Saccharomyces cerevisiae
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA350552 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR4453400.fastq.gz | Fastqsanger.gz | |||
| SRR4453401.fastq.gz | Fastqsanger.gz | |||
| SRR4453402.fastq.gz | Fastqsanger.gz | |||
| SRR4453403.fastq.gz | Fastqsanger.gz | |||
| SRR4453398.fastq.gz | Fastqsanger.gz |
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Project description:Fatty liver is a condition of excessive triglyceride accumulation in hepatocytes. Additionally, hepatocytes showed a high degree of fat droplet accumulation during excessive alcohol consumption and metabolic syndrome. However, the molecular mechanisms involved in fat droplet formation remain unknown. This study used an in vitro fatty liver formation model of the human liver cancer cell line HepG2 to comprehensively search for fat droplet formation-related genes whose expression changes during fat droplet formation. Microarray analysis with extracted total RNA determined the genes that are involved in fat droplet formation and confirmed their expression by real-time polymerase chain reaction after culturing HepG2 cells in a culture medium containing 0, 50, 200, and 500 μM of oleic acid for 24 h. The results revealed 142 genes demonstrating increased expressions by >2.0 fold with oleic acid treatment and 426 genes demonstrating decreased expressions. Perilipin 2 (PLIN2) was estimated as the gene most closely associated with fatty liver. Lipid droplet formation in HepG2 upregulated PLIN2 in an oleic acid-treated concentration-dependent manner. These results indicate the involvement of genes in oleate treatment-induced lipid droplet formation in HepG2, particularly PLIN2 may play an important role.
2023-12-01 | GSE248166 | GEO
Project description:The liver has a high demand for phosphatidylcholine (PC) particularly in overnutrition where reduced phospholipid levels have been implicated in the development of non-alcoholic fatty liver disease (NAFLD). Whether other pathways exist in addition to de novo PC synthesis that contribute to hepatic PC pools remains unknown. Here, we identified the lysophosphatidylcholine (LPC) transporter Mfsd2a as critical for maintaining hepatic phospholipid pools. Hepatic Mfsd2a expression was induced in patients having NAFLD and in mice in response to dietary fat via glucocorticoid receptor action. Mfsd2a liver-specific deficiency in mice (L2aKO) led to a robust NASH-like phenotype within just two weeks of dietary fat challenge associated with reduced hepatic phospholipids containing linoleic acid. Reducing dietary choline intake in L2aKO mice exacerbated liver pathology and deficiency of liver phospholipids containing polyunsaturated fatty acids (PUFA). Treating hepatocytes with LPC containing oleate and linoleate, two abundant blood-derived LPCs, specifically induced lipid droplet biogenesis and contributed to phospholipid pools, while LPC containing the omega-3 fatty acid DHA promoted lipid droplet formation and suppressed lipogenesis. This study revealed that PUFA containing LPCs drive both hepatic lipid droplet formation, suppress lipogenesis and sustain hepatic phospholipid pools--processes that are critical for protecting the liver from excess dietary fat.
2023-07-27 | GSE173545 | GEO
Project description:Phospholipase A2 group VI (PLA2G6, also called iPLA2β) has been implicated in male fertility, neuronal disorders, and metabolic diseases. However, its therapeutic effects on metabolic disorders remain elusive. We investigated the effects of Pla2g6 suppression on glucose and lipid metabolism. Systemic inhibition of Pla2g6 in high-fat diet-fed mice reduced hepatic lipid droplet formation without altering the levels of serum triglycerides and fasting blood glucose. Suppression of liver-specific Pla2g6 utilizing the short-hairpin RNA knockdown technique using an adenovirus vector (Ad-shPLA2G6) altered phospholipid and fatty acid metabolites and suppressed hepatic lipid accumulation, serum triglyceride, fasting glucose, and insulin levels. Additionally, Ad-shPLA2G6 treatment downregulated lipid biosynthesis-related genes but upregulated peroxisomal fatty acid oxidation-related genes. These findings indicate that targeting hepatic Pla2g6 modulates phospholipid and fatty acid metabolites and improves glucose and lipid metabolism, suggesting Pla2g6 as a potential therapeutic target in metabolic disorders, including type 2 diabetes mellitus and metabolic dysfunction-associated steatotic liver disease.
