| First Author | Schneider AJ | Year | 2019 |
| Journal | Gene Expr Patterns | Volume | 34 |
| Pages | 119075 | PubMed ID | 31669249 |
| Mgi Jnum | J:281428 | Mgi Id | MGI:6377533 |
| Doi | 10.1016/j.gep.2019.119075 | Citation | Schneider AJ, et al. (2019) Sox9 in mouse urogenital sinus epithelium mediates elongation of prostatic buds and expression of genes involved in epithelial cell migration. Gene Expr Patterns 34:119075 |
| abstractText | Previous studies identified Sox9 as a critical mediator of prostate development but the precise stage when Sox9 acts had not been determined. A genetic approach was used to delete Sox9 from mouse urogenital sinus epithelium (UGE) prior to prostate specification. All prostatic bud types (anterior, dorsolateral and ventral) were stunted in Sox9 conditional knockouts (cKOs) even though the number of prostatic buds did not differ from that of controls. We concluded that Sox9 is required for prostatic bud elongation and compared control male, control female, Sox9 cKO male and Sox9 cKO female UGE transcriptomes to identify potential molecular mediators. We identified 702 sex-dependent and 95 Sox9-dependent genes. Thirty-one genes were expressed in both a sex- and Sox9-dependent pattern. A comparison of Sox9 cKO female vs control female UGE transcriptomes revealed 74 Sox9-dependent genes, some of which also function in cell migration. SOX9 regulates, directly or indirectly, a largely different profile of genes in male and female UGE. Eighty-three percent of Sox9-dependent genes in male UGE were not Sox9-dependent in female UGE. Only 16 genes were Sox9-dependent in the UGE of both sexes and seven had cell migration functions. These results support the notion that Sox9 promotes cell migration activities needed for prostate ductal elongation. |
