G9a is transactivated by C/EBPβ to facilitate mitotic clonal expansion during 3T3-L1 preadipocyte differentiation

Li, Shu Fen; Guo, Liang; Qian, Shu Wen; Liu, Yuan; Zhang, You You; Zhang, Zhi Chun; Zhao, Yue; Shou, Jianyong; Tang, Qi; Li, Xi

doi:10.1152/ajpendo.00608.2012

Cited by 29 publications

(23 citation statements)

References 52 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…G9a plays important roles in various biological processes and has been shown to be a repressor of adipogenesis (27). In 3T3-L1 cells, a transient induction of G9a by C/EBP␤ was detected during MCE (32). Then, G9a inhibited PPAR␥ and C/EBP␣ expression through H3K9 dimethylation of their promoters.…”

Section: Role and Mechanism Of C/ebp␤ In Mitotic Clonal Expansionmentioning

confidence: 99%

Transcriptional Regulation of Adipocyte Differentiation: A Central Role for CCAAT/Enhancer-binding Protein (C/EBP) β

Guo

Tang

2015

Journal of Biological Chemistry

Self Cite

282

230

View full text Add to dashboard Cite

A detailed understanding of the processes controlling adipogenesis is instrumental in the fight against the obesity epidemic. Adipogenesis is controlled by a transcriptional cascade composed of a large number of transcriptional factors, among which CCAAT/enhancer-binding protein (C/EBP) ␤ plays an essential role. During 3T3-L1 adipocyte differentiation, C/EBP␤ is induced early to transactivate the expression of C/EBP␣ and peroxisome proliferator-activated receptor ␥ (PPAR␥), two master transcription factors for terminal adipocyte differentiation. Studies in recent years have revealed many new target genes of C/EBP␤, implicating its participation in many other processes during adipogenesis, such as mitotic clonal expansion, epigenetic regulation, unfolded protein response, and autophagy. Moreover, the function of C/EBP␤ is highly regulated by post-translational modifications, which are crucial for the proper activation of the adipogenic program. Advances toward elucidation of the function and roles of the post-translational modification of C/EBP␤ during adipogenesis will greatly improve our understanding of the molecular mechanisms governing adipogenesis.Adipose tissue is not only a key depot for energy storage but is also involved in the dynamic regulation of metabolism (1). The upsurge of adipose tissue mass plays a central role in obesity-related complications such as type 2 diabetes, hypertension, hyperlipidemia, and arteriosclerosis (2). Both the increase of adipocyte size (hypertrophy) and the increase of adipocyte number (hyperplasia) are major contributors to the development of obesity (3). Thus, a tight control of adipocyte development and function is critical in maintaining whole body energy homeostasis, and a full understanding of the mechanisms regulating adipose formation would provide precious information on the way to control of obesity.Much of our knowledge of adipocyte differentiation has been obtained by studying adipocyte cell culture models. The 3T3-L1 cell line is one of the best studied cellular models (4). Upon the treatment with differentiation inducers (a combination of 3-isobutyl-1-methylxanthine, dexamethasone, and insulin), growth-arrested 3T3-L1 preadipocytes re-enter the cell cycle, a process referred to as mitotic clonal expansion (MCE), 2 which contributes to the hyperplasia of adipocytes. The adipogenic gene expression program is initiated during and after 2-3 rounds of MCE, ultimately leading to terminal adipocyte differentiation (5).The adipogenic program requires a cascade of multiple transcription factors (6), among which is CCAAT/enhancer-binding protein ␤ (C/EBP␤), an important transcriptional factor belonging to the leucine zipper family. Knockdown of C/EBP␤ in 3T3-L1 preadipocytes blocks adipogenesis (7,8), whereas its overexpression is sufficient to induce 3T3-L1 adipocyte differentiation without the hormonal inducers normally required (9). The functional importance of C/EBP␤ during adipocyte development has also been demonstrated in vivo. Disruption of the C/EBP␤ gene in...

show abstract

Section: Role and Mechanism Of C/ebp␤ In Mitotic Clonal Expansionmentioning

confidence: 99%

Transcriptional Regulation of Adipocyte Differentiation: A Central Role for CCAAT/Enhancer-binding Protein (C/EBP) β

Guo

Tang

2015

Journal of Biological Chemistry

Self Cite

282

230

View full text Add to dashboard Cite

show abstract

“…Although some C/EBPβ-regulated genes have been found, there are still a lot unknown. Our laboratory used ChIP-onchip experiments to identify a series of C/EBPβ target genes at the early stage of 3T3-L1 preadipocyte differentiation (27,(31)(32)(33)(34), among which is KLF10. In the current study, we demonstrated that the expression profile of KLF10 positively correlated with that of C/EBPβ during 3T3-L1 preadipocyte differentiation (Fig.1).…”

Section: Resultsmentioning

confidence: 99%

Krüppel-like factor 10 (KLF10) is transactivated by the transcription factor C/EBPβ and involved in early 3T3-L1 preadipocyte differentiation

Liu

Peng

Guo

et al. 2018

Journal of Biological Chemistry

Self Cite

View full text Add to dashboard Cite

“…77 Furthermore, CEBPb activates G9a expression during mitotic clonal expansion reiterating a role for G9a in proliferation of preadipocytes. 78 In contrast to G9a, knockdown of SETDB1 decreased myogenic differentiation through downregulation of MyoD and myogenin expression indicating that SETDB1 is required for their expression and differentiation. However, surprisingly, overexpression of SETDB1 does not promote differentiation.…”

Section: Function In Cellular Differentiation and Senescencementioning

confidence: 94%

“…Similar to SUV39H1, G9a inhibits adipogenic differentiation. [76][77][78] This inhibition is mediated via repression of PPARg expression as well as activation of Wnt10a expression, a negative regulator of adipogenesis. Deletion of G9a or inhibition of its activity with BIX01294, reduced H3K9me2 on PPARg promoter but, interestingly, increased H3K9ac at the Wnt10a promoter.…”

Section: Function In Cellular Differentiation and Senescencementioning

confidence: 99%

A drive in SUVs: From development to disease

2017

View full text Add to dashboard Cite

Progression of cells through distinct phases of the cell cycle, and transition into out-of-cycling states, such as terminal differentiation and senescence, is accompanied by specific patterns of gene expression. These cell fate decisions are mediated not only by distinct transcription factors, but also chromatin modifiers that establish heritable epigenetic patterns. Lysine methyltransferases (KMTs) that mediate methylation marks on histone and non-histone proteins are now recognized as important regulators of gene expression in cycling and non-cycling cells. Among these, the SUV39 sub-family of KMTs, which includes SUV39H1, SUV39H2, G9a, GLP, SETDB1, and SETDB2, play a prominent role. In this review, we discuss their biochemical properties, sub-cellular localization and function in cell cycle, differentiation programs, and cellular senescence. We also discuss their aberrant expression in cancers, which exhibit de-regulation of cell cycle and differentiation.

show abstract

G9a is transactivated by C/EBPβ to facilitate mitotic clonal expansion during 3T3-L1 preadipocyte differentiation

Cited by 29 publications

References 52 publications

Transcriptional Regulation of Adipocyte Differentiation: A Central Role for CCAAT/Enhancer-binding Protein (C/EBP) β

Transcriptional Regulation of Adipocyte Differentiation: A Central Role for CCAAT/Enhancer-binding Protein (C/EBP) β

Krüppel-like factor 10 (KLF10) is transactivated by the transcription factor C/EBPβ and involved in early 3T3-L1 preadipocyte differentiation

A drive in SUVs: From development to disease

Contact Info

Product

Resources

About