The Martin lab is interested in understanding the mechanisms that control the early steps in organogenesis in the vertebrate embryo, and the subsequent outgrowth and patterning of the developing organs. We are particularly interested in the roles played by members of the Fibroblast Growth Factor (FGF) family of signaling molecules and their antagonists in these processes. For the most part we use genetic analysis in mice to uncover the functions of these molecules in the developing embryo.

Selected Publications

Shim, K., Minowada, G. Coling, D. E., and Martin, G. R. (2005). Sprouty2, a mouse deafness gene, regulates cell fate decisions in the auditory sensory epithelium by antagonizing FGF signaling. Dev. Cell 8, 553-564.

Grieshammer, U., Cebri·n, C., Ilagan, R., Meyers, E. N., Herzlinger, D. and Martin, G. R. (2005). FGF8 is required for cell survival at distinct stages of nephrogenesis and for regulation of gene expression in nascent nephrons. Development 132, 3847-3857.

Lu, P., Minowada, G., and Martin, G.R. (2006). Increasing Fgf4 expression in the mouse limb bud causes polysyndactyly and rescues the skeletal defects that result from loss of Fgf8 function. Development 133, 33-42.

Klein, O.D., Minowada, G., Peterkova, R., Kangas, A., Yu, B.D., Lesot, H., Peterka, M., Jernvall, J. and Martin, G. R. (2006). Sprouty genes control diastema tooth development via bidirectional antagonism of epithelial-mesenchymal FGF signaling. Dev. Cell 11, 181-190.

Craniofacial and Mesenchymal Biology home page

Fat cells in culture

Osteoblast depositing
bone matrix

The UCSF Program in Craniofacial and Mesenchymal Biology

FACULTY

Gail Martin

Organogenesis

The UCSF Program
in Craniofacial and Mesenchymal Biology