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ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-seq and CUT&RUN)

ABSTRACT: ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-seq and CUT&RUN)

PROVIDER: PRJNA1009853 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25765200_1.fastq.gz	Fastqsanger.gz
	SRR25765200_2.fastq.gz	Fastqsanger.gz
	SRR25765201_1.fastq.gz	Fastqsanger.gz
	SRR25765201_2.fastq.gz	Fastqsanger.gz
	SRR25765202_1.fastq.gz	Fastqsanger.gz

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ACSS2 mediates an epigenetic pathway to regulate maternal β-cell adaptation and progression of gestational diabetes (ATAC-seq and CUT&RUN)

Project description:Maternal pancreatic β-cell state is adapted to accommodate gestation metabolism. Defects in this process may cause gestational diabetes mellitus (GDM), with risk factors including a high-calorie diet during pregnancy. However, the regulatory mechanism of maternal β-cell adaptation is largely unknown. Using single-cell transcriptome combining genetic analyses, we discovered a precise process of β-cell adaptation in mice which is associated with progression of metabolic stress-related β-cell dysfunction, increased acetyl-CoA biosynthesis, and gene element-specific histone acetylation. STAT3 recruits p300 to promote histone acetylation levels of pregnancy-associated genes, and Acetyl-CoA Synthetase 2 (ACSS2) enhances this process. High-fat feeding causes hyperacetylation of chromatin that is specifically opened during pregnancy, which results in overexpression of genes that impair β-cell functions and, consequently, hyperglycemia. However, these impairments can be rescued by β-cell-specific deletion of Acss2. Therefore, our study reveals a precise adaptation process in β-cells at the single-cell level during pregnancy and a specific epigenetic pathway that regulates this process. We also explain the epigenetic regulatory mechanism by which a high-fat diet can lead to GDM and identify ACSS2 as a potential molecular target for controlling the progression of GDM.

2025-01-26 | GSE241773 | GEO

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

Project description:Maternal pancreatic Beta-cell state is adapted to accommodate gestation metabolism. Defects in this process may cause gestational diabetes mellitus (GDM), with risk factors including a high-calorie diet during pregnancy. However, the regulatory mechanism of maternal Beta-cell adaptation is largely unknown. Using single-cell transcriptome combining genetic analyses, we discovered a precise process of Beta-cell adaptation in mice which is associated with progression of metabolic stress-related Beta-cell dysfunction, increased 40393969acetyl-CoA biosynthesis, and gene element-specific histone acetylation. STAT3 recruits p300 to promote histone acetylation levels of pregnancy-associated genes, and Acetyl-CoA Synthetase 2 (ACSS2) enhances this process. High-fat feeding causes hyperacetylation of chromatin that is specifically opened during pregnancy, which results in overexpression of genes that impair Beta-cell functions and, consequently, hyperglycemia. However, these impairments can be rescued by Beta-cell-specific deletion of Acss2. Therefore, our study reveals a precise adaptation process in Beta-cells at the single-cell level during pregnancy and a specific epigenetic pathway that regulates this process. We also explain the epigenetic regulatory mechanism by which a high-fat diet can lead to GDM and identify ACSS2 as a potential molecular target for controlling the progression of GDM.

2025-01-26 | GSE241770 | GEO

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

Project description:ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

| PRJNA1009847 | ENA

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

Project description:ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes (scRNA-Seq)

| PRJNA1009841 | ENA

ACSS2 mediates an epigenetic pathway to regulate maternal Beta-cell adaptation and progression of gestational diabetes

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

2025-01-26 | GSE241776 | GEO

Acetyl-CoA metabolism by ACSS2 regulates neuronal histone acetylation and long-term memory [RNA-seq]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and direct regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Global survey of gene expression in CAD cells and differentiated CAD neurons following lentiviral knockdown of ACSS2 or ATP citrate lyase (ACL) (and control = scramble hairpin); survey of hippocampal gene expression changes associated with retrieval of fear memory, after ACSS2-AAV knockdown or in EGFP-AAV control (comparison of 0h vs. 1h post-memory retrieval).