2026-05-07 | GSE310622 | GEO
Project description:Immature bovine cumulus-oocytes complexes (COCs) with several layers of tightly packed cumulus cells and a homogeneous, darkish ooplasm are considered to be of good quality, whereas COCs exhibiting cytoplasmatic granulation are frequently observed but routinely discarded. This study compared the protein and lipid landscape, as well as the developmental competence, of immature cattle oocytes with either granulated or homogeneous ooplasm but similarly compact cumulus investment. Nile Red staining revealed increased lipid droplet accumulation, greater heterogeneity in droplet size, and formation of droplet clusters in granulated oocytes. Lipidomics via ESI-IT MS corroborated these findings by discovering a significantly higher content of phosphatidylcholines and a trend toward increased levels of free fatty acids in granulated compared to homogeneous oocytes. Protein profiling via LC-MS/MS was performed to characterize the molecular features of granulated oocytes in more detail. In total, 2136 proteins were detected, with only minor differences between the proteomes of granulated and homogenous oocytes. All ten proteins classified as differentially expressed displayed a lower abundance in granulated oocytes - seven were directly associated with peroxisomal lipid metabolism and peroxisome formation, mitochondrial function, and autophagy initiation. Protein interaction analysis revealed methyl-branched fatty acid metabolic process and fatty acid alpha-oxidation as enriched pathways with the highest strength. Granulated oocytes displayed significantly higher cleavage and blastocyst formation rates following in vitro embryo production than homogeneous oocytes, indicating superior developmental competence. Granulated oocytes thus represent a distinct, lipid‑rich phenotype with configured peroxisomal and mitochondrial pathways that, contrary to current selection practice, can enhance early embryonic development.
2026-05-27 | PXD071722 | Pride
Project description:Mycobacterium tuberculosis (Mtb) infection of macrophages reprograms cellular lipid metabolism to promote the formation of cytosolic lipid droplets. While it is clearly known that intracellular Mtb utilize host derived fatty acids and cholesterol to fuel a majority of its biosynthetic demands, the role of macrophage lipid metabolism on the bacteria’s ability to access the intracellular lipid pool remains controversial. We have utilized a CRISPR genetic knockdown approach to, systematically and comprehensively, characterize the role of macrophage fatty acid metabolism on the intracellular growth of Mtb. Our analyzes demonstrate that knockdown of lipid import, sequestration and metabolism genes collectively impair the intracellular growth of Mtb in macrophages. We further demonstrate that modulating fatty acids homeostasis in macrophages impair Mtb replication by enhancing production of pro-inflammatory cytokines, restricting the bacteria access to nutrients and increasing oxidative stress in a manner which is surprisingly divergent. We also demonstrate that impaired macrophage lipid droplet biogenesis is restrictive to intracellular Mtb growth. However, increased induction of lipid droplet formation by downstream blockade of fatty acid oxidation does not rescue the impaired Mtb growth phenotypes. Our work provides a characterization of macrophage fatty acid homeostasis and how its modulation impacts Mtb intracellular growth.
2024-06-24 | GSE270571 | GEO
Project description:Peroxisomes are ubiquitous organelles that mediate central metabolic functions, such as fatty acid β-oxidation, as well as diverse tissue- and organism-specific processes. Membrane contact sites, regions of close apposition with other organelles for direct communication, are central to several aspects of their life cycle. Pex3 is a conserved multifunctional peroxisomal transmembrane protein that is involved in the insertion of peroxisomal membrane proteins, in pexophagy, and in the formation of membrane contact sites. Here, we show that high Pex3 levels in Saccharomyces cerevisiae induce the formation of peroxisome clusters surrounded by lipid droplets, mediated by peroxisome-peroxisome and peroxisome-lipid droplet contact sites. This clustering occurs independently of Pex3 partners in other processes Pex19, Inp1, and Atg36. The cytosolic domain of Pex3 binds peroxisomes, suggesting a direct role in homotypic contact site formation. Lipid droplet-peroxisome contact sites require the lipid droplet-localized triacylglycerol lipase Tgl4, which is enriched at this interface along with other lipases. Pex3 overexpression in Drosophila melanogaster similarly alters peroxisome and lipid droplet morphology and promotes contact site formation. Together, our results offer novel molecular insights into homotypic peroxisome contact sites and peroxisome-lipid droplet contact sites across species.
2025-05-22 | PXD063514 | Pride
Project description:Palm and coconut oils are linked to cardiovascular disease and diabetes because of their high saturated fatty acid (SFA) content but exactly how exogenous SFAs, but not unsaturated fatty acids (UFA), are toxic to cells remains unknown. In insulin-producing, β-cells of the Islets of Langerhans, loss of which exacerbates diabetes, we found that SFAs but not UFAs were toxic because they disable a highly conserved lipid droplet biogenesis machinery. We show that palmitate (a major SFA of these oils), but not palmitoleic or oleic, S-acylates the highly conserved ER-resident FITM2 protein, required for lipid coalescence and droplet budding from the ER. The S-acylation marks FITM2 for ubiquitination and proteosomal degradation, leaving SFAs within the ER instead safe sequestration within lipid droplets. ER-stress ensues with rapid induction of ER stress leading to β-cell apoptosis. Specific deletion of FITM2 in β-cells disrupts calcium signaling and key β-cell TFs and exacerbates high fat diet-induced ER stress and diabetes. Rescue by overexpression ameliorates ER-stress and β-cell apoptosis thus demonstrating an important link between lipid species and cell ability to sequester them away from the ER in the form of lipid droplets.
