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Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels

ABSTRACT: Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels

PROVIDER: PRJNA418909 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6301950_1.fastq.gz	Fastqsanger.gz
	SRR6301950_2.fastq.gz	Fastqsanger.gz
	SRR6301951_1.fastq.gz	Fastqsanger.gz
	SRR6301951_2.fastq.gz	Fastqsanger.gz
	SRR6301952_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Tafazzin Regulates Cell State by Modulating Phosphatidylethanolamine and Phosphatidylserine levels

Project description:Inhibiting tafazzin a cardiolipin remodeling enzyme reduces stemness of AML by modulating the level of phosphatidylserine

2019-03-28 | GSE107045 | GEO

Genome-wide analysis of gene transcription in myocardium of the doxycycline inducible Tafazzin shRNA knockdown mouse model of Barth syndrome

Project description:Analysis of the transcriptome of cardiac tissue from mice trangenically engineered with a doxycycline inducible Tafazzin shRNA knockdown to mimic the loss of function of Tafazzin in Barth syndrome. ShRNA induced knockdown mice were compared to wildtype littermates also fed the doxycyline diet. The hypothesis was to investigate adaptive metabolic and compensatory gene transcriptional changes in myocardium of the mouse model of Barth syndrome Total RNA obtained from 2 month old cardiac tissue from the doxycycline inducible shRNA Tafazzin knockdown mouse model of Barth syndrome compared to wildtype littermates also fed 625 mg/Kg doxycycline diet

2011-11-05 | E-GEOD-33452 | biostudies-arrayexpress

Reduced basal insulin secretion from islets isolated from tafazzin deficient mice is associated with reduced mitochondrial function

Project description:Tafazzin is a transacylase which causes the content and molecular structure of cardiolipin (CL) to be altered in the inner mitochondrial membrane. The enzymatic machinery responsible for oxidative respiration are localized to the inner mitochondrial membrane and require CL for activity. As a result, tafazzin is critical for maintaining mitochondrial function. In beta-cells, which are the insulin secreting cells in pancreatic islets, mitochondrial function is linked to insulin secretion. We previously established that tafazzin knock-down mice were lean and maintained insulin sensitivity compared to the obese insulin resistant control litter mates. However, it was unknown whether tafazzin deficiency also influenced insulin secretion in the establishment of the lean phenotype. Using X week-old mice, we ascertained that the number of beta-cells was similar between genotypes. Ex vivo insulin secretion under low glucose conditions was reduced (52%) from islets isolated from tafazzin knock-down mice. Consistent with this tafazzin knock-down mice exhibited reduced fasting insulin plasma insulin levels. Measurement of mitochondrial oxygen consumption revealed that basal oxygen consumption was reduced (58%) in islets from tafazzin-deficient animals. The addition of etomoxir, an inhibitor of mitochondrial fatty acid translocation, significantly elevated basal mitochondrial respiration (5-fold) in islets from tafazzin knockdown mice, indicating a significant fatty acid-mediated inhibitory effect. In contrast, etomoxir lacked any measurable effect on control wild-type islets. The altered mitochondrial function identified in taffazin knock-down islets was not associated with reduced CL content or elevated oxyCL species. Our experiments indicate that tafazzin plays a key role in regulating normal islet beta-cell function.

2021-07-31 | GSE136242 | GEO

Impaired phosphatidylethanolamine metabolism activates a reversible stress response that detects and resolves mutant mitochondrial precursors

Project description:Phosphatidylethanolamine made in mitochondria has long been recognized as an important precursor for phosphatidylcholine production that occurs in the endoplasmic reticulum (ER). Recently, the strict mitochondrial localization of the enzyme that makes PE in the mitochondrion, phosphatidylserine decarboxylase 1 (Psd1), was questioned. Since a dual localization of Psd1 to the ER would have far-reaching implications, we initiated our study to independently re-assess the subcellular distribution of Psd1. Our results support the unavoidable conclusion that the vast majority, if not all, of functional Psd1 resides in the mitochondrion. Through our efforts, we discovered that mutant forms of Psd1 that impair a self-processing step needed for it to become functional are dually localized to the ER when expressed in a PE-limiting environment. We conclude that severely impaired cellular PE metabolism provokes an ER-assisted adaptive response that is capable of identifying and resolving nonfunctional mitochondrial precursors.

