Dr. Dressler studied Bioengineering and Chemical Engineering before receiving his Ph.D. in Molecular Genetics from the University of Pennsylvania. He was a post-doctoral fellow in the lab of Peter Gruss at the Max Planck Institute for Biophysical Chemistry where he helped discover the Pax gene family and characterized the Pax2 gene in the developing kidney and nervous system. As a staff fellow at the National Institute of Child Health and Human Development he began his studies on Pax2 and kidney development and disease. His lab showed that Pax2 was expressed in renal progenitor cells and in renal carcinoma and Wilms' tumor, but not in normal adult proximal tubules. Using genetic and biochemical models, he showed that deregulation of Pax2 led to severe kidney abnormalities. After coming to Michigan as a HHMI Assistant Investigator, he showed that glial-cell derived neurotrophic factor was the ligand for the c-ret tyrosine kinase and promoted renal epithelial cell migration in the developing kidney. The Dressler lab went on to discover the Kielin/Chordin-like Protein (KCP), the first secreted enhancer of BMP signaling and showed that this protein was important for mediating fibrotic disease in the kidney and liver. The lab also discovered PTIP, and adaptor protein that links the Pax family of DNA binding proteins to the MLL family of histone H4, lysine 4 methyltransferases. This work defined a new paradigm for how developmental regulatory proteins can imprint cell lineage specificity through epigenetic modification of the genome.

 How do cells know when and where to differentiate within the context of a developing multicellular organism? That is a fundamental question in biology whose relevance transcends all aspects of gene regulation, cellular phenotype and stability, tissue regeneration, and disease progression. Using the kidney and reproductive tract as a model tissue, the lab studies how these tissues are derived from the mesoderm, what genes and proteins determine the fate of specific mesoderm, how these developmental regulatory processes are disturbed in disease, and how such processes are reactivated in regeneration. Genetically engineered mouse models and biochemical analyses are used to study protein complexes that specify the renal epithelium and the female reproductive tract. How developmental signaling pathways are co-opted in chronic and acute renal disease is also under investigation, with particular emphasis on BMPs and TGF-beta. Based on our recent discoveries, several projects underway utilize the Chemical Genomics Core to screen for novel small molecules that may be lead compounds for developing new therapies for chronic and acute renal disease.