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Expression data from 4-week-old mouse liver

ABSTRACT: mRNA degradation critically contributes to liver development and function. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify deregulated genes in the livers lacking CNOT3, a core subunit of the CCR4-NOT complex.

ORGANISM(S): Mus musculus

PROVIDER: GSE114508 | GEO | 2019/02/21

REPOSITORIES: GEO

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Expression data from 1-week-old mouse liver

Project description:mRNA degradation critically contributes to liver development and function. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify deregulated genes in the livers lacking CNOT3, a core subunit of the CCR4-NOT complex.

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Expression data from embryonic day 16.5 or postnatal day 3 mouse liver

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Expression data from mouse white adipose tissue lacking CNOT3, a core subunit of the CCR4-NOT complex

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Expression data from mouse embryonic fibroblasts

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Expression data from mouse embryonic fibroblasts

Project description:In addition to transcriptional regulation, mRNA degradation critically contributes to gene expression as shown by various biological analysis. The CCR4-NOT complex serves as a major deadenylase that initiates mRNA degradation. We used microarrays to identify CCR4-NOT targets by searching for genes specifically stablized in the absence of CNOT3, a core subunit of the CCR4-NOT complex. Primary mouse embryonic fibroblasts (MEFs) were used for RNA extraction and hybridization on Affymetrix microarrays. CNOT3-knockdown MEFs were generated by Cre-mediated somatic recombination. We treated both control and CNOT-knockdown (CNOT3KD) MEFs with a transcriptional inhibitor, actinomycin D to focus on a stability of mRNAs.

2015-09-01 | E-GEOD-67418 | biostudies-arrayexpress

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).

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Expression data from A549 human lung adenocarcinoma cells with and without knockdown against CNOT3

Project description:The physiological importance of mRNA degradation through the CCR4-NOT deadenylase has recently been highlighted. For example, mutation in CNOT3, a gene coding for sCNOT3 subunit of the CCR4-NOT complex, is found to be associated with T-cell acute lymphoblastic leukemia, T-ALL, though its contribution to other cancers has not been reported. To identify the taget mRNAs of CNOT3 in human non-small cell lung cancer (NSCLC), we performed the microarray analysis using A549 cells with and without knockdown against CNOT3.

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

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Cnot3-dependent mRNA deadenylation safeguards the pluripotent state

Project description:Poly(A)-tail length and mRNA deadenylation play important roles in post-transcriptional gene regulation. Here, we report the regulation of mRNA expression, half-life, and polysome association in mouse embryonic stem cells by the Cnot3 subunit in the Ccr4-Not mRNA deadenylase complex.

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