A Deficiency Screen to Identify Regions of the Third Chromosome that Genetically Interact with Activated Abl. Lacey Berry, Traci L. Stevens. Biology, Randolph-Macon College, Ashland, VA.

   Abl nonreceptor tyrosine kinases are a highly conserved family of proteins that are essential in the development of multicellular organisms. Chronic myelogenous leukemia, a genetic disorder in humans, is linked to expression of Bcr-Abl, an activated form of Abl. Expression of the mutant Bcr-Abl in cell culture alters actin structures and cell migration. Studies in Drosophila have shown that the Abl protein plays a critical role in the ability of cells to migrate and communicate with neighboring cells in vivo. Expression of activated Abl in Drosophila disrupts dorsal closure and head involution, processes that require regulated cell migration. The pathways by which Abl receives signals from the cell surface and that link Abl to the actin cytoskeleton remain largely unknown, and the goal of our laboratory is to characterize proteins that work with Abl to regulate cell migration during development. In order to identify genes that function in Abl pathways, we are conducting a genetic screen to identify regions of the genome that contain genes that genetically interact with activated Abl expression during embryonic development. In this study, we identified ten deficiencies of the third chromosome that enhanced the phenotypes associated with Bcr-Abl expression when compared to the control. Three pairs of these interacting deficiencies overlap, and thus, each of these pairs is likely to represent a single interacting gene that falls in the region of overlap. Therefore, these ten interacting deficiencies represent seven independent genomic regions that are likely to contain genes that function in Abl signaling pathways. In the future, these interacting regions will be narrowed down to pinpoint single genes that encode proteins that work along with Abl in regulating cell migration.