In this proposal I will investigate signaling cascades that control branching at the nerve-terminal. The basis for this research will be three recently identified mutants that specifically alter nerve-terminal branching. Loss-of-function in the mutant cap ta in haddock (chad) leads to an increase in terminal branching, while loss-of-function in the mutant red rackham (rerak) leads to a decrease in terminal branching. Over- expression of the strung-out (stout) gene in muscle leads to an increase in nerve-terminal branching, indicating an alteration to a retrograde signaling pathway. chad and stout have been identified and are novel genes. I propose to identify the gene responsible for the rerak phenotype. I also propose to further characterize the phenotypes of these three mutations by analyzing their development live with GFP lines that specifically light up the synapse. In addition, I propose to do a series of electrophysiological experiments with these branching mutants that will test the importance of nerve-terminal branching for synaptic function and activity-dependent plasticity.

Agency
National Institute of Health (NIH)
Institute
National Institute of Neurological Disorders and Stroke (NINDS)
Type
Postdoctoral Individual National Research Service Award (F32)
Project #
1F32NS011066-01
Application #
6207310
Study Section
Special Emphasis Panel (ZRG1-MDCN-7 (01))
Program Officer
Finkelstein, Robert
Project Start
2001-09-30
Project End
Budget Start
2001-09-30
Budget End
2002-09-29
Support Year
1
Fiscal Year
2000
Total Cost
$37,516
Indirect Cost
Name
University of California San Francisco
Department
Biochemistry
Type
Schools of Medicine
DUNS #
073133571
City
San Francisco
State
CA
Country
United States
Zip Code
94143