David M. Ornitz,
M.D., Ph.D.

Alumni Endowed Professor

Department of Molecular Biology and Pharmacology

Washington University
School of Medicine

Campus Box 8103
660 South Euclid Avenue
Saint Louis, MO
63110

dornitz@wustl.edu

 

 



More information about David Ornitz and his laboratory: bio sketch, research interests, selected publications and laboratory resources.


Selected laboratory protocols, such as: alkaline plasmid prep, BrdU immunohistochemistry, LacZ embryo staining, RNase protection assay and many others.


Information and graphics concerncing fibroblast growth factor research, such as: FGF family tree, FGFR mutations, FGF specificity data and more.


Information on vestibular system projects; QuickTime movie of a mouse swim test in the Ornitz lab. The goal of this work is to identify the genes required for otoconia biosynthesis and the function of the gravity receptor.


Four types of projects are ongoing in the laboratory.

The first focuses on the role of FGFs in brain development. We are examining the developmental function of FGFs in cerebellar development. We have shown that FGF8 and FGF17 cooperate to regulate growth of midline cerebellar tissues. We are now investigating whether FGF18, a closely related FGF, is also involved in cerebellar development.

The second project involves the conditional inactivation of FGF receptor 2 in developing neuroblast and glial cells. Future studies will target FGFR2 inactivation to more defined sets of cells.

The third project involves FGF14 knockout mice. These mice develop neurological defects yet undergo normal development. These mice have provided an extremely useful tool to understand mechanisms of neuronal signaling in the basal ganglia and cerebellum.

The fourth project involves the axon guidance molecule slt3 and its role in mouse development.


Mice lacking FGF9 have defects in lung branching and lung mesoderm proliferation. These mice also have a male to female sex reversal secondary to decreased growth of testicular mesenchyme and failure of normal Sertoli and Lydig cell development.


Apert Syndrome manifests itself in premature ossification and fusion of the sutures between the developing flat bones of the skull; osseous fusion of digits and phalangeal joints; soft-tissue syndactyly in hands and feet; and in central nervous system malformations and mental retardation.


Links to other programs within the School of Medicine, and to other areas of interest.



This website is maintained by Laura Kyro. Latest update to this page: September 2004.