*** 9513334 Abmayr The proposed studies focus on the role of nautilus, the Drosophila homologue of the myogenic regulatory gene family that includes MyoD, in myogenesis. Embryos homozygous for deficiencies that delete nautilis are missing a distinct subset of mesodermal cells. Several of these muscles are missing in embryos mutant for daughterless, the putative partner of nautilus, and the spitz group genes, an EGF-like signaling cascade involved in dorsal/ventral axis determination. Additional studies have revealed that nautilus is capable of converting cells from non-muscle origins to somatic muscles, and of altering the developmental program of somatic muscle fibers in which it is not normally expressed. These results suggest that nautilus induces myogenic differentiation, and that some cells are converted to a myogenic program by expression of bHLH-containing myogenic genes. The proposed experiments are designed to address various aspects of the above findings. These include characterizing potential point mutations and/or overlapping deficiencies that affect only the nautilus gene. Results of these studies will provide critical information indicating whether nautilus is necessary to specify particular muscle progenitors or, rather, simply induces their differentiation program. In related studies, the origin and developmental status of ectopic muscles that form in response to nautilus will be explored to aid in understanding its role. Additional studies will search for interactions between nautilus and genes that cause similar or related mutant phenotypes. For example, the observation that daughterless mutant embryos exhibit a more severe mutant phenotype than that of the nautilus deficiencies suggests that it may interact with proteins that have yet to be identified. ***
