Ectopic expression of mir-3 affects mef2 and tinman levels

Loss of nautilus (MyoD) gene function results in a variable phenotype affecting muscle formation in embryos and larvae, larval movement, pupal eclosion, egg deposition, adult mobility and survival. mir-3 over expression disrupts muscle formation in the embryo while affecting protein production from the dMef2 and tinman genes, global regulators of the muscle transcriptional network. We propose the complex phenotype in the nautilus null is due to the disruption of the regulatory interactions provided by the 8-miR cluster. The results demonstrate that nautilus is an integral regulator of the miRNA circuitry buffering the transcriptional network directing muscle development. Two-condition experiment, wild type (w1118) vs. mutant (mir-3 ectopic expressionl). Biological replicates: 3 wild type, 3 mutants, independently isolated. One of the biological replicate was dye swaped to avoid dye bias.