The goal of this project is to understand more fully the mechanisms of gene regulation during eukaryotic development. The approach is to study selected loci having mutations that perturb regulatory functions. One system of interest involves the interaction of the zeste and white loci in Drosophila melanogaster. The mutation of z1 represses normal white locus (w+) function to give yellow eye color, but only if there are two w+ genes that are paired or proximate. This position-dependent regulatory phenomenon is called transvection. We are studying mutations of white locus that interact with z1 in ways that modify the transvection effort. For example, wzm gives a mottled eye color in a single dose, but only in a z1 background; otherwise it is wild type. The wzm mutation resulted from the insertion of the retrovirus-like transposon BEL in the 5'-most intron of the white locus, very near the sites where the zeste protein is known to bind, wzm is mildly unstable and has produced a series of other alleles including a transposition of an X chromosome segment containing white into the third chromosome. In the new position, the white locus produces a wild-type phenotype except when the transposition is homozygous and the z1 mutation is present. The transposition produces a mosaic eye-color that is nonautonomous and nonclonal in expression, marking a dramatic change from the autonomous, clonal patterns seen in the non-transposed wzm and its derivatives. The molecular analyses of these mutant alleles are being done to determine the basis for the modified expression of white and its interaction with zeste.
