smetana and touch insensitive larvae B, Two Genes Involved in Hearing and Male Fertility in Drosophila. R.G. Kavlie ¹, E. Sivan-Loukianova ², L.P. Morris ², M. Kernan ³, D.F. Eberl ^1,2. 1) Interdepartmental Genetics, University of Iowa, Iowa City, IA; 2) Department of Biological Sciences, University of Iowa, Iowa City, IA; 3) Department of Neurobiology and Behavior, State University of New York at Stony Brook, Stony Brook, NY.

   We are studying mutations in two different genes, smetana (smet) and touch insensitive larvae B (tilB). Flies with these mutations are deaf, and the adult males are sterile. We believe mutations in these genes cause axonemal defects in the ciliated neurons of Johnstons organ, the hearing organ of the adult fly, and axonemal defects in the sperm flagellum. smet has been mapped to polytene position 39E1-E2. We identified two overlapping deficiencies, Rev4 and R6 that delete smet. By performing PCR on the deficiency homozygotes we have narrowed the region where deficiency overlap may occur. Through P-induced male recombination we have further narrowed the region in which smet lies to between the insertion site of the P-element BG01034 and the gene cryptocephal. Deficiency mapping has placed tilB at map position 20A between the genes flamenco and wings apart. Transmission electron microscopy (TEM) of the sperm tail has been used to show that smet/Df flies are missing the inner dynein arms of their axonemes. Further ultrastructural analysis of the Johnstons organ shows that both the inner and outer dynein arms are missing in tilB mutants. We are currently sequencing the strongest candidates for smet and defining their expression patterns. Also we are inducing imprecise excision of the BG01034 P-element to induce a smaller smet deficiency. Finally we are using TEM to identify the ultrastructural defects in smet mutants. Our long-term goals are to identify and clone the smet and tilB genes and to understand their molecular function in chordotonal organ and sperm tail axonemes.