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Genome wide H3K9ac and SAGA occupancy at OX growth phase and RC quiescent phase of yeast metabolic cycle

ABSTRACT: We found acetyl-CoA levels increase when cells are committed to growth. We also found 3 components of the SAGA complex, Spt7p, Sgf73p and Ada3p as well as histones are dynamically acetylated in tune with the acetyl-CoA levels. ChIP-seq study reveals SAGA and H3K9ac predominantly occupy growth genes at the OX growth phase of the yeast metabolic cycle indicating acetyl-CoA levels may drive growth gene transcription program through acetylation of these proteins. Examination of H3K9ac and SAGA binding over two timepoints using H3 and Input as controls

ORGANISM(S): Saccharomyces cerevisiae

SUBMITTER: Ling Cai

PROVIDER: E-GEOD-28734 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Acetyl-CoA induces cell growth and proliferation by promoting the acetylation of histones at growth genes.

Cai Ling L Sutter Benjamin M BM Li Bing B Tu Benjamin P BP

Molecular cell 20110501 4

The decision by a cell to enter a round of growth and division must be intimately coordinated with nutrient availability and its metabolic state. These metabolic and nutritional requirements, and the mechanisms by which they induce cell growth and proliferation, remain poorly understood. Herein, we report that acetyl-CoA is the downstream metabolite of carbon sources that represents a critical metabolic signal for growth and proliferation. Upon entry into growth, intracellular acetyl-CoA levels ...[more]

PMID: 21596309

Similar Datasets

Genome wide H3K9ac and SAGA occupancy at OX growth phase and RC quiescent phase of yeast metabolic cycle

Project description:We found acetyl-CoA levels increase when cells are committed to growth. We also found 3 components of the SAGA complex, Spt7p, Sgf73p and Ada3p as well as histones are dynamically acetylated in tune with the acetyl-CoA levels. ChIP-seq study reveals SAGA and H3K9ac predominantly occupy growth genes at the OX growth phase of the yeast metabolic cycle indicating acetyl-CoA levels may drive growth gene transcription program through acetylation of these proteins.

2011-05-19 | GSE28734 | GEO

A high-resolution view of transcription and chromatin states across distinct metabolic states in budding yeast

Project description:Under continuous, glucose-limited conditions, budding yeast exhibit robust metabolic cycles associated with major oscillations of gene expression and metabolic state. However, how such fluctuations might be coordinately linked to changes in chromatin status is less well understood. Here, we examine the correlated genome-wide transcription and chromatin states across the yeast metabolic cycle (YMC) at unprecedented temporal resolution, revealing a "just in time supply chain" by which specific cellular processes such as ribosome biogenesis are coordinated in time with remarkable precision. We identify distinct chromatin and splicing patterns associated with different gene categories and determine the relative timing of chromatin modifications to maximal transcription. Additionally, we interrogate chromatin modifier occupancy and observe subtly distinct spatial and temporal patterns compared to the modifications themselves. Furthermore, we identify multiple lysine mutants in H3 or H4 tails that disrupt metabolic cycling, supporting a potentially cooperative role of histone modifications in the YMC. 16 time points RNA-seq and ChIP-seq of 8 histone marks over one metabolic cycle, 14 time points ChIP-seq of 3 chromatin modifiers over one metabolic cycle

2014-08-31 | E-GEOD-52339 | biostudies-arrayexpress

Glucose Starvation Induces a Switch in the Histone Acetylome for Activation of Gluconeogenic and Fat Metabolism Genes [RNA-seq]

Project description:Acetyl-CoA is a key intermediate in metabolism situated at the intersection of many metabolic pathways. The reliance of histone acetylation on acetyl-CoA enables gene expression to be coordinated with metabolic state. Previous studies have linked abundant histone acetylation to activation of genes involved in cell growth or tumorigenesis. However, under glucose starvation, the extent to which histone acetylation is important for gene expression remains poorly understood. Here, we use a yeast starvation model to unravel a dramatic alteration in global occupancy of histone acetylation following carbon starvation. We observe a shift in the location of histone acetylation marks from growth-promoting genes to genes required for gluconeogenesis and fat metabolism. This switch is mediated by both the histone deacetylase Rpd3 and the Gcn5p/SAGA acetyltransferase. Our findings reveal a striking specificity for histone acetylation in promoting pathways that generate acetyl-CoA for oxidation when intracellular acetyl-CoA is limiting .

