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Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ChIP-seq]

ABSTRACT: Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ChIP-seq]

PROVIDER: PRJNA1042644 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26874169.fastq.gz	Fastqsanger.gz
	SRR26874170.fastq.gz	Fastqsanger.gz
	SRR26874171.fastq.gz	Fastqsanger.gz
	SRR26874172.fastq.gz	Fastqsanger.gz
	SRR26874173.fastq.gz	Fastqsanger.gz

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Methionine availability influences essential H3K36me3 dynamics during cell differentiation

Project description:Methionine availability influences essential H3K36me3 dynamics during cell differentiation

| PRJNA1042641 | ENA

Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ATAC-seq]

Project description:Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ATAC-seq]

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Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ChIP-seq]

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

Methionine availability influences essential H3K36me3 dynamics during cell differentiation [ATAC-seq]

2023-11-30 | GSE248197 | GEO

Methionine availability influences essential H3K36me3 dynamics during cell differentiation.

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. 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.

| S-EPMC10690240 | biostudies-literature

Methionine availability influences essential H3K36me3 dynamics during cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-30 | GSE248199 | GEO

Dietary methionine starvation impairs acute myeloid leukemia progression

Project description:Targeting altered tumor cell metabolism might provide an attractive opportunity for patients with acute myeloid leukemia (AML). An amino acid dropout screen on primary leukemic stem cells and progenitor populations revealed a number of amino acid dependencies, of which methionine was one of the strongest. By using various metabolite rescue experiments, NMR-based metabolite quantifications and 13C-tracing, polysomal profiling, and ChIP-seq, we identified that methionine is used predominantly for protein translation and to provide methyl groups to histones via S-adenosylmethionine for epigenetic marking. H3K36me3 was consistently the most heavily impacted mark following loss of methionine. Methionine depletion also reduced total RNA levels, enhanced apoptosis and induced a cell cycle block. ROS levels were not increased following methionine depletion and replacement of methionine with glutathione or N-acetylcysteine could not rescue phenotypes, excluding a role for methionine in controlling redox balance control in AML. Although considered to be an essential amino acid, methionine can be recycled from homocysteine. We uncovered that this is primarily performed by the enzyme methionine synthase and only when methionine availability becomes limiting. In vivo, dietary methionine starvation was not only tolerated by mice, but also significantly delayed both cell line and patient-derived AML progression. Finally, we show that inhibition of the H3K36-specific methyltransferase SETD2 phenocopies much of the cytotoxic effects of methionine depletion, providing a more targeted therapeutic approach. In conclusion, we show that methionine depletion is a vulnerability in AML that can be exploited therapeutically, and we provide mechanistic insight into how cells metabolize and recycle methionine.

2022-12-21 | GSE220236 | GEO

Genome-wide H3K4me3 and gene expression before and after methionine restriction in human cancer cells and mouse liver

Project description:In this study, we compared genomic H3K4me3 and gene expression profiles before and after methionine restriction in human cancer cells and mouse liver. The goals are to understand the influences of nutrient availability on genomic architecture of histone modification and gene expression.

2018-01-01 | GSE103602 | GEO

Copper Availability Influences the Transcriptomic Response of C. albicans to Fluconazole Stress

Project description:Copper Availability Influences the Transcriptomic Response of C. albicans to Fluconazole Stress

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Characterization of methionine dependence in melanoma cells [HumanMethylationEPIC]

Project description:Dietary methionine restriction is associated with a reduction in tumor growth in preclinical studies and an increase in lifespan in animal models. The mechanism by which methionine restriction inhibits tumor growth while sparing normal cells is incompletely understood, except for the observation that normal cells can utilize methionine or homocysteine interchangeably (methionine independence) while most cancer cells are strictly dependent on methionine availability. Here, we compared a typical methionine dependent and a rare methionine independent melanoma cell line. We show that replacing methionine, a methyl donor, with homocysteine generally induced hypomethylation in gene promoters. This decrease was similar in methionine dependent versus methionine independent cells. There was only a low level of pathway enrichment, suggesting that the hypomethylation is generic rather than gene specific. Whole proteome and transcriptome were also analyzed. This analysis revealed that contrarily to the effect on methylation, the replacement of methionine with homocysteine had a much greater effect on the transcriptome and proteome of methionine dependent cells than methionine independent cells. Interestingly, the methionine adenosyltransferase 2A (MAT2A), responsible for the synthesis of s-adenosylmethionine from methionine, was equally strongly upregulated in both cell lines. This suggests that the absence of methionine is equally detected but trigger different outcomesin methionine dependent versus independent cells. Our analysis reveals the importance of cell cycle control, DNA damage repair, translation, nutrient sensing, oxidative stress and tight junctions in the cellular response to methionine stress in melanoma.

2023-05-03 | GSE225944 | GEO

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