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FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia

ABSTRACT: FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia

PROVIDER: PRJNA656759 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12435775_1.fastq.gz	Fastqsanger.gz
	SRR12435775_2.fastq.gz	Fastqsanger.gz
	SRR12435776_1.fastq.gz	Fastqsanger.gz
	SRR12435776_2.fastq.gz	Fastqsanger.gz
	SRR12435777_1.fastq.gz	Fastqsanger.gz

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FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia

Project description:Hematopoietic stem cells (HSC) activity is tightly controlled to ensure the integrity of the hematopoietic system during the organism’s lifetime. How the HSC compartment maintains its long-term fitness in condition of chronic stresses associated with systemic metabolic disorders is poorly understood. In this study, we show that obesity functionally affects the long-term function of the most immature engrafting HSC subpopulation. We link this altered regenerative activity to the oxidative stress and the aberrant constitutive activation of the AKT signaling pathway that characterized the obese environment. In contrast, we found minor disruptions of the HSC function in obese mice at steady state, suggesting that active mechanisms could protect the HSC compartment from its disturbed environment. Consistent with this idea, we found that FOXO proteins in HSCs isolated from obese mice become insensitive to their normal upstream regulators such as AKT, even during intense oxidative stress. We established that hyperglycemia, a key condition associated with obesity, is directly responsible for the alteration of the AKT-FOXO axis in HSCs and their abnormal oxidative stress response. As a consequence, we observed that HSCs isolated from a hyperglycemic environment display enhanced resistance to oxidative stress and DNA damage. Altogether, these results indicate that chronic metabolic stresses associated with obesity and/or hyperglycemia affect the wiring of the HSCs and modify their oxidative stress response. These data suggest that the uncoupling of FOXO to its environmental regulators could be a key adaptive strategy that promotes the survival of the HSC compartment in obesity.

2021-08-18 | GSE156085 | GEO

FOXO activity adaptation safeguards the hematopoietic stem cell compartment in hyperglycemia.

Project description:Hematopoietic stem cell (HSC) activity is tightly controlled to ensure the integrity of the hematopoietic system during the organism's lifetime. How the HSC compartment maintains its long-term fitness in conditions of chronic stresses associated with systemic metabolic disorders is poorly understood. In this study, we show that obesity functionally affects the long-term function of the most immature engrafting HSC subpopulation. We link this altered regenerative activity to the oxidative stress and the aberrant constitutive activation of the AKT signaling pathway that characterized the obese environment. In contrast, we found minor disruptions of the HSC function in obese mice at steady state, suggesting that active mechanisms could protect the HSC compartment from its disturbed environment. Consistent with this idea, we found that FOXO proteins in HSCs isolated from obese mice become insensitive to their normal upstream regulators such as AKT, even during intense oxidative stress. We established that hyperglycemia, a key condition associated with obesity, is directly responsible for the alteration of the AKT-FOXO axis in HSCs and their abnormal oxidative stress response. As a consequence, we observed that HSCs isolated from a hyperglycemic environment display enhanced resistance to oxidative stress and DNA damage. Altogether, these results indicate that chronic metabolic stresses associated with obesity and/or hyperglycemia affect the wiring of the HSCs and modify their oxidative stress response. These data suggest that the uncoupling of FOXO from its environmental regulators could be a key adaptive strategy that promotes the survival of the HSC compartment in obesity.

| S-EPMC7656925 | biostudies-literature

A phase separated active subnuclear compartment safeguards repressive chromatin domains [iCLIP]

Project description:A phase separated active subnuclear compartment safeguards repressive chromatin domains [iCLIP]

| PRJNA937859 | ENA

A phase separated active subnuclear compartment safeguards repressive chromatin domains [RNA-seq]

Project description:A phase separated active subnuclear compartment safeguards repressive chromatin domains [RNA-seq]

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [ChIP-seq]

Project description:A phase separated active subnuclear compartment safeguards repressive chromatin domains [ChIP-seq]

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A phase separated active subnuclear compartment safeguards repressive chromatin domains [TSA-seq]

Project description:A phase separated active subnuclear compartment safeguards repressive chromatin domains [TSA-seq]

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An RNA-dependent and phase-separated active subnuclear compartment safeguards repressive chromatin domains

Project description:An RNA-dependent and phase-separated active subnuclear compartment safeguards repressive chromatin domains

| PRJNA937858 | ENA

Foxo signaling declines with age

Project description:We performed RNA-seq for WT and foxo mutant flies, by combining with Dr. Baihua's foxo chip-seq data, we found 101 foxo-repressed and 300 foxo-activated genes. By analyzing expression change of these genes during age, we found foxo-repressed genes became activated, while foxo-activated genes became repressed, suggesting foxo signaling declines with age.

2018-11-14 | GSE122470 | GEO

daf-16/FoxO isoform-specific deletion mutants

Project description:FoxO transcription factors promote longevity across taxa. How they do so is poorly understood. In the nematode Caenorhabditis elegans, the A- and F-isoforms of the FoxO transcription factor DAF-16 extend life span in the context of reduced DAF-2 insulin-like growth factor receptor (IGFR) signaling. To elucidate the mechanistic basis for DAF-16/FoxO-dependent life span extension, we performed an integrative analysis of isoform-specific daf-16/FoxO mutants. In contrast to previous studies suggesting that DAF-16F plays a more prominent role in life span control than DAF-16A, isoform-specific daf-16/FoxO mutant phenotypes and whole transcriptome profiling revealed a predominant role for DAF-16A over DAF-16F in life span control, stress resistance, and target gene regulation. Integration of these data sets enabled the prioritization of a subset of 92 DAF-16/FoxO target genes for functional interrogation. Among 29 genes tested, two DAF-16A-specific target genes significantly influenced longevity. Our discovery of new longevity genes underscores the efficacy of our integrative strategy while providing a general framework for identifying specific downstream gene regulatory events that contribute substantially to transcription factor functions. As FoxO transcription factors have conserved functions in promoting longevity and may be dysregulated in aging-related diseases, these findings promise to illuminate fundamental principles underlying aging in animals. Whole-transcriptome profiling of daf-16/FoxO isoform-specific deletion mutants in the long-lived daf-2(e1370) background. Included are daf-16 wild-type, daf-16 null mutation, daf-16a/f mutation, two independent daf-16a mutations, and daf-16f mutation. N2 wild-type controls are also included.

2015-08-27 | E-GEOD-72426 | biostudies-arrayexpress

FOXO in mouse brain

Project description:Gene expression in FOXO KO vs WT brain

2018-02-13 | GSE102137 | GEO