Rachel Katherine Miller, PhD, is a tenured associate professor of pediatrics in the Pediatric Research Center at McGovern Medical School at UTHealth Houston and an internationally recognized developmental biologist whose research advances fundamental understanding of kidney development, tubulogenesis, and congenital renal disease. She also serves as director of the Genetics & Epigenetics Graduate Program (2024–2026) at the MD Anderson Cancer Center UTHealth Houston Graduate School of Biomedical Sciences (GSBS), where she leads academic strategy, curriculum innovation, and trainee success initiatives across one of the institution’s largest graduate programs.
Dr. Miller’s research focuses on the molecular regulation of nephron formation, epithelial morphogenesis, and Wnt/planar cell polarity (PCP) signaling, using Xenopus laevis as a powerful vertebrate model of human congenital disease. Her laboratory has produced several field shaping discoveries, including:
Her work is frequently highlighted in scientific media including Genes to Genomes, The Well, The Scientist, Xenbase, The Scoop, and the NIH Director’s Blog, reflecting its broad impact.
Nationally, Dr. Miller has served on the NIH DEV2 Study Section through multiple terms as an ad hoc reviewer from 2023–2025. She is frequently invited to present her research or contribute expertise at NIH workshops, international Xenopus conferences, and developmental nephrology meetings. She has delivered seminars at leading institutions including Emory University, the University of Kansas Medical Center, University of Michigan, Baylor College of Medicine, the Marine Biological Laboratory, the NIH, University of Zurich, Northwestern University, and Mount Sinai.
Dr. Miller is deeply committed to mentorship, training, and building scientific communities. She has served on nearly 70 graduate student committees, including doctoral advisory committees, doctoral examining committees, and master’s advisory committees, in addition to faculty mentorship and departmental committees. She has mentored postdoctoral fellows, medical fellows, PhD and MS students, and undergraduates who have earned nationally competitive fellowships (TL1, T32, K level awards), endowed scholarships, and faculty positions.
She plays a central role in multi institutional training infrastructures, serving as Co Director of the HAI KUH Networking Core of the NIH funded U2C/TL1 Houston Area Incubator for Kidney, Urologic, and Hematologic Research Training Program, where she leads cross institutional networking, trainee integration, and professional development programming across the Texas Medical Center.
Internationally, she is an instructor (2025–2029) for the prestigious Cold Spring Harbor Laboratory course, “Cell & Developmental Biology of Xenopus: Gene Discovery & Disease,” following earlier roles as lecturer and co-instructor. Her contributions to scientific education and leadership have been recognized through numerous honors, including the 2025 D. Dudley and Judy White Oldham Faculty Award, 2024 Breakthrough Discoveries Symposium Award, multiple GSBS commendations, and early career recognition from the National Xenopus Resource, the Society for Developmental Biology, and the Genetics Society of America.
Dr. Miller earned her B.A. in Biology and Physics, Magna Cum Laude, from DePauw University, her PhD in Genetics and Molecular Biology from Emory University, and completed advanced postdoctoral training and Odyssey Fellowship work in Cell and Developmental Biology at the University of Texas MD Anderson Cancer Center.
Her research continues to expand the mechanistic understanding of kidney development, deepen the modeling of human congenital disorders, and promote the use of Xenopus as a uniquely powerful system for studying developmental biology and birth defects.
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.