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Phosphatidic acid in gene expression-Phosphatidic acid in gene expression

ABSTRACT: au10-12_pa - phosphatidic acid in gene expression - Role of DGK in gene expression - Compounds were added 4h before cell harvesting.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE35872 | GEO | 2012/03/01

SECONDARY ACCESSION(S): PRJNA151927

REPOSITORIES: GEO

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phosphatidic acid in gene expression-Phosphatidic acid in gene expression

Project description:au10-12_pa - phosphatidic acid in gene expression - Role of DGK in gene expression - Compounds were added 4h before cell harvesting. 6 dye-swap - treated vs untreated comparison

2012-03-01 | E-GEOD-35872 | biostudies-arrayexpress

Disturbed intramitochondrial phosphatidic acid transport impairs cellular stress signaling

Project description:Disturbed intramitochondrial phosphatidic acid transport impairs cellular stress signaling

| PRJNA674653 | ENA

Interactome analysis of human phospholipase D and phosphatidic acid-associated protein network

Project description:Using a systematic proteomic approach, we define the protein-protein interaction network for PLD superfamily and phosphatidic acid in human cells and reveal diverse cellular signaling events involved for this key protein family and lipid.

2022-01-16 | PXD029183 | Pride

Disturbed intramitochondrial phosphatidic acid transport impairs cellular stress signaling

Project description:Lipid transfer proteins of the Ups1/PRELID1 family facilitate the transport of phospholipids across the intermembrane space of mitochondria in a lipid-specific manner. Heterodimeric complexes of yeast Ups1/Mdm35 or human PRELID1/TRIAP1 shuttle phosphatidic acid (PA) synthesized in the endoplasmic reticulum (ER) to the inner membrane, where it is converted to cardiolipin (CL), the signature phospholipid of mitochondria. Loss of Ups1/PRELID1 proteins impairs the accumulation of CL and broadly affects mitochondrial structure and function. Unexpectedly and unlike yeast cells lacking the cardiolipin synthase Crd1, Ups1 deficient yeast cells exhibit glycolytic growth defects, pointing to functions of Ups1-mediated PA transfer beyond CL synthesis. Here, we show that the disturbed intramitochondrial transport of PA in ups1D cells leads to altered phospholipid composition of the ER membrane, independent of disturbances in CL synthesis. The impaired flux of PA into mitochondria is associated with the increased synthesis of phosphatidylcholine (PC) and a reduced phosphatidylethanolamine (PE)/PC ratio in the ER of ups1D cells which suppresses the unfolded protein response (UPR). Moreover, we observed inhibition of TORC1 signaling in these cells. Activation of either UPR by ER protein stress or of TORC1 signaling by disruption of its negative regulator, the SEACIT complex, increased cytosolic protein synthesis and restored glycolytic growth of ups1D cells. These results demonstrate that PA influx into mitochondria is required to preserve ER membrane homeostasis and that its disturbance is associated with impaired glycolytic growth and cellular stress signaling.

2021-01-21 | GSE160861 | GEO

Disturbed intramitochondrial phosphatidic acid transport impairs cellular stress signaling

