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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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RNA-seq to identify the role of mRNA decay in mouse adipose tissues

ABSTRACT: The CCR4-NOT deadenylase complex has a critical function to trigger mRNA decay and various biological events. To understand roles of the complex in adipocyte function, we compare RNA expression between control and Cnot complex-deficient brown and white adipose tissues.

INSTRUMENT(S): Illumina HiSeq 2500

ORGANISM(S): Mus musculus

SUBMITTER: Toru Suzuki

PROVIDER: E-MTAB-8366 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The CCR4-NOT Deadenylase Complex Maintains Adipocyte Identity.

Takahashi Akinori A Takaoka Shohei S Kobori Shungo S Yamaguchi Tomokazu T Ferwati Sara S Kuba Keiji K Yamamoto Tadashi T Suzuki Toru T

International journal of molecular sciences 20191024 21

Shortening of poly(A) tails triggers mRNA degradation; hence, mRNA deadenylation regulates many biological events. In the present study, we generated mice lacking the Cnot1 gene, which encodes an essential scaffold subunit of the CCR4-NOT deadenylase complex in adipose tissues (Cnot1-AKO mice) and we examined the role of CCR4-NOT in adipocyte function. Cnot1-AKO mice showed reduced masses of white adipose tissue (WAT) and brown adipose tissue (BAT), indicating abnormal organ ...[more]

PMID: 31652943

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Roles of mRNA decay in liver development

Project description:mRNA decay machineries play important roles in various biological events. Among them, Cnot deadenylase complex has a critical function to trigger mRNA decay. To understand roles of the complex in liver development, we compare RNA expression between control and Cnot complex-deficient liver.

2019-02-01 | E-MTAB-7182 | biostudies-arrayexpress

Examination of mRNA decay rate in mature adipocytes

Project description:The CCR4-NOT deadenylase complex has a critical function to trigger mRNA decay and various biological events. To understand roles of the complex in adipocyte function, we compare mRNA half-lives between control and Cnot complex-deficient mature adipocytes from iWAT and BAT.

2019-10-24 | E-MTAB-8371 | biostudies-arrayexpress

RIP-seq of livers in C57BL/6J mice with antibodies against Cnot3, Ago2, and BRF1

Project description:Shortening of polyadenosine (poly(A)) tails (deadenylation) is the initial step in the decay of most mRNAs. The CCR4-NOT complex is the major deadenylase in mammals. Interaction of Cnot1 with RNA binding proteins, including the miRNA-induced silencing complex (miRISC), which includes Argonaute (Ago) and GW182 as core proteins, and the TTP family of AU-rich element (ARE)-binding proteins (TTP and BRF1/2), recruits the CCR4-NOT complex to the 3’-untranslated regions (3’-UTR) of mRNAs, leading to their degradation. This experiment aimed to determine the binding affinity of the CCR4-NOT complex, Ago2, and BRF1 with their target mRNAs in liver. Liver isolated from C57BL/6J wild-type mice at 8 weeks of age was solubilized in TNE buffer for 30 min at 4ºC. Lysate was incubated with antibodies against Cnot3, Ago2, and BRF1 for 1 hr at 4ºC, and then incubated with Dynabeads (Invitrogen) for 2 hr at 4ºC. mRNAs in immune complexes were isolated using Isogen II. 100 ng of total RNA was used for RNA-seq library preparation with TruSeq Stranded mRNA Library Prep Kit for NeoPrep. 150 base-pair pair-end read RNA-seq was performed with Hiseq 3000/4000 PE Cluster Kit and Hiseq 3000/4000 SBS Kit on Hiseq4000.

