mtb-infected mice or Mycobacterium marinum-infected zebrafish. AG interacted with carbohydrate recognition domain (CRD) 2 of galectin-9 with high affinity, and galectin-9 associated with transforming growth factor β-activated kinase 1 (TAK1) via CRD2 to trigger subsequent activation of extracellular signal-regulated kinase (ERK) as well as induction of the expression of matrix metalloproteinases (MMPs). Moreover, deletion of galectin-9 or inhibition of MMPs blocked AG-induced pathological impairments in the lung, and the AG-galectin-9 axis aggravated the process of Mtb infection in mice. These results demonstrate that AG is an important virulence factor of mycobacteria and galectin-9 is a novel receptor for Mtb and other mycobacteria, paving the way for the development of novel effective TB immune modulators.

2021-02-17 | GSE166850 | GEO

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