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First published online 13 July 2009
doi: 10.1242/jcs.046276

Journal of Cell Science 122, 2760-2768 (2009)
Published by The Company of Biologists 2009
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Research Article

Growth arrest induces primary-cilium formation and sensitizes IGF-1-receptor signaling during differentiation induction of 3T3-L1 preadipocytes

Di Zhu1, Shuo Shi2, Hongzhong Wang1 and Kan Liao1,*

1 State Key Laboratory of Molecular Biology, Institute of Biochemistry and Cell Biology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China
2 Institute for Nutritional Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China

* Author for correspondence (e-mail: kliao{at}sibs.ac.cn)

Accepted 11 May 2009

The first stage of 3T3-L1 adipocyte differentiation is growth arrest, which is achieved by contact inhibition at confluence. In growth-arrested confluent 3T3-L1 preadipocytes, {alpha}-tubulin acetylation and primary-cilium formation were induced. The blockade of primary-cilium formation by suppressing IFT88 or Kif3a inhibited 3T3-L1 adipocyte differentiation. IGF-1 (IGF-I)-receptor signaling, which is essential for differentiation induction, was sensitized by the formation of a primary cilium in confluent 3T3-L1 preadipocytes. The receptor located in primary cilium was more sensitive to insulin stimulation than that not located in cilia. During cilium formation, insulin receptor substrate 1 (IRS-1), one of the important downstream signaling molecules of the IGF-1 receptor, was recruited to the basal body at which it was phosphorylated on tyrosine by the receptor kinase in cilia. Akt-1, an important signal molecule of the IGF-1 receptor in adipocyte differentiation, was also activated at the basal body. These IGF-1-receptor signaling processes were all inhibited in IFT88- or Kif3a-knockdown cells. Thus, the primary cilium and its basal body formed an organized signaling pathway for the IGF-1 receptor to induce adipocyte differentiation in confluent 3T3-L1 preadipocytes.

Key words: Primary cilium, IGF-1 receptor, {alpha}-tubulin acetylation, Growth arrest, Adipocyte differentiation, 3T3-L1 cell


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