Investigating the possible roles of a GPCR family in hemocyte migration. D.E. Siekhaus¹, M. Starz-Gaiano¹, P. Kunwar¹, R. Bainton², U. Heberlein², R. Lehmann¹. 1) Dept. of Developmental Genetics, NYUSOM, Skirball Institute, New York, NY; 2) Dept. of Neuroscience, University of California, San Francisco, San Francisco, CA.

   Regulated cell migration is essential for immune system function and unregulated cell migration contributes to the spread of cancer. Blood cells in Drosophila represent an attractive system to study the control of cell migration throughout the body. Embryonic blood cells in Drosophila are formed in the cephalic mesoderm during Stage 9 and then migrate in a stereotyped pattern to achieve an even dispersal throughout the embryo by Stage 15. Mutants in the VEGF Receptor are clearly deficient in one part of this migration, from the dorsal regions of the head into the tail (Cho et al., Cell 108, 865-876). Yet different signaling pathways might mediate earlier and later migratory steps. We have identified a predicted GPCR called 1631 that is expressed in hemocytes from Stage 9 to Stage 11 during their migration from the cephalic mesoderm to three distinct directions within the head. Mutants in this gene display no obvious defects in hemocyte migration. Yet 1631 has two close homologs in Drosophila, one of which, tre-1, is maternally provided and is required for the initial steps of germ cell migration. We are investigating the hemocyte migration phenotypes of flies carrying mutations of combinations of these GPCRs, as well as flies mutant for these GPCRs and the VEGFR.