Rachel K. Miller, PhD
- Associate Professor, Pediatric Research Center
- Adjunct Associate Professor, Department of Genetics, The University of Texas MD Anderson Cancer Center
- Co-Director, Program in Genetics and Epigenetics, MD Anderson UTHealth Houston Graduate School of Biomedical Sciences
- Co-Chair, Women Faculty Forum, McGovern Medical School, UT Health Houston
Education
- B.A., Biology and Physics
- DePauw University, 2001
- Ph.D., Genetics and Molecular Biology
- Emory University, Atlanta, Georgia, 2007
- Postdoctoral and Odyssey Fellow, Developmental and Cell Biology
- The University of Texas MD Anderson Cancer Center, Houston, Texas, 2007-2012; Instructor 2012-2013
Areas of Interest
Research Interests
Although congenital anomalies of the kidney and urinary tract (CAKUT) are the predominant birth defects diagnosed in the prenatal period and are the most common cause of pediatric end stage renal disease, only 13% of cases have a known monogenic cause. CAKUT can result in defects in the formation of nephrons, which are required for the function of the kidney. During kidney development, early beta-catenin-mediated Wnt signaling, which is required for nephric mesenchyme condensation into epithelia, transitions to planar cell polarity (PCP)-mediated Wnt signaling, resulting in morphogenesis and differentiation of the nephron. A balance between beta-catenin and PCP signaling is thus critical in kidney formation and maintenance, with disruption of this balance promoting cystic diseases and kidney cancers. Our laboratory uses Xenopus (frog) embryos to understand how cells communicate via Wnt signaling to coordinate nephron formation and how this process goes awry giving rise to CAKUT.