An Evi1-C/EBPβ Complex Controls Peroxisome Proliferator-Activated Receptor γ2 Gene Expression To Initiate White Fat Cell Differentiation

Ishibashi, Jeff; Firtina, Zeynep; Rajakumari, Sona; Wood, Kathleen H.; Conroe, Heather M.; Steger, David J.; Seale, Patrick

doi:10.1128/mcb.06529-11

Cited by 23 publications

(23 citation statements)

References 49 publications

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“…Following growth arrest, efficient induction of 3T3-L1 cell differentiation is accompanied by mitotic clonal expansion (MCE) [28]. Studies have shown that EVI1 stimulates cell proliferation [29] and this property may stimulate MCE, contributing to the enhanced expression of adipogenic markers observed here, which are consistent with previous observations [11].…”

Section: Discussionsupporting

confidence: 91%

“…The relative abundance of splice variants has not been determined in this study but others have shown that general EVI1 expression is low in proliferating preadipocytes, transiently peaks during chemical stimulation of differentiation then is low again for the remaining programme [11].…”

Section: Discussionmentioning

confidence: 79%

“…Recent studies show that EVI1 also participates in adipogenesis [11] [12]. These studies show that EVI1 converts nonadipogenic cells to adipocytes and knockdown (KD) suppresses preadipocyte differentiation by impairing CCAAT/Enhancer-binding protein-beta (CEBPβ) assisted induction of peroxisome proliferator-activated receptor-gamma 2 (PPARγ 2 ).…”

Section: Introductionmentioning

confidence: 99%

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EVI1 Mediated Stimulation of 3T3-L1 Preadipocyte Differentiation Is CtBP Dependent

Ireland¹,

Alhasan²,

Craft³

et al. 2017

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Myelodysplasia syndrome 1 (MDS1) and Ecotropic viral integration site 1 (EVI1) complex (MECOM) locus encode multiple isoforms of the EVI1 protein that are essential for normal vertebrate development and when inappropriately expressed play a significant role in malignancy and in particular leukaemias. However, the function of individual EVI1 isoforms is not fully understood. Recently, EVI1 or PRDM3, which is structurally closely related to the brown adipose tissue determining factor PRDM16, was shown to be required for differentiation of adipocytes. In this study, we show that 3T3-L1 preadipocytes sustain expression of all Evi1 isoforms examined, including Mds1-Evi1, Evi1FL, Evi1Δ324, Evi1FL + 9 and Evi1Δ105 throughout the adipogenesis differentiation programme. We also show that differentiation markers are enhanced by enforced expression of either Evi1, Evi1FL + 9 or Evi1Δ105 isoforms. Interestingly 3T3-L1 differentiation markers are also moderately enhanced by enforced expression of Evi1Δ324, which lacks part of the N-terminal zinc finger domain (ZF1), demonstrating a biological activity for this particular isoform. Enforced expression of an Evi1 mutant lacking C-terminal binding protein (CtBP) co-repressor protein binding activity fails to stimulate 3T3-L1 differentiation markers and may have dominant negative activity, causing partial inhibition of this developmental programme. These studies show that multiple EVI1 isoforms are expressed in adipocytes and can stimulate adipogenic markers in a manner that is partially independent of the ZF1 DNA binding domain but fully dependent upon interaction with co-repressor CtBP proteins.

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Section: Discussionsupporting

confidence: 91%

Section: Discussionmentioning

confidence: 79%

Section: Introductionmentioning

confidence: 99%

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EVI1 Mediated Stimulation of 3T3-L1 Preadipocyte Differentiation Is CtBP Dependent

Ireland¹,

Alhasan²,

Craft³

et al. 2017

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“…Primary inguinal cells were grown and differentiated as above with the inclusion of 1 µM rosiglitazone through differentiation. Oil-Red-O, virus production, and transfection assays were performed as described previously (Ishibashi et al 2012). The following constructs were used in cell culture: pMX-BRG1 (Hans Schöler; Addgene, plasmid no.…”

Section: Cell Culturementioning

confidence: 99%

EBF2 transcriptionally regulates brown adipogenesis via the histone reader DPF3 and the BAF chromatin remodeling complex

et al. 2017

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The transcription factor early B-cell factor 2 (EBF2) is an essential mediator of brown adipocyte commitment and terminal differentiation. However, the mechanisms by which EBF2 regulates chromatin to activate brown fat-specific genes in adipocytes were unknown. ChIP-seq (chromatin immunoprecipitation [ChIP] followed by deep sequencing) analyses in brown adipose tissue showed that EBF2 binds and regulates the activity of lineage-specific enhancers. Mechanistically, EBF2 physically interacts with the chromatin remodeler BRG1 and the BAF chromatin remodeling complex in brown adipocytes. We identified the histone reader protein DPF3 as a brown fat-selective component of the BAF complex that was required for brown fat gene programming and mitochondrial function. Loss of DPF3 in brown adipocytes reduced chromatin accessibility at EBF2-bound enhancers and led to a decrease in basal and catecholamine-stimulated expression of brown fat-selective genes. Notably, Dpf3 is a direct transcriptional target of EBF2 in brown adipocytes, thereby establishing a regulatory module through which EBF2 activates and also recruits DPF3-anchored BAF complexes to chromatin. Together, these results reveal a novel mechanism by which EBF2 cooperates with a tissue-specific chromatin remodeling complex to activate brown fat identity genes.

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“…The increased level of the development of fat and creates adipose tissue obesity which mediates insulin resistance 14 . The PPAR-γ plays the major regulator for adipogenesis, which expressed specifically in adipose tissue [15][16][17] . It was found that adiponectin is directly affected by obesity and the correlation between adiponectin and Body Mass Index 18 .…”

mentioning

confidence: 99%

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2017

IJPSR

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The present study was initiated to quantify the Isoflavones content that accumulated in soybean transgenics with RnPPARγ gene by using high performance liquid chromatography. The effects of methanolic leaves extract of transformed soybean in 3T3-L 1 adipocyte cell line. The RnPPARγ transgenic soybean variety JS335 was developed and transgenics were confirmed by PCR and Southern blot techniques. The quantification of isoflavones compounds by HPLC showed that methanolic leaves extracts of transformed soybean contained Genistein (1.67µg/g extract), Daidzein (2.76µg/g extract), Rutin (32.06µg/g extract) and Quercetin (48.40µg/g extract) and methanolic leaves extracts of nontransformed soybean contained Genistein (1.23µg/g extract), Daidzein (2.33µg/g extract), Rutin (26.16µg/g extract) and Quercetin (43.03µg/g extract) by comparing the chromatogram of the reference standards. In the present study revealed that secondary metabolite content was higher in the transformed plant than non-transformed plants. After treatment of transformed methanolic leaves, extracts on 3T3-L 1 mature adipocytes significantly ameliorated lipid droplet accumulation and droplet reduction in adipocytes might be the result of lipid metabolism by lipolysis.

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An Evi1-C/EBPβ Complex Controls Peroxisome Proliferator-Activated Receptor γ2 Gene Expression To Initiate White Fat Cell Differentiation

Cited by 23 publications

References 49 publications

EVI1 Mediated Stimulation of 3T3-L1 Preadipocyte Differentiation Is CtBP Dependent

EVI1 Mediated Stimulation of 3T3-L1 Preadipocyte Differentiation Is CtBP Dependent

EBF2 transcriptionally regulates brown adipogenesis via the histone reader DPF3 and the BAF chromatin remodeling complex

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