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Expression data from the liver of wild-type and Cnot3+/- mice: Fasted

ABSTRACT: 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. To examine the underlying mechanisms by which CNOT3 is involved in the control of metabolic balance, we compared the gene expression profiles of wild-type and Cnot3+/- mice using Affymetrix microarray technology. We chose to analyze the liver because the CNOT3 level in the liver was affected by the feeding condition and because the liver plays a major role in glucose and lipid metabolism. The livers were isolated from 12-week-old wild-type and Cnot3+/- mice (n = 2 for each genotype).

ORGANISM(S): Mus musculus

SUBMITTER: Masahiro Morita

PROVIDER: E-GEOD-18924 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from the liver of wild-type and Cnot3+/- mice: Fed vs Fasted

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

Expression data from the liver of wild-type and Cnot3+/- mice: Fasted

2011-12-09 | GSE18924 | GEO

Expression data from the liver of wild-type and Cnot3+/- mice: Fed vs Fasted

2011-12-09 | GSE18925 | GEO

Expression data from the liver of wild-type and Cnot3+/- mice

Project description:This SuperSeries is composed of the following subset Series: GSE18924: Expression data from the liver of wild-type and Cnot3+/- mice: Fasted GSE18925: Expression data from the liver of wild-type and Cnot3+/- mice: Fed vs Fasted Refer to individual Series

2011-12-09 | E-GEOD-18926 | biostudies-arrayexpress

Regulation of B cell early development by CNOT3

Project description:The CCR4-NOT complex, bearing poly(A) deadenylation activity, is a highly conserved regulator that is involved in biological control; however its action mechanisms and physiological targets remain unclear. Using genetic deletion of the CNOT3 subunit of this complex in early B cell progenitors, we show that CNOT3 plays a critical role in pro- to pre-B cell transition. CNOT3 participated in controlling germline transcription, compaction of the immunoglobulin heavy chain (Igh) locus, and Igh rearrangement, and in destabilizing tumor suppressor p53 mRNA. Moreover, by genetic ablation of p53 or introduction of pre-rearranged Igh transgene, the B cell developmental defect in the Cnot3 knockout background could be partly rescued, suggesting that CCR4-NOT complex exerts critical control in B cell differentiation processes by co-utilizing transcriptional and post-transcriptional mechanisms. Pro-B cells mRNA profiles of Mb1(cre/+) and Cnot3(fl/fl)Mb1(cre/+) mice were generated by deep sequencing using Illumina HiSeq 1500

2015-07-23 | E-GEOD-64455 | biostudies-arrayexpress

Gene expression profile of Cnot3(+/+) & Cnot3 (∆/∆) pro-B cells

Project description:To study the role Cnot3 in early B cells development, RNASeq analysis of pro-B cells (B220+ and CD43+) was performed in tamoxifen treated Cnot3(fl/fl) RERTCre and Cnot3+/+;RERTCre mice.

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Regulation of B cell early development by CNOT3

2015-07-23 | GSE64455 | GEO

Comparative proteomic study on liver lipid droplets and mitochondria from mouse housed in different temperatures

Project description:Laboratory mice are standardly housed around 23ºC, setting them under chronic cold stress. Metabolic changes of liver in mice housed under thermoneutral, standard and cold temperatures remain unknown. Here we isolated lipid droplets and mitochondria from their livers for comparative proteomic study to investigate the changes. According to proteomic analysis, mitochondrial TCA cycle and retinol metabolism were enhanced while oxidative phosphorylation was no obviously affected under cold condition, suggesting liver mitochondria may increase TCA cycle capacity in biosynthetic pathways as well as retinol metabolism to help liver to adapt. Based on proteomic and immunoblotting results, Perilipin 5 and major urinary proteins were increased significantly while mitochondrial pyruvate carrier was decreased dramatically under cold condition, indicating a role they may play.

2019-07-02 | PXD014224 | Pride

Transcriptome wide analysis of Cnot3 target mRNA in mouse hearts

Project description:Through RNA immunoprecipitation with anti-Cnot3 antiboy from mouse heart lysates and RNA-seq (Cnot3 RIP-seq) and gene ontology analyses, we show the comprehensive picute of cardiac Cnot3 target genes.

2018-08-31 | GSE103629 | GEO

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse

Project description:The conserved phosphoprotein MAF1 is the main known direct repressor of RNA polymerase III (Pol III). MAF1 is phosphorylated and inactivated by the nutrient-sensing TORC1 kinase, making MAF1 a nutrient effector for Pol III transcription. MAF1 has been associated with lipid metabolism in D. melanogaster, C. elegans, and the mouse. However, whereas downregulation of Maf1 generally increases lipogenesis, Maf1-/- mice are lean even under a High Fat (HF) diet. Here we compared Maf1-/- mice fed a Chow diet with mice lacking Maf1 specifically in hepatocytes (Maf1hep-/- mice) fed either a Chow or HF diet. Unlike Maf1-/- mice, Maf1hep-/- mice become slightly heavier than control mice at an old age and much earlier under a HF diet, with increased adiposity. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and subtle changes in protein accumulation that are consistent with increased lipogenesis. RNAseq and metabolite profiling indicate that liver phenotypes of Maf1-/- mice are strongly influenced by systemic inter-organ communication. Notable changes observed in the three phenotypically distinct cohorts include downregulation of Mouse Urinary Proteins, upregulation of Cyp2a4 expression, suggestive of an alteration of Growth Hormone levels or secretion pattern, and downregulation of Angiogenin, a phenomenon that might be directly linked to increased Pol III occupancy of tRNA genes in the main Angiogenin promoter region.

2023-11-28 | PXD040086 | Pride

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