Bmpr1a and Bmpr1b Essential for Cartilage Formation
Mar 30, 2005 - 6:45:00 AM
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To clarify the in vivo role of BMP signaling during chondrocyte development, Yoon et al. generated mice lacking the BMP receptors Bmpr1a and Bmpr1b in chondrocytes. The researchers showed that mice deficient in either Bmpr1a or Bmpr1b were able to form cartilage elements and had few skeletal defects, but Bmpr1a/Bmpr1b double mutants developed severe generalized chondrodysplasia, including delayed bone formation and shortened long bones.
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By Proceedings of the National Academy of Sciences,
[RxPG] Byeong Yoon et al. report that bone morphogenetic protein (BMP) signaling is essential for the generation of chondrocytes in vivo.
During development, chondrocytes proliferate and form the cartilage that acts as the template for bone formation. Previous studies have demonstrated that BMPs can promote differentiation of chondrocytes in vitro.
To clarify the in vivo role of BMP signaling during chondrocyte development, Yoon et al. generated mice lacking the BMP receptors Bmpr1a and Bmpr1b in chondrocytes. The researchers showed that mice deficient in either Bmpr1a or Bmpr1b were able to form cartilage elements and had few skeletal defects, but Bmpr1a/Bmpr1b double mutants developed severe generalized chondrodysplasia, including delayed bone formation and shortened long bones.
Cartilage condensations in double mutants were reduced in size because of decreased proliferation and increased apoptosis. The few cartilage condensations that developed were arrested in the prechondrocytic stage and never formed an organized growth plate. In addition, the mutant cartilage lacked Sox9, a transcription factor involved in early chondrocyte differentiation, as well as the downstream targets of Sox9, L-Sox5, and Sox6.
The authors conclude that Bmpr1a and Bmpr1b are functionally redundant during early chondrogenesis, and that BMP signaling is required for chondrocyte proliferation, survival, and differentiation in vivo.
Publication:
"Bmpr1a and Bmpr1b have overlapping functions and are essential for chondrogenesis in vivo" by Byeong S. Yoon, Dmitry A. Ovchinnikov, Isaac Yoshii, Yuji Mishina, Richard R. Behringer, and Karen M. Lyons
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Proceedings of the National Academy of Sciences of the United States of America
PNAS is one of the world's most-cited multidisciplinary scientific serials. Since its establishment in 1914, it continues to publish cutting-edge research reports, commentaries, reviews, perspectives, colloquium papers, and actions of the Academy. Coverage in PNAS spans the biological, physical, and social sciences. PNAS is published weekly in print, and daily online in PNAS Early Edition. The PNAS impact factor is 10.3 for 2003. PNAS is available by subscription.
PNAS is abstracted and/or indexed in: Index Medicus, PubMed Central, Current Contents, Medline, SPIN, JSTOR, ISI Web of Science, and BIOSIS.
Please note that the articles in PNAS report original research by independent authors and do not necessarily represent the views of the National Academy of Sciences or the National Research Council.
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