Format

Send to

Choose Destination
Matrix Biol. 1998 Mar;16(9):529-40.

Toward understanding SOX9 function in chondrocyte differentiation.

Author information

1
Department of Molecular Genetics, The University of Texas M.D. Anderson Cancer Center, Houston, USA.

Abstract

The transcription factors that trigger the determinative switch to chondrocyte differentiation in mesenchymal cells are still unknown. In humans, mutations in the gene for SOX9, a transcription factor with a DNA-binding domain similar to that of the mammalian testis-determining factor SRY, cause campomelic dysplasia, a severe dwarfism syndrome which affects all cartilage-derived structures. During mouse embryonic development, the Sox9 gene becomes active in all prechondrocytic mesenchymal condensations, and at later stages its expression is maintained at high levels in fully differentiated chondrocytes. A chondrocyte-specific enhancer in the gene for collagen type II (Col2a1), a characteristic marker of chondrocytes, is a direct target for SOX9, and ectopic expression of SOX9 in transgenic mouse embryos is sufficient to activate the endogenous Col2a1 gene in some tissues. These data suggest that SOX9 could have a major role in chondrogenesis. Studies are in progress to identify other target genes for SOX9 in chondrocytes and also other transcription factors that are believed to cooperate with SOX9 in the activation of chondrocyte-specific genes. Defining SOX9 function and the mechanisms that regulate SOX9 gene expression should contribute to a better understanding of chondrocyte differentiation.

PMID:
9569122
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center