Abstract
Because lethal heat shocks perturb a multitude of cellular processes, the primary lesions responsible for death from heat stress remain to be defined. In Drosophila, sublethal heat treatments produce developmental 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 organism as a whole. We have analyzed a particular developmental defect inducible in early embryos of Drosophila melanogaster. By molecular, phenotypic, and genetic criteria, we have found extensive parallels between this phenocopy and certain dominant mutations in the segmentation gene fushi tarazu (ftz). Our analysis of this phenocopy indicates that the crucial lesion is interference with proper turnover of ftz protein, resulting in ftz overexpression. Our results provide a novel explanation 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.
