Yu Lab
Molecular and Genetic Regulation of Organogenesis and Cancer
My laboratory studies the mechanisms that regulate cell growth and differentiation during organogenesis. During organogenesis, multipotent progenitors are recruited, new cell lineages emerge, and patterned tissues emerge from complex cell-cell interactions. Robust signals that regulate growth are required to produce reproducible shapes and sizes of organs in throughout the life of an organism and in all its progeny. Understanding this process will help identify the key molecules and signaling centers necessary to stimulate for organ regeneration and repair.
The ectoderm is an ideal model to study organogenesis and tissue regeneration. The ectoderm is capable of producing organs of diverse size and shape including skin, hair, teeth, glands, and feathers. In addition, some of these organs, e.g. the hair and mammary glands, are regenerated multiple times during the life of an organism.
It has been known that growth factor signals such as fibroblast growth factors (FGFs), epidermal growth factor (EGF) and others play a role in the epithelial-mesenchymal interactions necessary for patterning the ectoderm. Our laboratory studies the molecular and genetic mechanisms by which such classical growth factors participate in patterning the morphogenesis of both embryonic and postnatal structures including the apical ectodermal ridge (AER), hair follicle, and sweat glands. Using models of activated Ras or animals deficient in antagonists of receptor tyrosine kinases called Sproutys, we are studying how RTK signals in the ectoderm and underlying mesenchyme regulate the growth and pattern of each of these structures.
An additional model to study organogenesis is in cancer. Many of the same molecules that participate during organogenesis are also perturbed in cancers such as melanoma. The abnormal growth pattern of transformed melanocytes contributes to the clinical appearance and metastatic propensity of this cancer. We are interested in understanding how melanoma cells spread and how tissue remodeling contributes to the maintenance of metastatic tumors.
Contact: Benjamin D. Yu M.D., Ph.D.
Email: byu@ucsd.edu