Targeted disruption of the basic Krüppel-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, Yuko, Orkin, Stuart H., Bell-Anderson, Kim and Crossley, Merlin 2008, Targeted disruption of the basic Krüppel-like factor gene (Klf3) reveals a role in adipogenesis, Molecular and cellular biology, vol. 28, no. 12, pp. 3967-3978, doi: 10.1128/MCB.01942-07.

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Title Targeted disruption of the basic Krüppel-like factor gene (Klf3) reveals a role in adipogenesis
Author(s) 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, Yuko
Orkin, Stuart H.
Bell-Anderson, Kim
Crossley, Merlin
Journal name Molecular and cellular biology
Volume number 28
Issue number 12
Start page 3967
End page 3978
Publisher American Society for Microbiology
Place of publication Washington, D.C.
Publication date 2008-06
ISSN 0270-7306
Summary 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/ebpα promoter. We find that C/ebpα is derepressed in Klf3 and Ctbp knockout fibroblasts and adipocytes from Klf3 knockout mice. Chromatin immunoprecipitations confirm that Klf3 binds the C/ebpα promoter in vivo. These results implicate Klf3 and CtBP in controlling adipogenesis.
Notes (published April 2008)
Language eng
DOI 10.1128/MCB.01942-07
Field of Research 030405 Molecular Medicine
060199 Biochemistry and Cell Biology not elsewhere classified
Socio Economic Objective 970103 Expanding Knowledge in the Chemical Sciences
HERDC Research category C1.1 Refereed article in a scholarly journal
HERDC collection year 2008
Copyright notice ©2008, American Society for Microbiology
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Document type: Journal Article
Collections: Faculty of Health
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