Đang chuẩn bị liên kết để tải về tài liệu:
Báo cáo sinh học: "Hyperactive Wnt signaling changes the developmental potential of embryonic lung endoderm"

Tuyển tập các báo cáo nghiên cứu về sinh học được đăng trên tạp chí sinh học Journal of Biology đề tài: Hyperactive Wnt signaling changes the developmental potential of embryonic lung endoderm. | J. Biol. Journal of Biology BioMed Central Research article Open Access Hyperactive Wnt signaling changes the developmental potential of embryonic lung endoderm Tadashi Okubo and Brigid LM Hogan Address Department of Cell Biology Duke University Medical Center Durham NC 27710 USA. Correspondence Brigid Hogan. E-mail b.hogan@cellbio.duke.edu. Tadashi Okubo. E-mail t.okubo@cellbio.duke.edu Received 27 January 2004 Revised 29 March 2004 Accepted 23 April 2004 Published 8 June 2004 Journal of Biology 2004 3 11 The electronic version of this article is the complete one and can be found online at http jbiol.com content 3 3 11 2004 Okubo and Hogan licensee BioMed Central Ltd. This is an Open Access article verbatim copying and redistribution of this article are permitted in all media for any purpose provided this notice is preserved along with the article s original URL. Abstract Background Studies in many model systems have shown that canonical signaling through the pathway downstream of ligands of the Wnt family can regulate multiple steps in organogenesis including cell proliferation differentiation and lineage specification. In addition misexpression of the Wnt-family member Wingless in Drosophila imaginal disc cells can lead to transdetermination of progenitors from one lineage to another. Conditional deletion of the P-catenin component of the Wnt signaling pathway has indicated a role for Wnt signaling in mouse lung endoderm development. The full range of effects of this pathway which includes the transcription factor Lef1 has not been explored however. Results To explore this issue we expressed a constitutively active p-catenin-Lefl fusion protein in transgenic embryos using a lung-endoderm-specific promoter from the surfactant protein C gene. Transgenic lungs appeared grossly normal but internally they contained highly proliferative cuboidal epithelium lacking fully differentiated lung cell types. Unexpectedly microarray analysis and in situ hybridization revealed