2017-05-01 | E-GEOD-76853 | biostudies-arrayexpress

Acetyl-CoA metabolism by ACSS2 regulates neuronal histone acetylation and long-term memory [ChIP-seq]

Project description:Metabolic production of acetyl-CoA has been linked to histone acetylation and gene regulation, however the mechanisms are largely unknown. We show that the metabolic enzyme acetyl-CoA synthetase 2 (ACSS2) is a critical and directchum regulator of histone acetylation in neurons and of long-term mammalian memory. We observe increased nuclear ACSS2 in differentiating neurons in vitro. Genome-wide, ACSS2 binding corresponds with increased histone acetylation and gene expression of key neuronal genes. These data indicate that ACSS2 functions as a chromatin-bound co-activator to increase local concentrations of acetyl-CoA and to locally promote histone acetylation for transcription of neuron-specific genes. Remarkably, in vivo attenuation of hippocampal ACSS2 expression in adult mice impairs long-term spatial memory, a cognitive process reliant on histone acetylation. ACSS2 reduction in hippocampus also leads to a defect in upregulation of key neuronal genes involved in memory. These results reveal a unique connection between cellular metabolism and neural plasticity, and establish a link between generation of acetyl-CoA and neuronal chromatin regulation. Genome-wide examination of histone H3 and H4 acetylation, as well as ACSS2 binding, in undifferentiated CAD cells and differentiated CAD neurons; background adjusted by H3 ChIP or Input.

2017-05-01 | E-GEOD-76850 | biostudies-arrayexpress

NRF2 deficiency leads to inadequate beta cell adaptation during pregnancy and gestational diabetes

Project description:The late stages of mammalian pregnancy are accompanied by a mild increase in insulin resistance likely due to enhanced glucose demand of the growing fetus. Therefore, as an adaptive process to maintain euglycemia during pregnancy, maternal β-cell mass expands leading to increased insulin release. Defects in functional β-cell adaptive expansion during pregnancy can lead to gestational diabetes mellitus (GDM). While the exact mechanisms that promote GDM are poorly understood, GDM is associated with inadequate functional β-cell mass expansion and with a systematic increase of oxidative stress. Here, we show that NRF2 levels are upregulated in mouse β-cells at gestational day 15 (GD15). Inducible β-cell-specific Nrf2 deleted (βNrf2KO) mice display reduced β-cell proliferation, increased β-cell oxidative stress and lipid peroxidation, compromised β-cell function, and elevated β-cell death, leading to impaired β-cell mass expansion and dysregulated glucose homeostasis towards the end of pregnancy. Importantly, the gestational hormone 17-β-estradiol (E2) increases NRF2 levels, and downregulation of NRF2 suppresses E2-induced protection of β-cells against oxidative stress, suggesting that E2 exerts its antioxidant effects through activation of NRF2 signaling in β-cells. Collectively, these data highlight the critical role of NRF2 in regulating oxidative stress during the adaptive response of β-cells in pregnancy and identify NRF2 as a potential therapeutic target for GDM treatment.

2025-03-07 | GSE289077 | GEO

Gestational diabetes and human amniocytes

Project description:Context: Context: Gestational diabetes (GDM) has profound effects on the intrauterine metabolic milieu and is linked to obesity and diabetes in offspring, but the mechanisms driving these effects remain largely unknown. Alterations gene expression in amniocytes exposed to GDM in utero may identify potential mechanisms leading to metabolic dysfunction later in life. Objective: Objective: To profile changes in the transcriptome in human amniocytes exposed to GDM Methods: A nested case-control study was performed in second trimeseter amniocytes matched for offspring sex, maternal race/ethnicity, maternal age, gestational age at amniocentesis, gestational age at birth and gestational diabetes status. Sex-specific RNA-sequencing was completed and gene expression changes were identified. Results: Expression of interferon-stimulated genes was increased in GDM amniocytes accounting for 6 of the top 10 altered genes (q<0.05). Enriched biological pathways in GDM anmiocytes included pathways involving inflammation, the interferon response, fatty liver disease, monogenic diabetes and atherosclerosis. Conclusion: In a unique repository of human amniocytes exposed to GDM in utero, trancriptome analysis identified enrichment of inflammation and interferon-related pathways.

2020-05-15 | GSE150621 | GEO

Gestational diabetes and human amniocytes

Project description:Gestational diabetes and human amniocytes

| PRJNA632929 | ENA