2020-03-30 | E-MTAB-6941 | biostudies-arrayexpress

ChIP-seq of livers in control and Cnot1 tamoxifen-inducible liver-specific knockout mice

Project description:Gene expression is balanced by transcription and mRNA degradation. Shortening of polyadenosine (poly(A)) tails (deadenylation) is the initial step in the decay of most mRNAs. However, the mechanism by which deadenylation controls mRNA expression is not fully understood. This experiment aimed to determine changes in transcriptional activity in livers of control and Cnot1 tamoxifen-inducible liver-specific knockout mice. Control and Cnot1 tamoxifen-inducible liver-specific knockout mice placed on tamoxifen-containing food at 6 weeks of age for 2 weeks. Lysates from livers were subjected to ChIP assay with Histone H3 (tri methyl K4) (H3K4me3) antibody (ab8580; abcam) using SimpleChIP Enzyatic Chromatin IP Kit (#9003; Cell Signaling Technology). Libraries for DNA sequence were prepared from DNA isolated by ChIP assays with a KAPA Hyper Prep Kit (Illumina). 109 base-pair pair-end read DNA-seq was performed with Hiseq PE Rapid Cluster Kit v2-HS and Hiseq Rapid SBS Kit v2-HS (200 Cycle) on Illumina Hiseq2500.

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RNA-seq of livers in control and Cnot1 tamoxifen-inducible liver-specific knockout mice

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2020-03-30 | E-MTAB-5901 | biostudies-arrayexpress

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

Examination of mRNA decay rate in mouse embryonic fibroblasts

Project description:The CCR4-NOT dedadenylase complex is essential for mRNA decay and various biological events.To understand roles of the complex in mouse embryonic fibroblasts, we compared mRNA half-lives between control and Cnot complex-deficient mouse embryonic fibroblasts

2020-01-29 | E-MTAB-8287 | biostudies-arrayexpress

Human Pumilio proteins directly bind the CCR4-NOT deadenylase complex to regulate the transcriptome

Project description:Pumilio paralogs, PUM1 and PUM2, are sequence-specific RNA-binding proteins that are essential for vertebrate development and neurological functions. PUM1&2 function to negatively regulate gene expression by accelerating degradation of specific mRNAs. Here, we determined the repression mechanism and impact of human PUM1&2 on the transcriptome. We identified subunits of the CCR4-NOT (CNOT) deadenylase complex required for stable interaction with PUM1&2 and to elicit CNOT-dependent repression. Isoform-level RNA sequencing revealed broad co-regulation of target mRNAs through the PUM-CNOT repression mechanism. Functional dissection of the domains of PUM1&2 identified a conserved N-terminal region that confers the predominant repressive activity via direct interaction with CNOT. In addition, we show that the DCP2 mRNA decapping enzyme has an important role in repression by PUM1&2 N-terminal regions. Our results support a molecular model of repression by human PUM1&2 via direct recruitment of CNOT deadenylation machinery in a decapping-dependent pathway.

2021-09-09 | GSE159510 | GEO

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

The CCR4-NOT complex contributes to repression of Major Histocompatibility Complex class II transcription

Project description:The multi-subunit CCR4 (carbon catabolite repressor 4)-NOT (Negative on TATA) complex serves as a central coordinator of all different steps of eukaryotic gene expression. Accordingly, members of the CCR4-NOT complex have been implicated in a variety of biological functions. Here we performed a systematic and comparative analysis of cells where the CCR4-NOT subunits CNOT1, CNOT2 or CNOT3 were individually downregulated using doxycycline-inducible shRNAs. Microarray experiments showed that downregulation of either CNOT subunit resulted in elevated expression of major histocompatibility complex class II (MHC II) target genes which are found in a gene cluster on chromosome 6. Increased expression of MHC II genes after knock-down or knock-out of CNOT subunits was seen in a variety of cell systems and also in naïve macrophages from CNOT3 conditional knock-out mice. CNOT2-mediated repression of MHC II genes occurred independent from the master regulator class II transactivator (CIITA) and detectable changes of the chromatin structure at the chromosomal MHC II locus. CNOT2 downregulation resulted in an increased de novo transcription of mRNAs and tethering of CNOT2 to a regulatory region governing MHC II expression resulted in dimished transcription. These results expand the known repertoire of CCR4-NOT members for immune regulation and identify CNOT proteins as a novel group of corepressors serving to restrict inappropriate or exaggerated class II expression, which can be causative for various diseases.

2017-03-15 | GSE90474 | GEO

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