2022-01-06 | GSE178160 | GEO

Glucose Starvation Induces a Switch in the Histone Acetylome for Activation of Gluconeogenic and Fat Metabolism Genes [ChIP-seq]

2022-01-06 | GSE178159 | GEO

RNA-sequencing analysis of glucose and acetate regulated transcripts in glioblastoma cells

Project description:Our studies indicate that glucose and acetate can regulate histone acetylation by altering the acetyl-CoA concentrations in the cell. The purpose of this study was to to determine whether specific gene sets correlated with acetyl-CoA availability. We conclude that 10% of glucose-regulated genes are acetyl-CoA regulated genes (genes suppressed or induced by low glucose and reversed by acetate). Acetate usually regulated gene expression in the same direction as glucose, suggesting that acetyl-CoA is a key mediator of glucose-dependent gene expression. The experiments were performed in quadruplicates for each condition with a total of 12 samples

2014-08-05 | E-GEOD-57488 | biostudies-arrayexpress

Ethylamine versus succinate cells of Methylobacterium extorquens

Project description:In order to provide global information on gene expression during growth on C2 compounds, microarray analysis of M. extorquens AM1 cells was carried out, comparing ethylamine-grown cells to succinate-grown cells. This comparison has confirmed previous observations on the inducible nature of some of the enzymes involved in C2 metabolism, such as methylamine (and ethylamine) utilization system (mau), putative enzymes for converting acetaldehyde into acetate and acetyl-CoA, and enzymes of the ethylmalonyl-CoA pathway that has been proposed to operate for assimilation of acetyl-CoA into cell biomass. RNA from ethylamine-grown cells was compared to RNA from succinate-grown cells. Four biological replicates were carried out.

2010-05-14 | E-GEOD-20365 | 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

Chromatin immunoprecipitation of human Hela cells grown under serum starved condtions to identify new targets genes for ETS-domain transcription factor Elk-1

Project description:Chromatin immunoprecipitation coupled with microarray analysis (ChIP-chip) was carried out to identify new target genes for ETS-domain transcription factor Elk-1. Experiment was done in Hela cells under serum starved conditions.

2009-08-11 | E-MEXP-1527 | biostudies-arrayexpress

Chromatin immunoprecipitation of human HeLa cells grown under serum starved conditions to identify new target genes for ETS-domain transcription factor Elk-1

2009-08-11 | E-MEXP-2084 | biostudies-arrayexpress

Exercise prevents substrate overload of liver mitochondria by modification of the compensatory responses during chronic overnutrition

Project description:Exercise training is a potent treatment of NAFLD and hepatic insulin resistance. Here we provide molecular information about the hepatic mitochondrial metabolism in mice when chronic overnutrition (high-energy diet (HED) for 6 weeks) is combined with exercise training. Training reduced the hepatic triacylglycerol content, fasting insulin, and reversed glucose intolerance. Training modified the hepatic mitochondrial proteome with a decrease in enzymes related to pyruvate metabolism and entry of acetyl-CoA into the TCA cycle. Transcriptome data revealed down-regulation of glucose oxidation and lipogenesis. The mitochondrial respiratory capacity of trained HED-fed mice is increased despite reduced content of complex I. Training decreased diacylglycerol species and JNK phosphorylation, both of which can induce insulin resistance. Increased mitochondrial mass and oxidative capacity of the trained muscle further unburdens the liver from substrate overload. Together, when high fat and carbohydrate intake in mice is accompanied by exercise, the decline of mitochondrial function and insulin resistance can be prevented by modification of mitochondrial acetyl-CoA metabolism.

2022-02-16 | PXD024308 | Pride

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