Perturbation of RET signaling in the embryonic kidney.
We have used a RET-Ig fusion protein to disrupt signaling in the rat embryonic kidney development pathway. Treatment of embryonic kidney organ cultures with RET-Ig results in a decrease in branching of the ureteric bud and a down regulation in expression of the Wnt-11, Wnt-4, and ld genes. These data suggest that Wnt-11, Wnt-4, and ld function downstream of RET signaling in normal development. Expression of BMP-7, shh, and ptc were uneffected by RET-Ig treatment, implying that these genes are regulated independently of ret. We have also performed immunohistochemistry with a GFR alpha-1 specific polyclonal antisera to localize GFR alpha-1 protein expression in the developing kidney.
D000818:Animals; D001483:Base Sequence; D055419:Bone Morphogenetic Protein 7; D019485:Bone Morphogenetic Proteins / Q000235:genetics; D017931:DNA Primers / Q000235:genetics; D029721:Drosophila Proteins; D005326:Fetal Proteins / Q000235:genetics; D000080865:Formins; D018507:Gene Expression Regulation, Developmental; D051097:Glial Cell Line-Derived Neurotrophic Factor Receptors; D006023:Glycoproteins / Q000235:genetics; D053823:Hedgehog Proteins; D006801:Humans; D007150:Immunohistochemistry; D017403:In Situ Hybridization; D007668:Kidney / Q000196:embryology* / Q000378:metabolism*; D008565:Membrane Proteins / Q000235:genetics; D008840:Microfilament Proteins; D009687:Nuclear Proteins / Q000235:genetics; D009924:Organ Culture Techniques; D000072079:Patched Receptors; D011506:Proteins / Q000235:genetics; D011518:Proto-Oncogene Proteins / Q000235:genetics*; D051096:Proto-Oncogene Proteins c-ret; D051381:Rats; D020794:Receptor Protein-Tyrosine Kinases / Q000235:genetics*; D011956:Receptors, Cell Surface; D011993:Recombinant Fusion Proteins / Q000235:genetics; D015398:Signal Transduction; D015534:Trans-Activators; D016212:Transforming Growth Factor beta; D051153:Wnt Proteins; D060528:Wnt4 Protein