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JCS ePress online publication date 14 Feb 2006
doi: 10.1242/jcs.02792

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Research Article

PKB{alpha} is required for adipose differentiation of mouse embryonic fibroblasts


Anne Baudry, Zhong-Zhou Yang, and Brian A. Hemmings*
* Author for correspondence (e-mail: hemmings{at}fmi.ch)

Protein kinase B{alpha} (PKB{alpha}) is a key regulator of metabolism, proliferation and differentiation. We have explored the role of PKB{alpha} in adipogenesis using wild-type and PKB{alpha}-knockout mouse embryonic fibroblasts (MEFs) and show that lack of PKB{alpha} prevents MEF differentiation into adipocytes. Expression of ectopic PKB{alpha} in PKB{alpha}-deficient cells restores adipogenesis. We identified 80 genes whose expression was upregulated in wild-type MEFs during adipogenesis but whose expression was significantly reduced in PKB{alpha}-deficient MEFs under the same conditions. Significantly, the regulator of adipogenesis Krüppel-like transcription factor 15 gene expression was downregulated in PKB{alpha}-deficient MEFs but could be restored by expressing an active PKB{alpha} in the deficient cells. The level of lipocalin 2, renin 1 and receptor-activity-modifying protein 3 genes expressed by adipose cells was also decreased in PKB{alpha}-deficient MEFs, and are inhibited by LY294002 treatment during early adipocyte differentiation of 3T3-L1 cells. The results underscore an essential role for PKB{alpha} in the transcriptional program required for adipogenesis.
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