Activation of the innate immune system accelerates growth in cooperation with oncogenic Ras.

Innate immunity in Drosophila acts as an organismal surveillance system that measures external stimuli or cellular fitness and triggers context-specific responses to fight infections and maintain tissue homeostasis. However, uncontrolled activation of innate immune pathways can be detrimental to the system. In mammals, innate immune signaling is often overactivated in malignant cells and contributes to tumor progression. Drosophila tumor models have been instrumental in the discovery of interactions between pathways that promote tumorigenesis, but little is known about whether and how the Toll innate immune pathway interacts with oncogenes. Here we use a Drosophila epithelial in vivo model to investigate the interplay between Toll signaling and oncogenic Ras. Overall design: Total RNA was extracted from approximately 50 control or 30 tumor eye-antennal discs (EAD) per sample from larvae at 96 h AED (after egg deposition). We generated mRNA sequencing libraries from four different samples, each in biologically independent triplicates: (1) Control EADs (LacZ), (2) Control EADs after Toll pathway activation (Dorsal), (3) Tumor EADs (RasLacZ) and (4) Tumor EADs after Toll pathway activation (RasDorsal).