Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA120359 | ENA |
REPOSITORIES: ENA
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Project description:The Wnt/b-catenin signaling inhibits adipogenesis. Genome-wide profiling studies have revealed the enrichment of histone H3K27 methyltransferase PRC2 on Wnt genes. However, the functional significance of such a direct link between the two types of developmental regulators in mammalian cells, and the role of PRC2 in adipogenesis, remain unclear. Here we show PRC2 and its H3K27 methyltransferase activity are required for adipogenesis. PRC2 directly represses Wnt1, 6, 10a and 10b genes in preadipocytes and during adipogenesis. Deletion of the enzymatic Ezh2 subunit of PRC2 eliminates H3K27me3 on Wnt promoters and de-represses Wnt expression, which leads to activation of Wnt/b-catenin signaling and inhibition of adipogenesis. Ectopic expression of the wild type Ezh2, but not the enzymatically inactive F667I mutant, prevents the loss of H3K27me3 and the defects in adipogenesis in Ezh2-/- preadipocytes. The adipogenesis defects in Ezh2-/- cells can be rescued by expression of adipogenic transcription factors PPARa, C/EBPb, or inhibitors of Wnt/b-catenin signaling. Interestingly, Ezh2-/- cells show marked increase of H3K27 acetylation globally as well as on Wnt promoters. These results indicate that H3K27 methyltransferase PRC2 directly represses Wnt genes to facilitate adipogenesis, and suggest that acetylation and trimethylation on H3K27 play opposing roles in regulating Wnt expression. To identify additional PRC2-regulated genes in preadipocytes, we performed microarray analysis in Ezh2flox/flox preadipocytes infected with retroviruses expressing Cre or vector alone.
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Project description:The Wnt/b-catenin signaling inhibits adipogenesis. Genome-wide profiling studies have revealed the enrichment of histone H3K27 methyltransferase PRC2 on Wnt genes. However, the functional significance of such a direct link between the two types of developmental regulators in mammalian cells, and the role of PRC2 in adipogenesis, remain unclear. Here we show PRC2 and its H3K27 methyltransferase activity are required for adipogenesis. PRC2 directly represses Wnt1, 6, 10a and 10b genes in preadipocytes and during adipogenesis. Deletion of the enzymatic Ezh2 subunit of PRC2 eliminates H3K27me3 on Wnt promoters and de-represses Wnt expression, which leads to activation of Wnt/b-catenin signaling and inhibition of adipogenesis. Ectopic expression of the wild type Ezh2, but not the enzymatically inactive F667I mutant, prevents the loss of H3K27me3 and the defects in adipogenesis in Ezh2-/- preadipocytes. The adipogenesis defects in Ezh2-/- cells can be rescued by expression of adipogenic transcription factors PPARa, C/EBPb, or inhibitors of Wnt/b-catenin signaling. Interestingly, Ezh2-/- cells show marked increase of H3K27 acetylation globally as well as on Wnt promoters. These results indicate that H3K27 methyltransferase PRC2 directly represses Wnt genes to facilitate adipogenesis, and suggest that acetylation and trimethylation on H3K27 play opposing roles in regulating Wnt expression.
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Project description:To investigate miRNAs that implicate the process of adipogenesis by interacting with canonical Wnt/β-catenin signaling pathway, we constructed two cell models at first, and then investigated the expression profile of microRNAs by using Microarray. Based on the data of high throughput microarray, we identified 18 miRNAs which might promote adipogenesis by repressing WNT signaling, including mir-210, mir-148a, mir-194, mir-322 etc. On the other hand, we also identified 29 miRNAs which might repress adipogenesis by activation of WNT signaling, including mir-344, mir-27, and mir-181. The target genes involved in WNT signaling pathway of these identified miRNAs were also predicted through online tools.
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Project description:To investigate miRNAs that implicate the process of adipogenesis by interacting with canonical Wnt/β-catenin signaling pathway, we constructed two cell models at first, and then investigated the expression profile of microRNAs by using Microarray. Based on the data of high throughput microarray, we identified 18 miRNAs which might promote adipogenesis by repressing WNT signaling, including mir-210, mir-148a, mir-194, mir-322 etc. On the other hand, we also identified 29 miRNAs which might repress adipogenesis by activation of WNT signaling, including mir-344, mir-27, and mir-181. The target genes involved in WNT signaling pathway of these identified miRNAs were also predicted through online tools. Two cell models of 3T3-L1, i.e. activation and suppression of WNT signaling including four samples, i.e. preadipocytes, mature adipocytes (MDI induction), Lithium treated preadipocytes, MDI induction of Lithium treated preadipocytes. Each sample was replicated in triplicate.
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