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Function of FMRP-Mediated MAP1b Regulation in Neuronal Development
 
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Yue Feng, Ph.D.
Principal Investigator
Emory University

FRAXA Awards:
  $50,000 in 2006
  $32,000 from FRAXA in 2005, and an additional $18,000 thanks to the Wiser family and the Jack Kent Cooke Foundation.

by Yue Feng, 2/2005

We have a long-standing interest in understanding how FMRP controls translation of its mRNA targets, and how FMRP deficiency leads to misregulated protein production in fragile X syndrome. Our recent studies focus on brain development of the newborn Fmr1 KO mice; we have demonstrated the functional requirement of FMRP in repressing translation of MAP1B during the most active period of synapse development. We found that the lack of FMRP causes overproduction of MAP1B and aberrantly increased microtubule stability in brain neurons, which is a conceivable factor underlying the abnormal synapse development in the fragile X brain.

The goal of this project is to delineate the pathological consequence of misregulated MAP1B, as a result of lacking FMRP, in neuronal development as well as in epilepsy, and explore the possibility of correcting such abnormalities by manipulating MAP1B expression and microtubule dynamics in the fragile X neurons, by microtubule targeted drugs and ligands of neurotransmitter receptors. We believe these studies will provide important insights for identifying potential drug targets for the treatment of fragile X syndrome.




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