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Publication : Loss of Sox9 function results in defective chondrocyte differentiation of mouse embryonic stem cells in vitro.

First Author  Hargus G Year  2008
Journal  Int J Dev Biol Volume  52
Issue  4 Pages  323-32
PubMed ID  18415932 Mgi Jnum  J:133946
Mgi Id  MGI:3784676 Doi  10.1387/ijdb.072490gh
Citation  Hargus G, et al. (2008) Loss of Sox9 function results in defective chondrocyte differentiation of mouse embryonic stem cells in vitro. Int J Dev Biol 52(4):323-32
abstractText  The transcription factor Sox9 plays an important role during chondrogenesis. After early conditional inactivation of Sox9 in mesenchymal limb bud cells of mice, mesenchymal condensations as well as cartilage and bone are completely absent in the developing limbs. We analyzed chondrogenic differentiation of Sox9-/- mouse embryonic stem cells in vitro, using two clones with different targeted mutations. We found that the development of mature and hypertrophic chondrocytes is completely inhibited in the absence of Sox9 confirming that Sox9 is required for the formation of cartilage. In contrast, Sox9+/- mouse embryonic stem cells showed continous but reduced differentiation into mature chondrocytes. Interestingly, the formation of early chondrogenic condensations expressing characteristic marker genes such as scleraxis, Sox5 and Sox6 was not inhibited in the absence of Sox9 in vitro. Thus, we propose that the earliest step of chondrogenesis could be regulated by a non cell-autonomous function of Sox9.
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