Mapping histone acylations in mouse liver
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE101597 | GEO | 2017/10/01
SECONDARY ACCESSION(S): PRJNA394911
REPOSITORIES: GEO
Similar Datasets
Project description:Transcriptome analysis and mapping histone acylations in fasted mouse livers
| PRJNA394910 | ENA
Project description:We report application of RNA-seq to quantify gene expression changes in fasted mouse livers compared to re-fed controls.
2017-10-01 | GSE101596 | GEO
Project description:Metabolic homeostasis in mammals critically depends on the regulation of fasting-induced genes by CREB in the liver. Previous genome-wide analysis has shown that only a small percentage of CREB target genes are induced in response to fasting-associated signaling pathways. The precise molecular mechanisms by which CREB specifically targets these genes in response to alternating hormonal cues remain to be elucidated. We performed chromatin immunoprecipitation coupled to high-throughput sequencing of CREB in livers from both fasted and re-fed mice. In order to quantitatively compare the extent of CREB-DNA interactions genome-wide between these two physiological conditions we developed a novel, robust analysis method, termed the ‘single sample independence’ (SSI) test that greatly reduced the number of false positive peaks. We found that CREB remains constitutively bound to its target genes in the liver regardless of the metabolic state. Integration of the CREB cistrome with expression microarrays of fasted and re-fed mouse livers and ChIP-seq data for additional transcription factors revealed that the gene expression switches between the fasted and fed states are associated with co-localization of additional transcription factors at CREB sites. Our results support a model in which CREB is constitutively bound to thousands of potential target genes and combinatorial interactions between DNA-binding factors are necessary to achieve the specific transcriptional response of the liver to fasting. Furthermore, our genome-wide analysis identifies thousands of novel CREB target genes in liver, including a previously unknown role for CREB in regulating ER stress genes in response to nutrient influx. Individual livers were collected from 24hr fasted and re-fed mice, with 4 biological replicates per condition. Extracted RNA was hybridized to Agilent two-color arrays, using randomly paired fasted/re-fed replicates.
2013-05-01 | E-GEOD-45731 | biostudies-arrayexpress
Project description:Metabolic homeostasis in mammals critically depends on the regulation of fasting-induced genes by CREB in the liver. Previous genome-wide analysis has shown that only a small percentage of CREB target genes are induced in response to fasting-associated signaling pathways. The precise molecular mechanisms by which CREB specifically targets these genes in response to alternating hormonal cues remain to be elucidated. We performed chromatin immunoprecipitation coupled to high-throughput sequencing of CREB in livers from both fasted and re-fed mice. In order to quantitatively compare the extent of CREB-DNA interactions genome-wide between these two physiological conditions we developed a novel, robust analysis method, termed the M-bM-^@M-^Xsingle sample independenceM-bM-^@M-^Y (SSI) test that greatly reduced the number of false positive peaks. We found that CREB remains constitutively bound to its target genes in the liver regardless of the metabolic state. Integration of the CREB cistrome with expression microarrays of fasted and re-fed mouse livers and ChIP-seq data for additional transcription factors revealed that the gene expression switches between the fasted and fed states are associated with co-localization of additional transcription factors at CREB sites. Our results support a model in which CREB is constitutively bound to thousands of potential target genes and combinatorial interactions between DNA-binding factors are necessary to achieve the specific transcriptional response of the liver to fasting. Furthermore, our genome-wide analysis identifies thousands of novel CREB target genes in liver, including a previously unknown role for CREB in regulating ER stress genes in response to nutrient influx. CREB ChIP-seq was performed on mouse liver from fasted and re-fed mice, using 5 separate biological replicates for each condition. GR and C/EBP(beta) ChIP-seq were performed as single replicates on ad-lib fed mice.
2013-05-01 | E-GEOD-45674 | biostudies-arrayexpress
Project description:To determine hepatic gene expression changes in fasted state, we employed the microarray analysis. We collected the livers from 8-weeks-old male WT and CREBH KO mice in both fasted and fed ad lib states.
2020-01-11 | GSE143420 | GEO
Project description:We report the RNA-Sequencing data for the livers of C57BL/6J mice fed ad libitum or were fasted for 16 hour.
