Investigating the role of scribble alleles in Ras-induced tumorigenesis in Drosophila melanogaster eye-antennal imaginal discs

Abstract

Epithelial tumours are characterized by uncontrolled cell proliferation, often driven by the activation of proto-oncogenes and the inactivation of tumour suppressor genes. While clinical data on tumour progression continues to accumulate, the precise molecular mechanisms linking genetic alterations to pathological outcomes remain incompletely understood. Drosophila melanogaster serves as an excellent model organism for studying both developmental biology and disease processes, including tumorigenesis, due to its conserved signalling pathways that regulate cell growth and invasion. This study investigates the interaction between different alleles of the scribble gene, a key regulator of apicobasal polarity in epithelial cells, and the oncogene RasV12, using genetic mosaic analysis in the eye-antennal imaginal discs of Drosophila. The primary aim is to assess whether the hypomorphic allele scrib5 can preserve tissue organization and control cell proliferation when co-expressed with RasV12. The results demonstrate that Scrib5 and RasV12 act synergistically, leading to pronounced tissue overgrowth and disruption of epithelial architecture.