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Homo sapiens

ABSTRACT: Histone demethylation and c-MYC activation enhance translational capacity in response to amino acid restriction [ChIP-seq]

PROVIDER: PRJNA391384 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR5725120.fastq.gz	Fastqsanger.gz
	SRR5725130.fastq.gz	Fastqsanger.gz
	SRR5725121.fastq.gz	Fastqsanger.gz
	SRR5725131.fastq.gz	Fastqsanger.gz
	SRR5725122.fastq.gz	Fastqsanger.gz

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Histone demethylation and MYC activation enhance translational capacity in response to amino acid restriction

Project description:Histone demethylation and MYC activation enhance translational capacity in response to amino acid restriction

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Project description:Histone demethylation and c-MYC activation enhance translational capacity in response to amino acid restriction [RNA-seq]

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Coordinated Histone Methylation Loss and MYC Activation Promote Translational Capacity Under Amino Acid Restriction

Project description:Coordinated Histone Methylation Loss and MYC Activation Promote Translational Capacity Under Amino Acid Restriction

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Coordinated Histone Methylation Loss and MYC Activation Promote Translational Capacity Under Amino Acid Restriction

Project description:Epigenetic mechanisms underlying cellular adaptation to and recovery from nutrient deficiency are incompletely understood. Here, we report an adaptive epigenetic response to amino acid (AA) restriction that primes cells for rapid recovery. Depriving human cells of AAs led to selective loss of histone H4 lysine 20 monomethylation (H4K20me1) from gene bodies and increased MYC binding at promoters genome-wide, with strongest effects at ribosomal protein and translation initiation genes. Although AA restriction reduced overall protein synthesis, it was accompanied by increased translational capacity through upregulation of protein synthesis genes and accumulation of monomeric ribosomes. Combined SETD8, the H4K20 methyltransferase, depletion and MYC over-expression in nutrient-rich media was necessary and sufficient to recapitulate the transcriptional and functional effects of AA restriction. These findings suggest that cells respond to AA deprivation through coordinated chromatin and transcriptional changes that anticipate nutrient restoration and promote rapid recovery of protein synthesis when AAs are replenished.

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Effect of folic acid deprivation on H3K27me3 and H3K9me2 upon OTX treatment

Project description:Deciphering the impact of metabolic intervention on response to anticancer therapy represents a path toward improved clinical responses. Here, we identify amino acid-related pathways connected to the folate cycle whose activation predicts sensitivity to MYC-targeting therapies in acute myeloid leukemia (AML). We establish that folate restriction and deficiency of the rate-limiting folate-cycle enzyme, MTHFR ― which exhibits reduced-function polymorphisms in about 10% of Caucasians ― enhance resistance to MYC targeting by BET and CDK7 inhibitors in cell lines, primary patient samples and syngeneic mouse models of AML. Further, this effect is abrogated by supplementation with the MTHFR enzymatic product, CH3-THF. Mechanistically, folate cycle disturbance reduces H3K27/K9 histone methylation, and activates a SPI1 transcriptional program counteracting the effect of BET inhibition. Our data provide a rationale for screening MTHFR polymorphisms and the folate cycle status to exclude patients least likely and nominate those most likely to benefit from MYC-targeting therapies.

2020-10-12 | GSE152440 | GEO

Effect of folic acid deprivation on on transcriptome upon OTX treatment

2020-10-12 | GSE152441 | GEO

Histone demethylation and c-MYC activation enhance translational capacity in response to amino acid restriction [ChIP-seq]

Project description:Nutrient limitation may elicit adaptive epigenetic changes but the nature and mechanisms of the cellular response to specific nutrient deficiencies are incompletely understood. We report that depriving human cells of amino acids (AAs) induces specific loss of H4K20me1 from gene bodies and elevated binding of c-MYC at promoters genome-wide. These effects are most pronounced at ribosomal protein and translation initiation genes, which are upregulated, leading to enhanced protein synthetic capacity. Combination of H4K20 methyltransferase depletion and c-MYC over-expression in rich media is required and sufficient to recapitulate the effects of AA restriction. Our data reveal an unexpected and epigenetically implemented increase in translational capacity when AAs are limiting, likely to safeguard the proteome by making effective use of limited resources.

2024-12-31 | GSE100302 | GEO

Histone demethylation and c-MYC activation enhance translational capacity in response to amino acid restriction [RNA-seq]

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Disrupting the Myc-Tfeb circuit confers vulnerabilities targeting amino acid homeostasis and provokes metabolic anergy

Project description:Metabolic reprogramming sustains cancer cell anabolism, and MYC oncoproteins control many aspects of this response. Normal cells adapt to nutrient-limiting conditions by activating autophagy, which is required for amino acid (AA) homeostasis. Surprisingly, here we report the autophagy-lysosomal pathway is suppressed by Myc in normal B cells, in premalignant and neoplastic B cells of Eµ-Myc transgenic mice, and in MYC-driven human Burkitt lymphoma. Myc suppresses autophagy by antagonizing expression and function of TFEB, a master regulator of autophagy/lysosome genes. Notably, compensatory mechanisms that sustain AA pools in MYC-expressing B cells include marked increases in AA transport and coordinate induction of the proteasome. Finally, reactivation of the autophagy-lysosomal pathway by constitutively active TFEB disables the malignant state, by perturbing mitochondrial functions and disrupting proteasome activity, amino acid transport, and disrupts amino acid and nucleotide metabolism, leading to growth arrest and apoptosis. This scenario provides therapeutic opportunities that disable MYC-driven tumorigenesis, including AA restriction and treatment with proteasome inhibitors.

2022-02-27 | GSE153570 | GEO

Translational Regulation of Metabolic Dynamics during Effector-Triggered Immunity

Project description:It is not fully known whether translational regulation also occurs in later stage immune responses, such as effector-triggered immunity (ETI), which often leads to strong metabolic dynamics. In this study, we performed a genome-wide ribosome profiling in Arabidopsis upon ETI activation and discovered that specific groups of genes were translationally regulated, especially metabolic genes in aromatic amino acid, phenylpropanoid, camalexin, and sphingolipid metabolism. The involvement of these components in the induction of ETI was confirmed by genetic analysis, amino acid profiling and exogeneous application of phenylalanine or an inhibitor of aromatic amino acid biosynthesis. Our findings provide new insight into the diverse translational regulation in the plant immune responses and demonstrate that translational coordination of metabolic gene expression is an important strategy for ETI activation.

2020-12-16 | GSE124115 | GEO

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