Perturbation of RET signaling in the embryonic kidney

• Published in: Developmental genetics 1999, Vol.24 (3-4), p.263-272
• Main Authors: Ehrenfels, Christian W., Carmillo, Paul J., Orozco, Olivia, Cate, Richard L., Sanicola, Michele
• Format: Article
• Language: English
• Subjects: Animals; Base Sequence; Bone Morphogenetic Protein 7; Bone Morphogenetic Proteins - genetics; DNA Primers - genetics; Drosophila Proteins; Fetal Proteins - genetics; Gene Expression Regulation, Developmental; GFRα-1; Glial Cell Line-Derived Neurotrophic Factor Receptors; Glycoproteins - genetics; Hedgehog Proteins; Humans; Immunohistochemistry; In Situ Hybridization; Kidney - embryology; Kidney - metabolism; kidney development; Membrane Proteins - genetics; Microfilament Proteins; Nuclear Proteins - genetics; organ culture; Organ Culture Techniques; Patched Receptors; Proteins - genetics; Proto-Oncogene Proteins - genetics; Proto-Oncogene Proteins c-ret; Rats; Receptor Protein-Tyrosine Kinases - genetics; Receptors, Cell Surface; Recombinant Fusion Proteins - genetics; RET; Signal Transduction; Trans-Activators; Transforming Growth Factor beta; Wnt Proteins; Wnt4 Protein
• ISSN: 0192-253X; 1520-6408
• DOI: 10.1002/(SICI)1520-6408(1999)24:3/4<263::AID-DVG9>3.0.CO;2-D

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 GFRα‐1 specific polyclonal antisera to localize GFRα‐1 protein expression in the developing kidney. Dev. Genet. 24:263–272, 1999. © 1999 Wiley‐Liss, Inc.