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DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE158173 | GEO | 2023/09/17

REPOSITORIES: GEO

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DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (RNA-Seq)

Project description:DDB1 is typically recognized as a component of the Cullin4 (CUL4)-RING E3 ubiquitin ligase complex. Here, we show that DDB1 functions independently of CUL4 to promote adipogenesis and diet-induced obesity. In contrast to depletion of CUL4A or CUL4B that stimulates adipogenesis, lack of DDB1 dramatically suppresses the process. Re-introduction of a DDB1 mutant that lacks the binding ability to CUL4A or CUL4B fully restores adipogenesis in DDB1-deficient preadipocytes. Furthermore, while inducibly knocking out Cul4a or Cul4b in mice aggravates diet-induced obesity, Ddb1+/- mice are lean on high-fat diet. Mechanistically, by binding the bromodomain-containing histone reader BRWD3, DDB1 is recruited to acetylated histones in the proximal promoters of immediate-early response genes, where it facilitates the release of paused RNA polymerase II (Pol II) and activates the transcription of these genes. Our findings have thus uncovered a mechanism of activating the transcriptional cascade in adipogenesis by DDB1-mediated release of paused Pol II.

2023-09-17 | GSE158172 | GEO

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-Seq)

2023-09-17 | GSE158171 | GEO

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-seq II)

2023-09-17 | GSE168136 | GEO

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity

Project description:DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity

| PRJNA664200 | ENA

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-Seq)

Project description:DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-Seq)

| PRJNA664202 | ENA

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (RNA-Seq)

Project description:DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (RNA-Seq)

| PRJNA664203 | ENA

DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-seq II)

Project description:DDB1 Binds Histone Reader BRWD3 to Activate the Transcriptional Cascade in Adipogenesis and Promote Onset of Obesity (ChIP-seq II)

| PRJNA706200 | ENA

Ramshackle (Brwd3) promotes light-induced ubiquitylation of Drosophila Cryptochrome by DDB1-CUL4-ROC1 E3 ligase complex.

Project description:Cryptochrome (CRY) is the primary circadian photoreceptor in Drosophila. It resets the circadian clock by promoting light-induced degradation of the clock proteins Timeless and Period, as well as its own proteolysis. The E3 ligases that ubiquitylate Timeless and Period before degradation are known and it is known that Drosophila (d) CRY is degraded by the ubiquitin-proteasome system as well. To identify the E3 ligase for dCRY we screened candidates in S2 cells by RNAi. Knockdown of each of the 25 putative F-box proteins identified by bioinformatics did not attenuate the light-induced degradation of dCRY. However, knockdown of a WD40 protein, Bromodomain and WD repeat domain containing 3 (Brwd3) (CG31132/Ramshackle) caused strong attenuation of dCRY degradation following light exposure. We found that BRWD3 functions as a Damage-specific DNA binding protein 1 (DDB1)- and CULLIN (CUL)4-associated factor in a Cullin4-RING Finger E3 Ligase (CRL4) that mediates light-dependent binding of dCRY to CUL4-ROC1-DDB1-BRWD3, inducing ubiquitylation of dCRY and its light-induced degradation. Thus, this study identifies a light-activated E3 ligase complex essential for light-mediated CRY degradation in Drosophila cells.

| S-EPMC3612607 | biostudies-literature

Peroxisome proliferator-activated receptor gamma recruits the positive transcription elongation factor b complex to activate transcription and promote adipogenesis.

Project description:Positive transcription elongation factor b (P-TEFb) phosphorylates the C-terminal domain of RNA polymerase II, facilitating transcriptional elongation. In addition to its participation in general transcription, P-TEFb is recruited to specific promoters by some transcription factors such as c-Myc or MyoD. The P-TEFb complex is composed of a cyclin-dependent kinase (cdk9) subunit and a regulatory partner (cyclin T1, cyclin T2, or cyclin K). Because cdk9 has been shown to participate in differentiation processes, such as muscle cell differentiation, we studied a possible role of cdk9 in adipogenesis. In this study we show that the expression of the cdk9 p55 isoform is highly regulated during 3T3-L1 adipocyte differentiation at RNA and protein levels. Furthermore, cdk9, as well as cyclin T1 and cyclin T2, shows differences in nuclear localization at distinct stages of adipogenesis. Overexpression of cdk9 increases the adipogenic potential of 3T3-L1 cells, whereas inhibition of cdk9 by specific cdk inhibitors, and dominant-negative cdk9 mutant impairs adipogenesis. We show that the positive effects of cdk9 on the differentiation of 3T3-L1 cells are mediated by a direct interaction with and phosphorylation of peroxisome proliferator-activated receptor gamma (PPARgamma), which is the master regulator of this process, on the promoter of PPARgamma target genes. PPARgamma-cdk9 interaction results in increased transcriptional activity of PPARgamma and therefore increased adipogenesis.

| S-EPMC2259259 | biostudies-literature

Monoalkylglycerol ether lipids promote adipogenesis.

Project description:The molecular mechanisms that lead to the generation of adipose tissue (adipogenesis) are of basic and biomedical interest. Cellular models of adipogenesis have proven extremely valuable in defining biomolecules-primarily genes and proteins-that regulate adipogenesis. Here, the analysis of differentiating adipocytes using an untargeted metabolomics approach led to the discovery of the monoalkylglycerol ethers as a natural class of adipocyte differentiation factors.

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