Yingzi Yang, Ph.D. Senior Investigator Genetic Disease Research Branch Head Developmental Genetics Section B.S. Fudan University, Shanghai, P.R. China, 1988 Ph.D. Cornell University, 1996 (301) 402-2034 (301) 402-2170 yingzi@mail.nih.gov Building 49, Room 4A68 49 Convent Dr, MSC 4472 Bethesda, MD 20892-4472 Selected Publications

Dr. Yang's laboratory studies vertebrate limb development and skeletal morphogenesis. Her goal is to understand the mechanisms by which molecular signals are transduced and integrated in a regulatory network, and to gain insight into key regulatory events during skeletogenesis. To that end, her lab focuses on the signaling mechanisms of Wnts and Hhs (hedgehogs) in the limb, and how abnormalities in these two signaling pathways lead to birth defects and tumor formation. Her lab's multidisciplinary approach combines the strength of mouse molecular genetics with embryology, functional genomics, and the cell and organ culture systems in the developing limb.

Skeletal morphogenesis starts from mesenchymal condensation, which ossifies either directly (intramembranous ossification) or indirectly through the formation of a cartilaginous shaft (endochondral ossification). Early in endochondral skeletogenesis, chondrocytes and osteoblasts differentiate from a homogeneous field of cells to form the skeletal anlagen. Later, cartilage and bone develop through a precisely coordinated process that involves the sequential maturation of chondrocytes and osteoblasts and the invasion of blood vessels. Early patterning signals, including Hhs, Wnts, FGFs and TGF superfamily members, provide temporal and spatial information when these skeletal anlagen are laid down, long before overt skeletogenesis. Dr. Yang's previous work provided insight into the regulation of this early limb patterning event. Her current research addresses how signaling molecules regulate the formation of skeletal elements in the limb, a later morphogenetic process. She seeks to understand several fundamental events in skeletal morphogenesis: the regulation of mesenchymal condensation; the differentiation of chondrocytes versus osteoblasts from mesenchymal progenitor cells; the coordination of chondrocyte proliferation with maturation; and the induction and maintenance of synovial joint formation.

Dr. Yang has made several discoveries in her current research efforts. She found that different Wnts play distinct roles in regulating chondrocyte differentiation. The canonical Wnt pathway induces synovial joint formation and determines cell differentiation of mesenchymal progenitors by inhibiting chondrogenesis while promoting osteogenesis. The non-canonical Wnt5a promotes chondrocyte differentiation by inhibiting the canonical Wnt signaling activity. In addition, she found that the canonical Wnt pathway interact with Ihh signaling pathway in distinct ways during different processes of skeletal morphogenesis and Wnt5a acts in parallel pathways with Ihh to coordinate chondrocyte maturation. Dr. Yang's lab is continuing to study how Wnt and Hh signaling pathways are integrated with other pathways in skeletal development and is now exploring the role of Wnt and Ihh signaling in bone diseases, such as osteoarthritis and bone tumors. Her lab is also actively investigating the molecular mechanism underlying the control of cell and tissue organization by the planar cell polarity pathway in both embryonic development and adult tissue homeostasis.

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Last Reviewed: February 10, 2009