Project description:Lipid transfer proteins of the Ups1/PRELID1 family facilitate the transport of phospholipids across the intermembrane space of mitochondria in a lipid-specific manner. Heterodimeric complexes of yeast Ups1/Mdm35 or human PRELID1/TRIAP1 shuttle phosphatidic acid (PA) synthesized in the endoplasmic reticulum (ER) to the inner membrane, where it is converted to cardiolipin (CL), the signature phospholipid of mitochondria. Loss of Ups1/PRELID1 proteins impairs the accumulation of CL and broadly affects mitochondrial structure and function. Unexpectedly and unlike yeast cells lacking the cardiolipin synthase Crd1, Ups1 deficient yeast cells exhibit glycolytic growth defects, pointing to functions of Ups1-mediated PA transfer beyond CL synthesis. Here, we show that the disturbed intramitochondrial transport of PA in ups1 cells leads to altered phospholipid composition of the ER membrane, independent of disturbances in CL synthesis. The impaired flux of PA into mitochondria is associated with the increased synthesis of phosphatidylcholine (PC) and a reduced phosphatidylethanolamine (PE)/PC ratio in the ER of ups1 cells which suppresses the unfolded protein response (UPR). Moreover, we observed inhibition of TORC1 signaling in these cells. Activation of either UPR by ER protein stress or of TORC1 signaling by disruption of its negative regulator, the SEACIT complex, increased cytosolic protein synthesis and restored glycolytic growth of ups1 cells. These results demonstrate that PA influx into mitochondria is required to preserve ER membrane homeostasis and that its disturbance is associated with impaired glycolytic growth and cellular stress signaling.

2021-01-22 | PXD022321 | Pride

New Era of Diacylglycerol Kinase, Phosphatidic Acid and Phosphatidic Acid-Binding Protein.

Project description: Not available

| S-EPMC7555651 | biostudies-literature

DLGAP1-AS2-Mediated Phosphatidic Acid Synthesis Activates YAP Signaling and Confers Chemoresistance in Squamous Cell Carcinoma [ATAC-Seq]

Project description:Squamous cell carcinomas (SCC) constitute a group of human malignancies that originate from the squamous epithelium. Most SCC patients experience treatment failure and relapse and have a poor prognosis due to de novo and acquired resistance to first-line chemotherapeutic agents. To identify chemoresistance mechanisms and explore novel targets for chemosensitization, we performed whole-transcriptome sequencing of paired resistant and parental SCC cells. We identified DLGAP1 antisense RNA 2 (D-AS2) as a crucial noncoding RNA that contributes to chemoresistance in SCC. Mechanistically, D-AS2 affected chromatin accessibility around the histone mark H3K27ac of FAM3 metabolism regulating signaling molecule D (FAM3D), reducing FAM3D mRNA transcription and extracellular protein secretion. FAM3D interacted with the Gαi-coupled G protein-coupled receptors (GPCRs) formyl peptide receptor 1 (FPR1) and FPR2 to suppress phospholipase D (PLD) activity, and reduced FAM3D increased PLD signaling. Moreover, activated PLD promoted phosphatidic acid (PA) production and subsequent nuclear translocation of yes-associated protein (YAP). Accordingly, in vivo administration of a D-AS2-targeting antisense oligonucleotide sensitized SCC to cisplatin treatment. In summary, this study shows that D-AS2/FAM3D-mediated PLD/PA lipid signaling is essential for SCC chemoresistance, suggesting D-AS2 can be targeted to sensitize SCC to cytotoxic chemotherapeutic agents.

2022-07-29 | GSE169502 | GEO

DLGAP1-AS2-Mediated Phosphatidic Acid Synthesis Activates YAP Signaling and Confers Chemoresistance in Squamous Cell Carcinoma [RNA-Seq]

2022-07-29 | GSE169631 | GEO

salmonell inva-Trancriptomic analysis in Salmonella typhimurium infection

Project description:au10-06_salmonella - salmonell inva - Transcriptomic analysis between Salmonella wt and differents mutants in type3 secretion system. - Plants were grown during 14 days in solid medium and were transfered to liquid medium during 16 h. at 9 am samonella was added to a final concentration of OD600=0.2

2012-04-07 | GSE36699 | GEO

Trancriptomic analysis in Salmonella typhimurium infection [invA_vs_14028s]

Project description:au10-06_salmonella_eduardob - inva_vs_14028s Transcriptomic analysis between Salmonella wt and different mutants in type3 secretion system. - Plants were grown during 14 days in solid medium and were transfered to liquid medium during 16 h. at 9 am samonella was added to a final concentration of OD600=0.2

2012-01-31 | GSE34664 | GEO

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