
pmid: 16378759
To identify genes and pathways not previously implicated in the mesenchymal-epithelial (M/E) interactions that are critical for normal mouse prostate development, we constructed six serial analysis of gene expression (SAGE) libraries. Bioinformatic analyses revealed expression of various members of numerous signalling pathways and the differential expression of several members of the wingless-related MMTV integration site (Wnt) signalling pathway. This pathway has not been previously implicated in prostate development thus expression of selected Wnt pathway members in the developing prostate was confirmed by RT-qPCR. Of particular interest, an antagonist of the Wnt pathway, secreted frizzled related protein 2 (Sfrp2), was highly expressed in the early prostate libraries and down regulated at later developmental stages. The expression levels of four Wnt ligands reported to interact with Sfrp2 were, therefore, examined by RT-qPCR. We found that only Wnt4 transcripts were detectable in the developing prostate. Expression of Sfrp2 was validated using RT-qPCR and localization of Sfrp2 transcripts and protein was carried out using in situ hybridization and immunofluorescence, respectively. These studies provide the first evidence that Wnt pathway members are expressed in the developing prostate. Functional analyses are now required to establish the biological significance of this observation.
Male, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Prostate, Computational Biology, Fluorescent Antibody Technique, Gene Expression Regulation, Developmental, Ligands, Mice, Inbred C57BL, Wnt Proteins, Mice, Microscopy, Fluorescence, Animals, In Situ Hybridization, Gene Library, Signal Transduction
Male, Reverse Transcriptase Polymerase Chain Reaction, Gene Expression Profiling, Prostate, Computational Biology, Fluorescent Antibody Technique, Gene Expression Regulation, Developmental, Ligands, Mice, Inbred C57BL, Wnt Proteins, Mice, Microscopy, Fluorescence, Animals, In Situ Hybridization, Gene Library, Signal Transduction
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