Drosophila melanogaster
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB16683 | ENA |
REPOSITORIES: ENA
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Project description:Single-cell ATAC sequencing (scATAC-seq) was performed on tumor tissue isolated from the cortex of immunocompetent mice bearing high-grade glioma. Animals were maintained on either a control diet or a methionine-restricted diet to investigate the effects of dietary methionine restriction on tumor viability and chromatin accessibility. This dataset enables characterization of chromatin remodeling and regulatory landscape changes within the tumor microenvironment in response to methionine restriction.
2026-05-22 | GSE331233 | GEO
Project description:Histone modifications are integral to epigenetics through their influence on gene expression and cellular status. While it's established that metabolism, including methionine metabolism, can impact histone methylation, the direct influence of methionine availability on crucial histone marks that determine the epigenomic process remains poorly understood. In this study, we demonstrate that methionine, through its metabolic product, S-adenosylmethionine (SAM), dynamically regulates H3K36me3, a cancer-associated histone modification known to influence cellular status, and myogenic differentiation of mouse myoblast cells. We further demonstrate that the methionine-dependent effects on differentiation are mediated in part through the histone methyltransferase SETD2, which senses methionine levels. Additionally, methionine restriction leads to preferential decreases in H3K36me3 abundance and genome accessibility of genes involved in myogenic differentiation. Importantly, the effects of methionine restriction on differentiation and chromatin accessibility can be phenocopied by the deletion of Setd2. Collectively, this study demonstrates that methionine metabolism through its ability to be sensed by chromatin modifying enzymes can have a direct role in influencing cell fate determination.
2023-11-30 | GSE248198 | GEO
Project description:Histone modifications are integral to epigenetics through their influence on gene expression and cellular status. While it's established that metabolism, including methionine metabolism, can impact histone methylation, the direct influence of methionine availability on crucial histone marks that determine the epigenomic process remains poorly understood. In this study, we demonstrate that methionine, through its metabolic product, S-adenosylmethionine (SAM), dynamically regulates H3K36me3, a cancer-associated histone modification known to influence cellular status, and myogenic differentiation of mouse myoblast cells. We further demonstrate that the methionine-dependent effects on differentiation are mediated in part through the histone methyltransferase SETD2, which senses methionine levels. Additionally, methionine restriction leads to preferential decreases in H3K36me3 abundance and genome accessibility of genes involved in myogenic differentiation. Importantly, the effects of methionine restriction on differentiation and chromatin accessibility can be phenocopied by the deletion of Setd2. Collectively, this study demonstrates that methionine metabolism through its ability to be sensed by chromatin modifying enzymes can have a direct role in influencing cell fate determination.
2023-11-30 | GSE248197 | GEO
Project description:Methionine restriction is known to extend lifespan in various model organisms including Drosophila melanogaster. In this analysis, we performed scRNAseq of Drosophila female midgut samples to understand the cell type specific response to methionine restriction.
2023-09-25 | GSE198149 | GEO
Project description:Epigenetic modifications on DNA and histones regulate gene expression by modulating chromatin accessibility to transcription machinery. Chromatin-modifying enzymes are dependent on metabolic intermediates for chromatin remodeling, linking nutrient availability and cellular metabolism to the cellular epigenetic landscape. Here we identify methionine as a key nutrient affecting T cell epigenetic reprogramming in CD4+ T helper (Th) cells. Using metabolomic approaches, we showed that methionine is rapidly taken up by activated T cells and then serves as the major substrate for the biosynthesis of S-adenosyl-L-methionine (SAM), the universal methyl donor for cellular methyltransferases. Conversely, methionine restriction (MR) depletes intracellular SAM pools, reduces global histone H3K4 methylation (H3K4me3) in T cells, and reduces H3K4me3 levels at the promoter regions of key genes involved in CD4+ Th17 cell proliferation and cytokine production. Applied to the mouse model of multiple sclerosis (experimental autoimmune encephalomyelitis), dietary methionine restriction reduced the expansion of pathogenic Th17 cells in vivo, leading to reduced T cell-mediated neuroinflammation and disease onset. Overall our data identify methionine as a key nutritional factor that shapes T cell proliferation, differentiation, and function in part through regulation of histone methylation in T cells.
2020-02-03 | GSE143321 | GEO
Project description:Methionine restriction sensitizes A549 cells with and without LKB1 to chemotherapy
2024-07-19 | GSE270333 | GEO
Project description:EBV uses latency III oncoproteins to drive abnormal B cell proliferation to establish lifelong latency, and oncoprotein+ B cells correlate to pathology in autoimmune diseases such as systemic lupus erythematosus and multi-sclerosis. EBV-driven B cell outgrowth shows unique features that are different from both cancerous and cytokine-activated B cells, especially in their metabolism. Building on our previous observation that EBV+ tumors depend on methionine for viral epigenetic regulation, we tested whether EBV latency III program B cells share a similar phenotype. Surprisingly, the effect of methionine restriction on latency III cells is distinct and far more drastic—reducing RPMI media methionine level to 10% completely blocked B cell transformation, and to 1% resulted in rapid death of LCL and latency III Burkitt cells. Transcriptomic and liquid chromatography mass spectrometry-based metabolomic analyses revealed that methionine restriction downregulated genes related to the pentose phosphate pathway which supports cystine reduction, and upregulated genes related to ferroptosis, a lipid peroxidation (LPO)-mediated cell death. Isotope-labeled amino acid tracing indicated that methionine was shunt to cysteine biosynthesis pathway. Methionine restriction can be rescued by a combination of quenching LPO (Fer-1 and DFO) and removing toxic cystine buildup (NAC and penicillamine). In mice models, either dietary methionine restriction or injection of engineered methioninase abolished lymphoblastoid cell line tumor growth without having effects on body weight, and refractory tumor cells upregulated pathways against LPO, and downregulated cystine intake, highlighting methionine’s multiple roles in antagonizing LPO and redox pressure via modulating cysteine metabolism. In tonsil organoid model, moderate methionine restriction blocks EBV+ cell outgrowth but did not affect T cell activation and normal germinal center development, implying therapeutic potential. In a B cell transformation assay with a panel of loss-of-function BAC viruses, we identify EBNA2, EBNA-LP, and LMP2A deletion provided protection.
2026-07-04 | GSE336950 | GEO
Project description:Methionine, a sulfur-containing essential amino acid, is a key component of dietary proteins important for protein synthesis, sulfur metabolism, antioxidant defense, and signaling. However, the role of methionine in cancer progression remains inconclusive. On one hand, dietary methionine restriction is known to repress cancer growth and improve cancer therapy in xenografted tumors. On the other hand, methionine is also critical for T cell activation and differentiation, making it a potential tumor suppression nutrient by enhancing T cell-mediated anti-tumor immunity. Here we investigated the interaction between dietary methionine, immune cells, and cancer cells by allografting CT26.WT mouse colon carcinoma cells into immunocompetent Balb/c mice or immunodeficient NSG mice, then analyzed how dietary methionine contents affect their growth. Our results show that dietary methionine restriction suppresses tumor growth in immunodeficient NSG mice but promotes tumor progression in immunocompetentt Balb/c mice.
2023-06-14 | GSE165993 | GEO
Project description:To explore putative connections between genetic methionine restriction and the retrograde response, we asked whether the altered transcriptional program of methionine-restricted cells required RTG3 (which is indispensible for retrograde signaling in yeast).
2014-04-10 | GSE56641 | GEO