Signaling by receptor tyrosine kinases (RTKs) is a mechanism implicated in developmental processes in organisms as distantly related as yeast and humans. Recently, protein tyrosine phosphatases (PTPases) have been implicated in RTK pathways. The Drosophila PTPase Corkscrew (Csw) is among the first PTPases whose gene mutations are allowing genetic analyses of function in vivo and has been functionally conserved through evolution. The experiments described here utilize genetic, cellular and molecular approaches to determine more precisely the role of Csw during embryogenesis. Therefore, this proposal addresses the following:
SPECIFIC AIM I. Determine genetic interactions between Csw and RTKs known to function during embryogenesis. Phenotypic analyses support an hypothesis that Csw functions in several RTK pathways during embryogenesis. To determine whether Csw functions in the DER and Btl RTK pathways experiments are designed to reveal genetic interactions between Csw and each of these RTKs.
SPECIFIC AIM II. Determine the role of Csw in RTK signalling during myogenesis. Preliminary results reveal a need for Csw for specification of both heart and muscle precursor cells during embryogenesis. Only a subset of muscle cells (and none of the heart cells) require the DER RTK suggesting that an additional RTK functions in mesoderm specification. Experiments are designed to elucidate the in vivo roles of Csw, as well as a candidate RTK, in the specification of these two mesodermally derived cell types.

Agency
National Institute of Health (NIH)
Institute
National Institute of General Medical Sciences (NIGMS)
Type
Predoctoral Individual National Research Service Award (F31)
Project #
5F31GM018903-04
Application #
6018324
Study Section
Special Emphasis Panel (ZRG2-CBY-1 (01))
Project Start
1999-09-30
Project End
Budget Start
1999-09-30
Budget End
1999-11-30
Support Year
4
Fiscal Year
1999
Total Cost
Indirect Cost
Name
Massachusetts General Hospital
Department
Type
DUNS #
City
Boston
State
MA
Country
United States
Zip Code
02199