Stage specific embryonic defects following heat shock in Drosophila

Abstract

AbstractHeat shock of pre‐adult Drosophila disrupts development and causes phenotypic abnormalities. Type of abnormality depends on developmental stage at time of shock. Defects probably result from disruption of stage specific processes by the heat shock response (which includes reduction of normal mRNA and protein production). This study uses heat shock to study stage specific processes in early development. Short, intense shocks (2–3 min, 42–43°C) are administered to carefully staged embryos within the first 5 h of development. Stage specific defects occur following shock at syncitial blastoderm or later. Abnormal segmentation follows shock at syncitial or cellular blastoderm. Segmentation is also disrupted by shocks 1 h after the onset of gastrulation, but not by shocks at the onset of gastrulation. Segmentation defects include phenocopies of pair rule mutants, which lack parts of alternate segments. Defective shortening of the germ band is common following shock at the onset of gastrulation. Germ band shortening normally occurs several hours after the time of shock; thus heat shock specifically affects control of a later developmental process. Development does not simply cease at the time of the distrupted process; rather a specific step in the developmental sequence is omitted or altered. Stage specific defects do not occur following pre‐blastoderm shock. Pre‐blastoderm eggs have few or no normal processes controlled by transcription, and poor ability to induce the heat shock response. This suggests that stage specific defects require disruption of transcription controlled processes. Pre‐blastoderm eggs survive a 3‐min shock less well than older eggs. The ability of older eggs to induce the heat shock response probably enhances survival. The mutant hairy was also investigated. Extreme alleles show a striking pair rule phenotype, while a weak allele does not. Heat shock of animals heterozygous or homozygous for the weak allele at blastoderm specifically increases the frequency of the extreme hairy phenotype. Thus heat shock may disrupt the same developmental process as is altered by the mutation.