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. 2007 Mar;12(3):377-89.
doi: 10.1016/j.devcel.2007.02.004.

V体育安卓版 - MEF2C transcription factor controls chondrocyte hypertrophy and bone development

Michael A Arnold  1 , Yuri Kim, Michael P Czubryt, Dillon Phan, John McAnally, Xiaoxia Qi, John M Shelton, James A Richardson, Rhonda Bassel-Duby, Eric N Olson
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MEF2C transcription factor controls chondrocyte hypertrophy and bone development

Michael A Arnold et al. Dev Cell. 2007 Mar.
Free article

Abstract (VSports app下载)

Chondrocyte hypertrophy is essential for endochondral bone development. Unexpectedly, we discovered that MEF2C, a transcription factor that regulates muscle and cardiovascular development, controls bone development by activating the gene program for chondrocyte hypertrophy. Genetic deletion of Mef2c or expression of a dominant-negative MEF2C mutant in endochondral cartilage impairs hypertrophy, cartilage angiogenesis, ossification, and longitudinal bone growth in mice. Conversely, a superactivating form of MEF2C causes precocious chondrocyte hypertrophy, ossification of growth plates, and dwarfism. Endochondral bone formation is exquisitely sensitive to the balance between MEF2C and the corepressor histone deacetylase 4 (HDAC4), such that bone deficiency of Mef2c mutant mice can be rescued by an Hdac4 mutation, and ectopic ossification in Hdac4 null mice can be diminished by a heterozygous Mef2c mutation VSports手机版. These findings reveal unexpected commonalities in the mechanisms governing muscle, cardiovascular, and bone development with respect to their regulation by MEF2 and class II HDACs. .

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