Training / Education
Ph.D. - Yale University - Neuroscience – May 2005 (Advisors: Mark S. Mooseker, Ph.D. and David G. Wells, Ph.D.
B.A. - Oberlin College - Biology - May 1999
Research Interests
Fragile X syndrome (FXS) is caused by the loss of fragile X mental retardation protein (FMRP), and understanding the function of this protein is essential to understanding the syndrome. Evidence suggests that FMRP (1) regulates the translation of specific mRNAs, (2) negatively regulates its own production, and (3) is made at synapses in response to the long-term depression (LTD) mediated by group 1 metabotropic glutamate receptors (Gp 1 mGluRs). Interestingly, mGluR-LTD is protein synthesis-dependent, and the "mGluR Theory" suggests that symptoms of FXS may be due to exaggerated mGluR-LTD mediated protein synthesis. The question then becomes- what proteins are produced during mGluR-LTD, and how might excessive production of these proteins result in FXS symptoms?
Grants / Awards
Ruth L. Kirschstein National Research Service Award Individual Fellowship (9/1/04-7/1/05)
National Fragile X Foundation Basic Science Grant (7/1/05-7/1/06)
FRAXA Postdoctoral Fellowship (7/1/06-present)
Publications
Krendel M, Osterweil EK, Mooseker MS. Myosin 1E
interacts with synaptojanin-1 and dynamin and is involved in
endocytosis.
FEBS Lett. 2007 Feb 20;581(4):644-50
Osterweil E, Wells DG, Mooseker MS. A role for myosin VI in postsynaptic structure and glutamate receptor endocytosis. J Cell Biol. 2005 Jan 17;168(2):329-38.
Graesser D, Solowiej A, Bruckner M, Osterweil E, Juedes A, Davis S, Ruddle NH, Engelhardt B, Madri JA. Altered vascular permeability and early onset of experimental autoimmune encephalomyelitis in PECAM-1-deficient mice. J Clin Invest. 2002 Feb;109(3):383-92. |
