Expression Profile Of SOX9 Research Articles

Harderian SOX9: Molecular characterization and its dimorphic expression in hamster

The molecular action of SOX9 can promote lipogenesis. Because the hamster Harderian gland (HG) synthesizes lipids and exhibits sexual dimorphism, this study aimed to identify and characterize Harderian SOX9. We examined the tissue distribution and expression profiles of SOX9 in hamster Mesocricetus auratus HGs. The full-length SOX9 cDNA sequence [3649-base pairs (bp)] contains an 81-bp 5′ untranslated region (UTR), a 3′ UTR of 2044-bp, an open reading frame (ORF) of 1524-bp, and a polyadenylation signal (AATAAA) at 19-bp upstream of poly(A) tail. The cDNA encodes a 507 amino acid protein containing the potential DNA-binding domain known as the HMG box. BLAST analysis revealed 99%, 99%, and 97% identity with the SOX9 of mouse, rat, and human, respectively. High expression levels were also observed in the testis, cerebellum, and hypothalamus. qPCR analysis demonstrated that SOX9 is expressed more abundantly in the HGs of males than in females. Sexually dimorphic expression of SOX9 suggests that differential expression between male and female HGs could be under the regulation of sex steroids. SOX9 might play a similar role in regulating exocrine secretions of lipids; these could occur downstream of FGF signaling – as found during embryogenesis – and/or androgen signaling.

The bone morphogenetic protein antagonist Noggin is regulated by Sox9 during endochondral differentiation.

Noggin has been described to be capable of binding bone morphogenetic proteins (BMP) and inhibiting BMP signaling by preventing the interactions of BMP with their receptors. Noggin expression during endochondral differentiation was analyzed to elucidate its potential role during chondrogenesis. Throughout mouse development, Noggin was expressed abundantly in the chondrocytic lineage as early as collagen type II RNA was detectable. In addition, a strong correlation was detected between Noggin expression and the expression profile of Sox9 during chondrogenesis. Sox9 (known to play an important role during chondrogenesis) and Noggin expression were investigated in the pluripotent mesenchymal cell line C3H10T1/2, stimulated by BMP-2. BMP-2 caused significant upregulation of Sox9 and Noggin expression in these cells. The upregulation of Noggin could be inhibited by introducing antisense oligonucleotides against Sox9 mRNA into the cells. Using mouse limb bud cultures, the role of Sox9 and Noggin during endochondral tissue differentiation was further studied. Treatment of cultures with Sox9 antisense oligonucleotides and/or Noggin protein caused significant alterations in limb morphogenesis and endochondral development. The data suggest that the transcriptional control of Noggin by Sox9 is a potent regulatory mechanism in chondrocyte differentiation.