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Downloaded from genesdev.cshlp.org on November 24, 2021 - Published by Cold Spring Harbor Laboratory Press Continuous expression of Cbfa1 in nonhypertrophic chondrocytes uncovers its ability to induce hypertrophic chondrocyte differentiation and partially rescues Cbfa1-deficient mice 1 1 2 1 1,3 Shu Takeda, Jean-Pierre Bonnamy, Michael J.Owen, Patricia Ducy, and Gerard Karsenty 1 2 Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas 77030, USA; Imperial Cancer Research Fund, London, England WC2A3PX, UK Chondrocyte hypertrophy is a mandatory step during endochondral ossification.Cbfa1-deficient mice lack hypertrophic chondrocytes in some skeletal elements, indicating that Cbfa1 may control hypertrophic chondrocyte differentiation.To address this question we generated transgenic mice expressing Cbfa1 in nonhypertrophic chondrocytes (1(II) Cbfa1).This continuous expression of Cbfa1 in nonhypertrophic chondrocytes induced chondrocyte hypertrophy and endochondral ossification in locations where it normally never occurs.To determine if this was caused by transdifferentiation of chondrocytes into osteoblasts or by a specific hypertrophic chondrocyte differentiation ability of Cbfa1, we used the 1(II) Cbfa1 transgene to restore Cbfa1 expression in mesenchymal condensations of the Cbfa1-deficient mice.The transgene restored chondrocyte hypertrophy and vascular invasion in the bones of the mutant mice but did not induce osteoblast differentiation.This rescue occurred cell-autonomously, as skeletal elements not
Genes & Development – Unpaywall
Published: Feb 15, 2001
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