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Adipocyte RNA-binding protein CELF1 promotes beiging of white fat through stabilizing Dio2 mRNA

ABSTRACT: Adipocyte RNA-binding protein CELF1 promotes beiging of white fat through stabilizing Dio2 mRNA

PROVIDER: PRJNA1263392 | ENA |

REPOSITORIES: ENA

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Adipocyte RNA-binding protein CELF1 promotes beiging of white fat through stabilizing Dio2 mRNA

Project description:RNA-binding proteins (RBPs) regulate diverse cellular processes at post-transcriptional level and play roles in adipocyte development. However, their involvement in the beiging of white fat remains unclear. Here we screened RBPs in inguinal adipose tissues in response to cold stimulation and identified CUG-BP Elav-like family member 1 (CELF1) as a novel regulator that promotes white fat beiging. Adipocyte-specific Celf1 deficiency impairs cold-induced beiging and reduces energy expenditure. Mechanistically, RNA immunoprecipitation RNA-seq (RIP-seq) and functional experiments revealed that CELF1 stabilizes the mRNA of the key thermogenic regulator Dio2 by binding to its 3'UTR, thereby promoting local triiodothyronine (T3) production. CELF1 augments isoproterenol-induced activation of beige adipocytes and increases mitochondria respiration capacity in vitro, and CELF1 overexpression ameliorates diet-induced obesity and metabolic dysfunction. Hence, our study identifies CELF1 as a physiological regulator of metabolic stress in activating thermogenesis and promoting energy expenditure at the post-transcriptional level, suggesting that targeting CELF1 to locally increase the T3 production may serve as a promising therapeutic strategy for combating obesity and related metabolic disorders.

2025-07-05 | GSE297248 | GEO

mRNA profiles of Celf1fl/fl and adipocyte-specific Celf1 deficiency (Celf1fl/fl AKO) in iWAT after acute cold stimulation

Project description:RNA-seq reveals the critical role of adipocyte Celf1 in cold-responsive thermogenic remodeling in inguinal white adipose tissue (iWAT). The cold-induced thermogenic program in iWAT was severely blunted in Celf1AKO mice, especially the obvious downregulation of Ucp1, Dio2, Elvol3, Tbx1, Cox7a1, and Cidea genes. The GO analysis revealed that the down-regulated genes were primarily involved in adaptive thermogenesis, temperature homeostasis, and mitochondrial-related processes, including lipid oxidation, fatty acid metabolism and so on. KEGG pathway analysis further showed that these down-regulated genes were involved in thermogenesis-related pathways, including thermogenesis, PPAR signaling, metabolic pathways, fatty acid degradation, and AMPK signaling. Together, these results suggest that adipocyte Celf1 deficiency impairs cold-induced iWAT thermogenic program.

2025-07-05 | GSE281771 | GEO

Adipocyte YTH N(6)-methyladenosine RNA-binding protein 1 protects against obesity by promoting white adipose tissue beiging in male mice

Project description:Obesity, one of the most serious public health issues, is caused by energy imbalance of energy intake and expenditure. N(6)-methyladenosine (m6A) RNA modification has been recently identified as a key regulator of obesity, while the detailed mechanism is elusive. Here, we found that YTH RNA binding protein 1 (YTHDF1), an m6A reader, acts as an essential regulator of white adipose tissue metabolism. The expression of YTHDF1 decreased in adipose tissue of mice fed a high-fat diet. Adipocyte-specific Ythdf1 deficiency exacerbated obesity-induced metabolic defects and inhibited beiging of inguinal white adipose tissue (iWAT) in mice. By contrast, mice with WAT-specific Ythdf1 overexpression were resistant to obesity and showed promotion of beiging. Mechanistically, YTHDF1 regulated the translation of diverse m6A-modified mRNAs. In particular, YTHDF1 facilitated the translation of bone morphogenetic protein 8b (Bmp8b) in an m6A-dependent manner to induce the beiging process. Together, these findings suggested that YTHDF1 may be an attractive therapeutic target for the management of obesity-associated diseases.

2023-02-02 | GSE197173 | GEO

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity

Project description:HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity

| PRJNA796298 | ENA

METTL3-mediated Klf9 mRNA stabilization contributes to white adipose tissue beiging

Project description:The induction of beige adipocytes in white adipose tissue (WAT), also known as WAT beiging, improves glucose and lipid metabolism. However, the regulation of WAT beiging at the posttranscriptional level remains elusive. Here, we report that METTL3, the methyltransferase of N6-methyladenosine (m6A) mRNA modification, is induced during WAT beiging in mice. Adipose-specific depletion of Mettl3 gene undermines WAT beiging. Transcriptomic analysis of m6A modifications and mRNA expression level reveals global reduction of m6A-modified mRNAs in Mettl3-depleted beige adipose tissue. In particular, METTL3-catalyzed m6A installation on Krüppel-like factor 9 (Klf9) mRNA prevents its degradation. We further demonstrate that the m6A reader protein IGF2BP3 mediates the stabilization of m6A-modified Klf9 mRNA. Overexpressioin of KLF9 protein reverses the impaired WAT beiging elicited by Mettl3 deletion. These findings uncover a novel epitranscriptional mechanism in WAT beiging and identify METTL3-KLF9 axis as a potential therapeutic target for obesity-associated disorders.

2023-02-03 | GSE178884 | GEO

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [scRNA-Seq]

Project description:HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [scRNA-Seq]

| PRJNA796303 | ENA

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ATAC-Seq]

Project description:HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ATAC-Seq]

| PRJNA795805 | ENA

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ChIP-Seq]

Project description:HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [ChIP-Seq]

| PRJNA795809 | ENA

HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [RNA-Seq]

Project description:HMGNs Regulate White Adipocyte Browning By Stabilizing Cell Identity [RNA-Seq]

| PRJNA795810 | ENA

Regulation of the mouse heart transcriptome by Celf1

Project description:The CUG-BP and ETR-3-like factor 1 (Celf1) RNA binding protein plays an important role in heart and muscle development, and is over-expressed in the disease myotonic dystrophy. Celf1 has known roles in regulation of RNA splicing, RNA stability, and protein translation. To identify transcriptome-wide targets of the Celf1 protein in heart, we performed RNA-Seq of polyA+ RNA from mice inducibly expressing Celf1 in the heart. Mice were engineered to express the reverse tetracycline trans-activator (rtTA) from a heart-specific alpha myosin heavy chain promoter, and an N-terminal Flag-tagged version of the LYLQ isoform of human Celf1 from a tet-inducible promoter. Mice were fed doxycycline to induce Celf1 expression in heart, and hearts were harvested from 3 mice each at 12 hour, 24 hour, 72 hour, and 7 day time points. To account for potential doxycycline-dependent effects, control mice were fed doxycycline for 72 hours but these mice did not contain the tet-inducible Celf1 cassette. In total, 15 hearts were analyzed by RNA-Seq.

2014-04-01 | E-GEOD-56185 | biostudies-arrayexpress

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