2020-12-11 | GSE162987 | GEO

Unsaturation of very-long-chain ceramides regulates hypoxia response by modulating ethylene signaling in Arabidopsis

Project description:Lipid remodeling is crucial for hypoxic tolerance in animals, whilst little is known about the hypoxia-induced lipid dynamics in plant cells. Here we performed a mass spectrometry-based analysis to survey the lipid profiles of Arabidopsis rosettes under various hypoxic conditions. We observed that hypoxia caused a significant increase in total amounts of phosphatidylserine, phosphatidic acid and oxylipins, but a decrease in phosphatidylcholine (PC) and phosphatidylethanolamine (PE). Particularly, significant gains in the polyunsaturated species of PC, PE and phosphatidylinositol, and losses in their saturated and mono-unsaturated species were evident during hypoxia. Moreover, hypoxia led to a remarkable elevation of ceramides and hydroxyceramides. Depletion of ceramide synthases LOH1, LOH2, and LOH3 enhanced plant sensitivity to dark submergence (DS), but displayed more resistance to submergence under light than wild type. Consistently, levels of unsaturated ceramide species (22:1, 24:1, and 26:1) predominantly declined in the loh1, loh2, and loh3 mutants under DS. Evidence that C24:1-ceramide interacted with recombinant CTR1 protein in vitro, enhanced ER-to-nucleus translocation of EIN2-GFP and stabilization of EIN3-GFP in vivo, suggests a role of ceramides in modulating ethylene signaling. The DS-sensitive phenotypes of loh mutants were rescued by a ctr1-1 mutation. Thus, our findings demonstrate that unsaturation of very-long-chain ceramides is a protective strategy for hypoxic tolerance in Arabidopsis. Arabidopsis Affymetrix GeneChip arrays were probed with RNAs isolated from leaves of untreated plants (controls) and plants upon hypoxia under light submergence for 48 h.

2016-07-24 | E-GEOD-59719 | biostudies-arrayexpress

Wild-type and tafazzin-deficient clones of granulocyte-monocyte progenitors (GMP), ER-HOXB8 conditionally immortalized, immature, in estrogen.

Project description:Evaluate changes in gene expression resulting from the loss of the gene TAZ (protein tafazzin). Tafazzin is an enzyme involved in cardiolipin maturation and cardiolipin is a phospholipid found only in the inner mitochondrial membrane. Gene expression profiling was performed in a murine granulocyte-monocyte progenitor in vitro cell system. We identified a limited number of changes in gene expression, which was not surprising given that the tafazzin protein is localized in the mitochondria and has a very specific enzymatic activity. Genes involved in cholesterol and fatty acid metabolism (Acss1, Acat2, Ldlr), apoptosis (Bcl2, Casp3, Casp6, Cycs), and ER-stress induced apoptosis (Ddit3, Atf4) were differentially expressed.

2020-05-22 | GSE151006 | GEO

Gene expression analysis of wild-type and Tafazzin-deficient granulocyte-monocyte progenitor (GMP) clones (ER-HOXB8 conditionally immortalized)

2020-05-22 | GSE151007 | GEO

Genome-wide analysis of gene transcription in myocardium of the doxycycline inducible Tafazzin shRNA knockdown mouse model of Barth syndrome

2011-11-05 | GSE33452 | GEO

Ptdsr-/- (phosphatidylserine receptor) fibroblasts

Project description:Phagocytosis of apoptotic cells is fundamental to animal development, immune function and cellular homeostasis. The phosphatidylserine receptor (Ptdsr) on phagocytes has been implicated in the recognition and engulfment of apoptotic cells and in anti-inflammatory signaling. Ptdsr is essential for the development and differentiation of multiple organs during embryogenesis. Ptdsr may thus have a novel, unexpected developmental function as an important differentiation-promoting gene. Moreover, Ptdsr is not required for apoptotic cell clearance by macrophages but seems to be necessary for the regulation of macrophage cytokine responses. Keywords: ptdsr, fibroblast, cDNA microarray experiments,

2007-03-01 | GSE6937 | GEO

The Mitochondrial Transacylase, Tafazzin, Regulates for AML Stemness by Modulating Intracellular Levels of Phospholipids.

Project description:Tafazzin (TAZ) is a mitochondrial transacylase that remodels the mitochondrial cardiolipin into its mature form. Through a CRISPR screen, we identified TAZ as necessary for the growth and viability of acute myeloid leukemia (AML) cells. Genetic inhibition of TAZ reduced stemness and increased differentiation of AML cells both in vitro and in vivo. In contrast, knockdown of TAZ did not impair normal hematopoiesis under basal conditions. Mechanistically, inhibition of TAZ decreased levels of cardiolipin but also altered global levels of intracellular phospholipids, including phosphatidylserine, which controlled AML stemness and differentiation by modulating toll-like receptor (TLR) signaling.

| S-EPMC7137093 | biostudies-literature

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