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Project description:Membrane contact sites between organelles are critical for transfer of biomolecules. Lipid droplets store fatty acids and form contacts with mitochondria, which regulate fatty acid oxidation and adenosine triphosphate production. Protein compartmentalization at lipid droplet-mitochondria contact sites and their effects on biological processes are poorly described. Using proximity-dependent biotinylation methods, we identify 71 proteins at lipid droplet-mitochondria contact sites, including a multimeric complex containing extended synaptotagmin (ESYT) 1, ESYT2, and VAMP Associated Protein B and C (VAPB). High resolution imaging confirms localization of this complex at the interface of lipid droplet-mitochondria-endoplasmic reticulum where it likely transfers fatty acids to enable -oxidation. Deletion of ESYT1, ESYT2 or VAPB limits lipid droplet-derived fatty acid oxidation, resulting in depletion of tricarboxylic acid cycle metabolites, remodeling of the cellular lipidome, and induction of lipotoxic stress. These findings were recapitulated in Esyt1 and Esyt2 deficient mice. Our study uncovers a fundamental mechanism that is required for lipid droplet-derived fatty acid oxidation and cellular lipid homeostasis, with implications for metabolic diseases and survival.
2025-04-28 | PXD060912 | Pride
Project description:part of a project: Granulocyte differentiation arrest in HAX1-deficient cells demonstrated in a new in vitro model of Kostmann disease, is caused by ineffective lipid droplet autophagy and fatty acids uptake. Molecular and metabolic mechanisms underlying congenital neutropenia in patients with HAX1 deficiency are not clear at the moment. It was demonstrated that HAX1 deficiency results in the arrest of neutrophil differentiation. Our studies of the effect of HAX1 deficiency on proteomic and metabolic profiles of promyelocytic cells have led to a conclusion that HAX1-deficient cells display differences in amino acid metabolism, specifically arginine, serine and aspartate. The analysis revealed significant upregulation of several proteins in HAX1-deficient cells, specifically argininosuccinate synthase (ASS1), an enzyme of arginine biosynthesis pathway, with the highest upregulation score, confirmed by Western blot. Moreover, Quantitative System Metabolism (QSM) analysis of the proteomic data has led to a conclusion, supported by specific tests, that fatty acid metabolism is affected in HAX1-deficient cells. This assumption was confirmed by experiments showing that the lipid droplet content is increased in HAX1-deficient cells, pointing to the accumulation of fatty acids that are not metabolized. Studies of autophagosome formation and function in HAX1 WT and knockout (KO) cells revealed that autophagy of lipid droplets is defective at the stage of the fusion with the lysosome. It is known that autophagy-dependent generation of free fatty acids is critical for neutrophil differentiation, therefore if HAX1 deficiency affects normal autophagy of lipids in promyeloblasts it should explain its effect on differentiation arrest.
2026-04-22 | PXD064511 | Pride
Project description:The combination of immune checkpoint blockade and chemotherapies is the standard-of-care for triple negative breast cancer (TNBC). However, initially responsive tumors can still develop recurrences, suggesting acquired resistance mechanisms that remain poorly understood. Herein, we discovered that TNBC cells surviving anti-PD-1 and chemotherapy treatment accumulated neutral lipids. Disrupting lipid droplet formation in cancer cells reversed resistance and mitigated the immunosuppressive microenvironment. Single-cell RNA sequencing revealed a subset of neutrophils exhibiting a lipid-laden phenotype similar to adjacent tumor cells. Mechanistically, tumor-derived extracellular vesicles carrying lipids including arachidonic acid (AA) mediated neutrophil reprogramming. Blocking dietary intake of omega-6 fatty acids or inhibiting fatty acid elongation for AA synthesis restored antitumor immunity and re-sensitized the resistant tumors to anti-PD-1 and chemotherapy treatment. In human patients, AA metabolism-related pathways correlated with neutrophil enrichment. Overall, we demonstrate how lipid accumulation in TNBC cells leads to immune suppression and therapy resistance.
2025-04-08 | GSE243099 | GEO