The mutant phenotype of nautilus. L. Balagopalan , C. Keller , S. Abmayr. Biochemistry and Mol. Biol., Pennsylvania State University, State College, PA.

   nautilus is the only apparent Drosophila homologue of the bHLH family of myogenic regulatory factors. Previous studies (Keller et. al., 1998.) described two overlapping deficiencies that remove the nau gene. The entire coding sequence is completely absent in each of these deficiencies and transheterozygous embryos exhibit no NAU expression. These embryos are missing a subset of muscles, but not the precursors to these muscles, indicating that nau plays a role in the differentiation of these precursors to mature muscle fibers. This muscle loss is tolerated through development and individuals lacking nau survive to adulthood. Interestingly, adult females that are transheterozygous for the deficiencies are sterile and lay eggs that appear to be unfertilized. Both the embryonic muscle phenotype and the adult female sterility phenotype are rescued by ectopic expression of nau, indicating that nau is responsible for both of these defects. In an effort to address whether lack of lethality was a consequence of maternally provided nau, RT-PCR analysis of mRNA isolated from either unfertilized eggs, 0-4 hr embryos, or ovaries was performed. To date, no nau products have been detected by this assay. However, as an independent method to determine if nau mRNA is provided maternally, germline clone analysis will be performed. To this end, the sterility phenotype was used as the basis for genetic screens to isolate a mutation specific for nau. Out of 5407 mutagenized chromosomes, two apparent muatations in nau have been recovered. One of them, nau¹⁸⁸, is a small deletion that removes the nau transcription start site, 5'UTR and Exon 1. Embryos that are genetically nau¹⁸⁸/Df(3R)nau-11a4 display the same somatic muscle phenotype as previously described for the deficiency transheterozygotes and do not exhibit detectable levels of NAU expression. These results suggest that nau¹⁸⁸ is a null allele. Experiments to generate germline clones with this mutation are currently in progress.