Hepatic lipid remodeling in cold exposure uncovers direct regulation of bis(monoacylglycero)phosphate lipids by Pla2g15
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1241305 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR32841061_1.fastq.gz | Fastqsanger.gz | |||
| SRR32841061_2.fastq.gz | Fastqsanger.gz | |||
| SRR32841062_1.fastq.gz | Fastqsanger.gz | |||
| SRR32841062_2.fastq.gz | Fastqsanger.gz | |||
| SRR32841063_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 8 |
Similar Datasets
Project description:Cold exposure is a selective environmental stress that elicits a rapid metabolic shift to maintain energy homeostasis. In response to cold exposure, the liver rewires the metabolic state shifting from glucose to lipid catabolism. By probing the liver lipids in cold exposure, we observed that the lysosomal bis(monoacylglycero)phosphate (BMP) lipids were rapidly increased during cold exposure. BMP lipid changes occurred independently of lysosomal abundance but were dependent on the lysosomal transcriptional regulator transcription factor EB (TFEB). Knockdown of TFEB in hepatocytes decreased BMP lipid levels and led to cold intolerance in mice. We assessed TFEB binding sites of lysosomal genes and determined that the phospholipase Pla2g15 regulates BMP lipid catabolism. Knockdown of Pla2g15 in mice increased BMP lipid levels, ablated the cold-induced rise, and improved cold tolerance. Knockout of Pla2g15 in mice and hepatocytes led to increased BMP lipid levels, that were decreased with re-expression of Pla2g15. Mutation of the catalytic site of Pla2g15 ablated the BMP lipid breakdown. Together, our studies uncover TFEB regulation of BMP lipids through Pla2g15 catabolism.
2025-03-25 | GSE292817 | GEO
Project description:Targeted lipidomic analyses of: acycarnitines in mouse plasma and liver; ceramides in lysosomes isolated from mouse liver; and bis(monoacylglycero)phosphate lipids in mouse liver and 293t cells.
2025-01-07 | MSV000096791 | MassIVE
Project description:Acinetobacter baumannii is an ESKAPE pathogen that rapidly develops resistance to antibiotics and persists for extended periods in the host or on abiotic surfaces. Survival in environmental stress such as phosphate scarcity, represents a clinically significant challenge for nosocomial pathogens. In the face of phosphate starvation, certain bacteria encode adaptive strategies, including the substitution of glycerophospholipids with phosphorus-free lipids. In bacteria, phosphatidylethanolamine, phosphatidylglycerol, and cardiolipin are conserved glycerophospholipids that can form lipid bilayers, particularly in the presence of other lipids. Here, we demonstrate that in response to phosphate limitation, conserved regulatory mechanisms induce alternative lipid production in A. baumannii. Specifically, phosphate limitation induces formation of three lipids, including amine-containing ornithine and lysine aminolipids. Mutations that inactivate aminolipid biosynthesis exhibit fitness defects relative to wild type in colistin growth and killing assays. Furthermore, we show that other Gram-negative ESKAPE pathogens accumulate aminolipids under phosphate limiting growth conditions, suggesting aminolipid biosynthesis may represent a broad strategy to overcome cationic antimicrobial peptide-mediated killing.
2024-10-02 | GSE276010 | GEO
Project description:Lipid accumulation by oleaginous microorganisms is of great scientific interest and biotechnological potential. While nitrogen limitation has been routinely employed, low-cost raw materials usually contain rich nitrogenous components, thus preventing from efficient lipid production. Inorganic phosphate (Pi) limitation has been found sufficient to promote conversion of sugars into lipids, yet the molecular basis of cellular response to Pi-limitation and concurrent lipid accumulation remains elusive. Here we performed multi-omic analyses of the oleaginous yeast Rhodosporidium toruloides to shield lights on Pi-limitation induced lipid accumulation. Samples were prepared under Pi-limited as well as Pi-replete chemostat conditions, and subjected to analysis at the transcriptomic, proteomic and metabolomic level. In total, 7970 genes, 4212 proteins and 123 metabolites were identified. Results showed that Pi-limitation facilitates up-regulation of Pi-associated metabolism, RNA degradation and triacylglycerol biosynthesis, while down-regulation of ribosome biosynthesis and tricarboxylic acid cycle. Pi-limitation leads to de-phosphorylation of adenosine monophosphate, the allosteric activator of isocitrate dehydrogenase key to lipid biosynthesis. It was found that NADPH, the key cofactor for fatty acid biosynthesis, is limited due to reduced flux through the pentose phosphate pathway and transhydrogenation cycle, and that this can be overcomed by overexpression of an endogenous malic enzyme. These phenomena are found distinctive from those under nitrogen-limitation. The information greatly enriches our understanding on microbial oleaginicity and Pi-related metabolism. Importantly, systems data may facilitate designing advanced cell factories for production of lipids and related oleochemicals.
