Two phases of myogenesis occur in Drosophila- the embryonic period during which larval muscles develop, and the pupal period during which adult muscles develop. Adult myogenesis is dependent on innervation and embryonic is not (Fernandes and Keshishian, 1999). This allows us to explore how the nerve may signal to myoblasts or organizer cells. This is important, because vertebrate skeletal muscles also depend on innervation for their development. We use the indirect flight muscles of the fly as a model system- these ar esome of the largest muscles in the fruifly. Based on previous studies [Fernandes and Keshishian, 2005], the influence of motor neurons on myoblast proliferation was proposed to be brought about through the founder cell. This has been confirmed by 2 sets of preliminary data (1) Ablation of founder cells causes a 30% reduction in BrDU positive myoblasts, which is similar to what is seen during denervation (2) Blocking EGF signal reception in myoblasts causes 20% reductions in proliferation and causes patterning defects in 95% of animals. To test if the motor neuron was the source of signals, we have used two approaches- Blocking the synthesis of EGF ligands and overexpressing the signals. The number of adult nuclei in sections of adult muscles can be used as an indicator of the extent of myoblast proliferation. Our results thus far show that spitz and vein are predominant EGF ligands that mediate the neuronal influence on organizer cells to influence myoblast proliferation. Blocking synthesis with RNAi caused decreased number of nuclei in adult muscles, and conversely overexpression caused an increase in the number of nuclei. Our results indicate that the EGF signaling pathway operates during the motor neuron mediated proliferation of myoblasts during myogenesis.