Candidate - Dr. Chung is a research associate with in depth knowledge about the role of steroid hormones, steroid receptors and growth factors during brain development. His past research was focused on the cellular and molecular mechanisms involved in the sexual differentiation of the brain. His immediate goal is to extend his academic and professional skills in order to enact his independent translational research program studying steroid hormone-dependent growth factor expression underlying CNS morphogenesis through extra-mural funding. This proposed K99/R00 proposal forms an integral part in this pursuit. Career development plan - Dr. Chung's proposed training activities consist of: 1) acquiring new research techniques associated with this proposal, 2) attend structured forums designed to promote periodic interactions with his mentors and disseminate his research data at local and national scientific meetings, 3) mentor and train undergraduate and graduate students in performing independent research projects. Environment - The research environment for the proposed training activities is well-suited. The primary sponsor, Dr. Tsai, is well-established in the field of neuroendocrinology with extramural funding and has an excellent record in the successful mentoring of undergraduates, graduates and postdoctoral fellows. Research - The studies are based on the hypothesis: Testosterone regulates the development of the neuroendocrine brain via the induction of fibroblast growth factor (FGF) 8/FGF receptor signaling. These studies examine how testosterone regulates FGF8/FGF receptor expression in the embryo brain, and investigate the consequences of FGF8 deficiency on brain development. Examination of this hypothesis will result in new insights about how the embryonic neuroendocrine brain is organized in a testosterone-dependent fashion.
Fibroblast growth factor (FGF) signaling has been implicated in the Kallmann syndrome, a human disease characterized by hypogonadotropic and hypogonadism associated with anosmia. Therefore, novel insights in how FGF expression is regulated by testosterone may help us better understand the mechanisms involved in the onset of Kallmann syndrome.
