THE BASIS FOR A HEAT-INDUCED DEVELOPMENTAL DEFECT - DEFINING CRUCIAL LESIONS

Because lethal heat shocks perturb a multitude of cellular processes, the primary lesions responsible for death from heat stress remain to b e defined. In Drosophila, sublethal heat treatments produce developmen tal anomalies that frequently mimic the effects of known mutations and are hence referred to as phenocopies. Mutations subject to phenocopy mimicry provide signposts to those biological processes most sensitive to heat and most important for the function and survival of the organ ism as a whole. We have analyzed a particular developmental defect ind ucible in early embryos of Drosophila melanogaster. By molecular, phen otypic, and genetic criteria, we have found extensive parallels betwee n this phenocopy and certain dominant mutations in the segmentation ge ne fushi tarazu (ftz). Our analysis of this phenocopy indicates that t he crucial lesion is interference with proper turnover of ftz protein, resulting in ftz overexpression. Our results provide a novel explanat ion for a heat-induced developmental defect. Perturbations in relative amounts of important regulatory proteins may be a common mechanism by which heat-shock phenocopies arise.