Analysis of Ras-Induced Overproliferation in Drosophila Hemocytes

Author:

Asha H1,Nagy Istvan2,Kovacs Gabor2,Stetson Daniel3,Ando Istvan1,Dearolf Charles R1

Affiliation:

1. Department of Pediatrics, Massachusetts General Hospital, Boston, Massachusetts 02114

2. Department of Molecular Biology, Massachusetts General Hospital, Boston, Massachusetts 02114

3. Institute of Genetics, Biological Research Center of the Hungarian Academy of Sciences, H-6701, Szeged, Hungary

Abstract

Abstract We use the Drosophila melanogaster larval hematopoietic system as an in vivo model for the genetic and functional genomic analysis of oncogenic cell overproliferation. Ras regulates cell proliferation and differentiation in multicellular eukaryotes. To further elucidate the role of activated Ras in cell overproliferation, we generated a collagen promoter-Gal4 strain to overexpress RasV12 in Drosophila hemocytes. Activated Ras causes a dramatic increase in the number of circulating larval hemocytes (blood cells), which is caused by cellular overproliferation. This phenotype is mediated by the Raf/MAPK pathway. The mutant hemocytes retain the ability to phagocytose bacteria as well as to differentiate into lamellocytes. Microarray analysis of hemocytes overexpressing RasV12  vs. Ras+ identified 279 transcripts that are differentially expressed threefold or more in hemocytes expressing activated Ras. This work demonstrates that it will be feasible to combine genetic and functional genomic approaches in the Drosophila hematopoietic system to systematically identify oncogene-specific downstream targets.

Publisher

Oxford University Press (OUP)

Subject

Genetics

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