Associate Professor
Washington University in St. Louis
Dr. Ma obtained his BA degree from the University of California Berkeley and his Ph.D. degree in biochemistry and molecular biology from the University of Southern California. He received his postdoctoral training from Brigham and Women's Hospital and Harvard Medical School. Research in the Ma lab focuses on understanding signaling pathways regulating organogenesis and how endocrine disruptors may affect development. He has a long-standing interest in the development and patterning of the female reproductive tract as well as uterine function during embryo implantation. His has spent 15 years studying the molecular mechanisms underlying DES-induced uterine metaplasia. His lab showed that DES changed uterine epithelial cell fate and altered their cellular metabolism by activating ectopic adipogenic program via Pparγ. More recently his lab demonstrated that DES influences uterine epithelial cell fate by antagonizing retinoic acid signaling during development. He has also focused his research effort on uterine receptivity and decidualization. Despite its importance during embryo implantation, the process of decidualization has not been systematically studied at the genetic level due to the lack of a suitable high-throughput screening tool. To address this challenge, his lab finished a genome-wide siRNA screen to identify genes crucially required during decidualization in humans as well as drugs that either inhibit or enhance this process which could be candidates for novel non-steroidal female contraceptives or IVF drugs, respectively. From the screening result, his lab identified retinoic acid signaling as a major pathway regulating decidualization and mice expressing a dominant negative retinoic acid receptor in the peri-implantation uterus are infertile.
Another major research focus in his lab is urogenital development. Through years of research, they have shown that Shh, Wnt, and Fgf signaling pathways are absolutely required during genital tubercle development as well as cloaca septation. Using mouse genetics, they showed that a conserved genetic pathway, Wnt/β-cateninSp8Fgf8, regulates the outgrowth of body appendages including limbs and genitalia. In addition, they uncovered a role for β-catenin in regulating male predilection to bladder cancer.