Targeted disruption of the basic Kruppel-like factor gene (Klf3) reveals a role in adipogenesis

Sue, Nancy, Jack, Briony H. A., Eaton, Sally A., Pearson, Richard C. M., Funnell, Alister P. W., Turner, Jeremy, Czolij, Robert, Denyer, Gareth, Bao, Shisan, Molero-Navajas, Juan Carlos, Perkins, Andrew, Fujiwara, Y, Orkin, Stuart H., Bell-Anderson, Kim and Crossley, Merlin (2008) Targeted disruption of the basic Kruppel-like factor gene (Klf3) reveals a role in adipogenesis. Molecular and cellular biology, 28 12: 3967-3978. doi:10.1128/MCB.01942-07

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Author Sue, Nancy
Jack, Briony H. A.
Eaton, Sally A.
Pearson, Richard C. M.
Funnell, Alister P. W.
Turner, Jeremy
Czolij, Robert
Denyer, Gareth
Bao, Shisan
Molero-Navajas, Juan Carlos
Perkins, Andrew
Fujiwara, Y
Orkin, Stuart H.
Bell-Anderson, Kim
Crossley, Merlin
Title Targeted disruption of the basic Kruppel-like factor gene (Klf3) reveals a role in adipogenesis
Journal name Molecular and cellular biology   Check publisher's open access policy
ISSN 0270-7306
Publication date 2008-06
Sub-type Article (original research)
DOI 10.1128/MCB.01942-07
Open Access Status File (Publisher version)
Volume 28
Issue 12
Start page 3967
End page 3978
Total pages 12
Place of publication Washington, DC, United States
Publisher American Society for Microbiology
Language eng
Abstract Krüppel-like factors (KLFs) recognize CACCC and GC-rich sequences in gene regulatory elements. Here, we describe the disruption of the murine basic Krüppel-like factor gene (Bklf or Klf3). Klf3 knockout mice have less white adipose tissue, and their fat pads contain smaller and fewer cells. Adipocyte differentiation is altered in murine embryonic fibroblasts from Klf3 knockouts. Klf3 expression was studied in the 3T3-L1 cellular system. Adipocyte differentiation is accompanied by a decline in Klf3 expression, and forced overexpression of Klf3 blocks 3T3-L1 differentiation. Klf3 represses transcription by recruiting C-terminal binding protein (CtBP) corepressors. CtBPs bind NADH and may function as metabolic sensors. A Klf3 mutant that does not bind CtBP cannot block adipogenesis. Other KLFs, Klf2, Klf5, and Klf15, also regulate adipogenesis, and functional CACCC elements occur in key adipogenic genes, including in the C/ebp{alpha} promoter. We find that C/ebp{alpha} is derepressed in Klf3 and Ctbp knockout fibroblasts and adipocytes from Klf3 knockout mice. Chromatin immunoprecipitations confirm that Klf3 binds the C/ebp{alpha} promoter in vivo. These results implicate Klf3 and CtBP in controlling adipogenesis.
Keyword Enhancer-binding-protein
Q-Index Code C1
Q-Index Status Provisional Code

Document type: Journal Article
Sub-type: Article (original research)
Collection: Institute for Molecular Bioscience - Publications
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