2021-02-26 | GSE159038 | GEO
Project description:Delayed access to feed following hatching has been associated with reduction in growth performance in chicks. However, the gene networks within the hypothalamus that regulate feed intake and metabolism, and the effects of fasting on those pathways are not well understood. The present experiment evaluated global hypothalamic gene expression in neonatal chicks using the Arizona Gallus gallus 20.7K Oligo Array v1.0 to elucidate genes and pathways regulated by feeding, fasting, and refeeding. Ten groups of chicks were sampled over four days post-hatch, including: control (at hatch), 24h fed, 24h fasted, 48h fed, 48h fasted, 48h fasted then 4h refed, 72h fed, 48h fasted then 24h refed, 96h fed, and 48h fasted then 48h refed. Non-esterified fatty acids were elevated, and triglycerides were decreased in fasted chicks at 24 and 48h, indicating that fasting induced physiological changes. Hypothalamic samples were collected from 16 chicks per group, and total RNA was extracted and pooled for hybridization (n=4). Expression patterns of selected genes were confirmed by quantitative real-time PCR. Two-fold differences in gene expression were detected in 1,272 genes between treatment groups, and of those, 119 genes were significantly (P<0.05) different. Assignment of gene ontology terms to the significant genes resulted in 34 different categories of biological processes, with 24% of genes participating in signal transduction, transport, or metabolic processes. Genes that were upregulated during fasting (and confirmed by qPCR) include FK506BP51, which is involved in the formation of steroid receptor complexes, and deiodinase type II, which is responsible for converting the thyroid hormone T4 into T3. Confirmed genes, downregulated due to fasting, included proopiomelanocortin and fatty acid binding protein 7. Other regulated genes were identified that play a role in feeding and obesity in other species, such as relaxin 3 and adrenergic receptor-β2. Further analysis of differentially regulated genes could provide new information regarding the role of the hypothalamus in feed intake and metabolism. Keywords: Metabolic perturbation
2008-10-18 | GSE13257 | GEO
Project description:Spatial heterogeneity and plasticity of the mammalian liver is critical for systemic metabolic homeostasis in response to fluctuating nutritional status. Here, we generated a high-resolution transcriptomic landscape of the livers from mice that were either fed chow (fed), fasted for 18 h (fasted), or fasted for 18 h and then refed for 6 h (refed) using spatial transcriptomics (ST) and quantified changes in gene expression. This work provides a critical foundation for future mechanistic studies of liver metabolic heterogeneity and plasticity, and will help to understand the zonated pathology during liver disease progression.
2023-01-12 | GSE222796 | GEO
Project description:Decay of mRNAs initiates with shortening of the poly(A) tail. Although the CCR4-NOT complex participates in deadenylation, how it becomes activates remain obscure. We show that complete deficiency in CNOT3, subunit 3 of this complex, is lethal in mice, but that heterozygotes survive as lean mice with hepatic and adipose tissues containing reduced lipid levels. Cnot3+/- mice have enhanced metabolic rates and remain lean on high-fat diets. We further provide evidence suggesting that CNOT3, by changing its level in response to feeding conditions, affects the activity of the CCR4-NOT deadenylase against poly(A) tails of specific mRNAs coding for proteins involved in metabolism of carbohydrates and fats. Because the levels of CNOT3 protein were decreased under fasting conditions and increased upon refeeding and because CNOT3 could be a positive regulator of the CCR4-NOT deadenylase, we hypothesized that the levels of CCR4-NOT target mRNAs would be lower in fed mice than in fasted mice. We compared the gene expression profiles of fed and fasted wild-type mice. Microarray analysis revealed that approximately 1,200 mRNA transcripts were down-regulated in the livers of fed mice. Of these mRNAs, 68 corresponded to the genes up-regulated in the livers of Cnot3+/- mice and fasted wild-type mice. A large number of the 68 identified genes encoded proteins involved in metabolism, especially lipid metabolism and growth. The livers were isolated from 8-week-old fed wild-type, fasted wild-type and fasted Cnot3+/- mice (n = 2 for each genotype).
2011-12-09 | E-GEOD-18925 | biostudies-arrayexpress
Project description:Metabolic homeostasis in mammals critically depends on the regulation of fasting-induced genes by CREB in the liver. Previous genome-wide analysis has shown that only a small percentage of CREB target genes are induced in response to fasting-associated signaling pathways. The precise molecular mechanisms by which CREB specifically targets these genes in response to alternating hormonal cues remain to be elucidated. We performed chromatin immunoprecipitation coupled to high-throughput sequencing of CREB in livers from both fasted and re-fed mice. In order to quantitatively compare the extent of CREB-DNA interactions genome-wide between these two physiological conditions we developed a novel, robust analysis method, termed the ‘single sample independence’ (SSI) test that greatly reduced the number of false positive peaks. We found that CREB remains constitutively bound to its target genes in the liver regardless of the metabolic state. Integration of the CREB cistrome with expression microarrays of fasted and re-fed mouse livers and ChIP-seq data for additional transcription factors revealed that the gene expression switches between the fasted and fed states are associated with co-localization of additional transcription factors at CREB sites. Our results support a model in which CREB is constitutively bound to thousands of potential target genes and combinatorial interactions between DNA-binding factors are necessary to achieve the specific transcriptional response of the liver to fasting. Furthermore, our genome-wide analysis identifies thousands of novel CREB target genes in liver, including a previously unknown role for CREB in regulating ER stress genes in response to nutrient influx.
2013-05-01 | GSE45731 | GEO