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Nutrient deprivation elicits a transcriptional and translational inflammatory response coupled to decreased protein synthesis

ABSTRACT: Nutrient deprivation elicits a transcriptional and translational inflammatory response coupled to decreased protein synthesis

PROVIDER: PRJNA472636 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7207260.fastq.gz	Fastqsanger.gz
	SRR7207270.fastq.gz	Fastqsanger.gz
	SRR7207280.fastq.gz	Fastqsanger.gz
	SRR7207290.fastq.gz	Fastqsanger.gz
	SRR7207300.fastq.gz	Fastqsanger.gz

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Nutrient deprivation elicits a transcriptional and translational inflammatory response coupled to decreased protein synthesis

Project description:Purpose: The goal of this study is to examine gene expression regulation at the transcriptional and translational levels in response to various forms of nutrient deprivation, and whether there are differences between isogenic transformed and non-transformed cells. Mehods: We apply high-throughput sequencing of ribosome footprints (ribosome profiling) and poly(A) RNA (RNA sequencing) in an isogenic pair of transformed (tamoxifen-treated) and non-transformed (ethanol control) MCF10A-ER-Src cells subjected to the metabolic stresses that differentially affect global protein synthesis (Figure 1): deprivation of glutamine (for 30min and 4 hours), glucose (4hours), cysteine/cystine (4hours) or leucine/isoleucine/valine (brach-chain aminoacids - BCAA) (4hours). The same experiments were also performed in transformed ER-Src MCF10A treated with torin1 (500nM) for 4 hours. Results: Genome-wide translational profiling of glutamine deprived ER-Src MCF10A cells (for 30 minutes) shows increased translation of uORFs-containing mRNAs and down-regulation of ribosomal protein mRNAs, which is followed by increased translation and transcription of cytokine and inflammatory mRNAs (after 4 hours of glutamine deprivation). The transcription and translation of inflammatory and cytokine mRNAs is also stimulated in response to 4 hours deprivation of glucose, cysteine/cystine and BCAA, with the extent of stimulation correlating with the i) decrease in global protein synthesis and ii) down-regulation of all translationally-repressed mRNAs or ribosomal protein mRNAs. Conclusions: Pro-inflammatory gene expression is associated with translational repression in response to short-term nutrient deprivation.

2018-07-01 | GSE114794 | GEO

Nutrient Deprivation Elicits a Transcriptional and Translational Inflammatory Response Coupled to Decreased Protein Synthesis.

Project description:Nutrient deprivation inhibits mRNA translation through mTOR and eIF2α signaling, but it is unclear how the translational program is controlled to reflect the degree of a metabolic stress. In a model of breast cellular transformation, various forms of nutrient deprivation differentially affect the rate of protein synthesis and its recovery over time. Genome-wide translational profiling of glutamine-deprived cells reveals a rapid upregulation of mRNAs containing uORFs and downregulation of ribosomal protein mRNAs, which are followed by selective translation of cytokine and inflammatory mRNAs. Transcription and translation of inflammatory and cytokine genes are stimulated in response to diverse metabolic stresses and depend on eIF2α phosphorylation, with the extent of stimulation correlating with the decrease in global protein synthesis. In accord with the inflammatory stimulus, glutamine deprivation stimulates the migration of transformed cells. Thus, pro-inflammatory gene expression is coupled to metabolic stress, and this can affect cancer cell behavior upon nutrient limitation.

| S-EPMC6419098 | biostudies-literature

Molecular mechanism of mice embryonic diapause induction by nutrient deprivation

Project description:To thoroughly characterize the diapaused blastocyst induced by ovariectomy, maternal starvation, and nutrient deprivation, we executed RNA-sequencing analyses for ND blastocysts at E4.5, DIA, Sta, K-PC, and K+0.02 blastocysts at E5.5.

2022-12-18 | GSE220804 | GEO

Transcriptomic profiling of human HAP1 cells before and after nutrient deprivation

Project description:Autophagy is a lysosomal degradation pathway critical for maintaining cellular homeostasis and viability, and is predominantly regarded as a rapid and dynamic cytoplasmic process. To improve our understanding of the transcriptional and epigenetic events associated with autophagy, we performed genome-wide transcriptomic and epigenomic profiling after nutrient deprivation in human wildtype and autophagy-deficient cells. We observed that nutrient deprivation leads to the transcriptional induction of numerous autophagy-associated genes. These transcriptional changes are reflected at the epigenetic level (H3K4me3, H3K27ac, and H3K56ac) and are independent of autophagic flux.

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Epigenetic profiling of human HAP1 cells before and after nutrient deprivation

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Human HAP1 cells before and after nutrient deprivation

Project description:Human HAP1 cells before and after nutrient deprivation

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The effect of nutrient deprivation on early life small intestine mucosal microbiome and host proteome

Project description:Nutrition has a vital role in shaping the intestinal microbiome. The impact of nutrients and the consequences of enteral deprivation on the small intestinal mucosal microbiota, specifically in early life, has not been well described. Our aim was to study the impact of enteral deprivation on the small intestine mucosal microbiome and to search for factors that shape this interaction in early life. Host seem to be the most dominant factor in the structure of the early life mucosal microbial small intestine community. Under conditions of nutrient deprivation, there are specific changes in host proteomics. Further research is needed to better define and understand this host-microbe-nutrition interaction in the small intestine.

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Transcriptional profiling of mouse pancreatic tumor cells under nutrient and oxygen deprivation condition

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Transcriptional profiling of human pancreatic tumor cells under nutrient and oxygen deprivation condition

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Transcriptomic changes in C3H10T1/2 cells exposed to lipid deprivation

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