2018-05-31 | GSE113097 | GEO
Project description:Brachypodium distachyon cultivar:Bis-1 Genome sequencing
| PRJNA337153 | ENA
Project description:Lipids play crucial roles in plant-microbe interactions, functioning as structural components, signaling molecules, and microbe-associated molecular patterns (MAMPs); however, the mechanisms underlying lipid perception and signaling pathways in plants remain largely unknown. This study investigates the immune responses triggered in Hordeum vulgare (barley) by lipid extracts from the root endophytic fungus Serendipita indica. We compare these responses to those elicited by the carbohydrate MAMP chitohexaose and the fungal sterol lipid ergosterol, a 5,7-diene oxysterol recognized as a MAMP in plants. Our results demonstrate that S. indica lipid extract induces hallmarks of pattern-triggered immunity (PTI) in barley. Ergosterol was identified as the main immunogenic component and was detected in the apoplastic fluid of S. indica-colonized barley roots. Using a multi-omics approach combining transcriptomics, phosphoproteomics, and metabolomics, our data provide evidence for the activation of phosphatidylinositol phosphate (PIP) signaling and diterpene biosynthesis upon exposure to fungal lipids. Furthermore, we show that phosphatidic acid (PA) enhances lipid-mediated apoplastic reactive oxygen species (ROS) production in barley. These findings indicate that plant lipids mediate immune responses to fungal lipids in barley, advancing our understanding of lipid perception and signaling in plant-microbe interactions.
2025-01-31 | PXD056788 | Pride
Project description:Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids' saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS.
2012-05-09 | GSE37670 | GEO
Project description:Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids' saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS.
2012-05-09 | GSE37826 | GEO
Project description:Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids' saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS.
2012-05-09 | GSE37664 | GEO
Project description:Lipids comprise 70% of the myelin sheath, and autoantibodies against lipids may contribute to the demyelination that characterizes multiple sclerosis (MS). We used lipid antigen microarrays and lipid mass spectrometry to identify bona fide lipid targets of the autoimmune response in MS brain and an animal model of MS to explore the role of the identified lipids in autoimmune demyelination. We found that autoantibodies in MS target a phosphate group in phosphatidylserine and oxidized phosphatidylcholine derivatives. Administration of these lipids ameliorated experimental autoimmune encephalomyelitis by suppressing activation and inducing apoptosis of autoreactive T cells, effects mediated by the lipids' saturated fatty-acid side chains. Thus, phospholipids represent a natural anti-inflammatory class of compounds that have potential as novel therapeutics for MS. Fig. 2A. Mini-Array I: IgG antibody reactivity to various glycero-3-phosphocholine lipids in CSF samples from patients with relapsing remitting MS and from control patients with other neurological disease. Lipid hits with the lowest FDR (q=0.029) were clustered according to their reactivity profiles. 47 different lipids were custom-spotted in duplicate using the CAMAG Automatic TLC Sampler (ATS4) robot to spray 200 nl of 10 to 100 pmol of lipids onto PVDF membranes affixed to the surface of microscope slides. The slides were probed with cerebrospinal fluid (CSF) from 24 human patient samples. 25 slides total: 13 relapsing-remitting MS, 11 other neurological disease, and 1 secondary Ab alone (not included in this submission). CSF diluted 1/20. HRP-conjugated secondary Ab (goat anti-human IgM/IgG) diluted 1/175. ECL for 3 minutes.
2012-05-08 | E-GEOD-37670 | biostudies-arrayexpress