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TFAM binding analysis at mitochondrial genome between Wild Type (Wt) and Actb-/- (KNO) Mouse Embryonic Fibroblast

ABSTRACT: Using Chromatin-immunoprecipitation and NGS, we investigated the binding of TFAM protein at mitochondrial genome between Actb+/+ Wild Type (WT) and Actb-/- (KO) Mouse Embryonic Fibroblast

ORGANISM(S): Mus musculus

PROVIDER: GSE109532 | GEO | 2018/01/24

REPOSITORIES: GEO

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TFAM binding analysis at mitochondrial genome between Wild Type (Wt) and Actb-/- (KNO) Mouse Embryonic Fibroblast

Project description:TFAM binding analysis at mitochondrial genome between Wild Type (Wt) and Actb-/- (KNO) Mouse Embryonic Fibroblast

| PRJNA431307 | ENA

Genome-wide maps of H3K9Me3, H3K27Me and Brg1 distribution between Wild Type (Wt) and Actb-/- (KNO) Mouse Embryonic Fibroblast

Project description:Using Chromatin-immunoprecipitation and NGS, we profiled the genome-wdie H3K9Me3, H3K27Me and Brg1 distribution between Wild Type (Wt) and Actb-/- (KNO) Mouse Embryonic Fibroblast

2017-07-01 | GSE100096 | GEO

Impaired TFAM expression promotes mitochondrial damage to drive fibroblast activation and fibrosis in systemic sclerosis

Project description:Objectives: The transcription factor TFAM is controlling the transcription of core proteins required for mitochondrial homeostasis. The aim of the current study was to investigate changes in TFAM expression in systemic sclerosis (SSc), to analyze mitochondrial function and to evaluate the consequences for fibroblast activation. Methods: The expression of TFAM was analyzed by immunofluorescence and Western blot. The effects of TFAM knockout were investigated in cultured fibroblasts and in bleomycin-induced skin and lung fibrosis and in TβRIact-induced skin fibrosis. Results: The expression of TFAM was downregulated in fibroblasts in SSc skin and in cultured SSc fibroblasts. The downregulation of TFAM was associated with decreased mitochondrial number and accumulation of damaged mitochondria with release of mtDNA, accumulation of deletions in mtDNA, metabolic alterations with impaired OXPHOS and release of the mitokine GDF15. Chronic, but not acute exposure of normal fibroblasts to TGFβ mimicked the finding in SSc fibroblasts with downregulation of TFAM and accumulation of mitochondrial damage. Downregulation of TFAM promotes fibroblast activation with upregulation of fibrosis-relevant GO-terms in RNASeq. Mice with fibroblast-specific knockout of TFAM are prone to fibrotic tissue remodeling with fibrotic responses even to NaCl instillation and enhanced sensitivity to bleomycin injection and TβRIact-overexpression. TFAM knockout fosters SMAD3 signaling to promote fibroblast activation. Conclusions: Alterations in the key mitochondrial transcription factor TFAM in response to prolonged activation of TGFβ and associated mitochondrial damage induce transcriptional programs that promote fibroblast-to-myofibroblast transition and drive tissue fibrosis.

2021-12-21 | GSE184356 | GEO

Genome-wide ChIP-Seq maps of EZH2 distribution between Wild Type (WT), Actb+/- (HET), and Actb-/- (KO) Mouse Embryonic Fibroblast

Project description:Genome-wide ChIP-Seq maps of EZH2 distribution between Wild Type (WT), Actb+/- (HET), and Actb-/- (KO) Mouse Embryonic Fibroblast

| PRJNA630705 | ENA

Next-generation sequencing analysis of chemically induced neurons from wild type (WT), Actb+/- (HET) and Actb-/- (KO) mouse embryonic fibroblasts (MEFs)

Project description:Purpose: The goals of this study are to use NGS to perform transcriptome profiling (RNA-seq) to find the difference of the transcriptomes of chemically induced neurons from wild type (WT), Actb+/- (HET) and Actb-/- (KO) mouse embryonic fibroblasts. Methods: MEFs were reprogramed into neurons by small chemical cocktails. Small chemical molecules were dissolved and diluted in DMSO and used at the following final concentrations: ISX9: 20 mM; Forskolin: 50 mM; CHIR99021: 20 mM; and I-BET151: 2 mM. In addition to the small molecules, the neuron induction medium (Neurobasal Medium) contains the following supplements: N2 (1X) and B27 (2X) supplements, GlutaMAX (1X), penicillin-streptomycin (100 µg/ml), bFGF (20 ng/ml), 100 µM cAMP, Non-essential Amino Acid (1X) and Trace element B (1X). MEFs were seeded to Matrigel-coated plate (1:30 dilution in pre-cold PBS and coat overnight at 4 oC, at a density of 200,000 cells per well in 6-well plate and 10,000 cells/well in 96 well plate. The MEFs were cultured in DMEM until confluent. When the cells are confluent, the DMEM was replaced with neuron induction medium with 4 small molecules. The induction medium was refreshed every two days for the first week and every 3 days for the remaining induction period until day 20. 3 biological replicates of total RNA were used for RNA-seq library preparation. Results: Using an optimized data analysis workflow, we identified neuronal gene programs induced during direct reprograming. The induction of neuronal programs were impaired in neurons from Actb-/- mouse embryonic fibroblasts. Conclusions: Our study shows that neuronal program induction was impaired in chemically induced neurons from Actb-/- mouse embryonic fibroblasts.

2018-04-27 | GSE113733 | GEO

SIRT3 Deacetylates TFAM to Promote Mitochondrial Biogenesis

Project description:SIRT3 is a NAD+-dependent mitochondrial protein deacetylase participating in the regulation of central metabolism and mitochondrial proteostasis. SIRT3 is downregulated in clear cell renal cell carcinoma (ccRCC), a main type of renal cancers, but the function of SIRT3 in tumorigenesis and development of ccRCC remains unknown. In this study, we established a SIRT3 overexpressed cell line to explore the changes of proteomics and metabolomics regulated by SIRT3 expression. Both the results of quantitative proteomics, metabolomics and acetylome showed overexpression of SIRT3 increased mitochondrial biogenesis and reversed the mitochondrial dysfunctions in ccRCC. We found SIRT3 could increase the activity of TFAM through modulation of TFAM transcription, degradation and acetylation level. The acetylation of TFAM K154 decreased while TFAM protein expression increased after SIRT3 overexpression. Further study revealed that SIRT3 could bind with TFAM, and decrease the acetylation of TFAM, promoting TFAM activity in mitochondrial biogenesis. Overall, our results present a new mechanism of SIRT3 in regulating mitochondrial functions, and the downregulation of SIRT3 in ccRCC lowers the activity of TFAM, subsequently inhibits the transcription of mitochondrial genes and mitochondrial biogenesis.

2018-08-14 | PXD009110 | Pride

Transcriptomic analysis of WT, Tfam+/-, Zbp1-/- and Tfam+/-Zbp1-/- mouse embryonic fibroblasts (MEFs)

Project description:The goal of this study was to compare the gene expression profiles of WT, Tfam+/-, Zbp1-/- and Tfam+/-Zbp1-/- MEFs.

2023-01-28 | GSE223553 | GEO

High levels of TFAM repress in vivo transcription of mitochondrial DNA

Project description:Mammalian mitochondrial DNA (mtDNA) is coated with mitochondrial transcription factor A (TFAM) and compacted into nucleoids. TFAM is not only the main component of mitochondrial nucleoids but its levels can also control mtDNA copy number. Here we show that the TFAM-to-mtDNA ratio is critical for maintaining normal mtDNA expression in different tissues of the mouse. BAC transgenic mice with a 1.5-fold increase in TFAM protein levels maintain a normal TFAM-to-mtDNA ratio in different tissues and as a consequence mitochondrial gene expression, nucleoid distribution and whole animal metabolism are all unaltered. In contrast, mice expressing TFAM from the CAG promoter in the ROSA26 locus have 4.5-fold increase of TFAM protein levels in heart and skeletal muscle and develop pathology leading to early postnatal lethality. The TFAM-to-mtDNA ratio varies widely between tissues in these mice and is very high in skeletal muscle where it causes strong repression of mtDNA expression and deficient oxidative phosphorylation (OXPHOS) despite normal mtDNA levels. In heart, mtDNA copy number is increased leading to a near normal TFAM-to-mtDNA ratio and maintained OXPHOS capacity. In the liver, mtDNA expression is maintained despite increased TFAM levels and normal mtDNA levels. Here, tissue-specific induction of the LONP1 protease and mitochondrial RNA polymerase (POLRMT) expression counteracts the silencing effect of high TFAM levels. We conclude that the TFAM-to-mtDNA ratio has an important role in maintaining mtDNA expression in vivo. TFAM acts as a general repressor of mtDNA expression and this effect can be counterbalance by tissue-specific expression of regulatory factors.

2021-08-18 | PXD023050 | Pride

TFAM-dependent mitochondrial metabolism is required for alveolar macrophages maintenance and homeostasis

Project description:In this report, we showed that TFAM deficiency caused impaired AM mitochondrial fitness, altered metabolism and defective lipid catabolic responses, leading to diminished AM quantity and altered AM phenotypes. We demonstrated that TFAM deficiency did not impair AM differentiation from their precursors, but caused reduced AM maintenance. RNA-seq experiment revealed that TFAM deficiency caused impaired AM self-renewal capability. We showed that TFAM deficiency in AMs caused impaired clearance of respiratory debris, surfactant and enhanced susceptibility to severe influenza virus infection. Finally, we found that influenza infection resulted in disruption of TFAM-mediated mitochondrial fitness and metabolism in AMs.

2021-11-07 | GSE188279 | GEO

TFAM ChIP-seq in HeLa cells

Project description:ChIP-seq data characterizing the occupancy of TFAM over the mitochondrial and nuclear genomes in HeLa cells. Characterization of mitochondrial and nuclear genome-wide TFAM binding in HeLa cells

2013-09-21 | E-GEOD-48176 | biostudies-arrayexpress

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