Fig. 1. Caspase-dependent cell death in bicoid and oskar mutants. (A-C) Schematic illustration of the wild-type (A), bicoid (B) and oskar (C) phenotypes. In each panel, the embryonic fate maps are shown on the left, the differentiated larvae on the right. During development, wild-type embryos specify five distinct regions along the anteroposterior axis that are visible in the larval cuticle as Acron (Ac), Head (He), Thorax (Th), Abdomen (Ab) and Telson (Te). Arrows indicate the polarity of the tissues. T1-3 and A1-8 denote thoracic and abdominal segments, respectively. In bicoid and oskar mutants, this pattern is severely affected and some of the regions are missing. In addition, in bicoid mutants, the anterior acron is transformed into a telson (B). Modified, with permission, from Nüsslein-Volhard et al. (Nüsslein-Volhard et al., 1987). (D-F) Lateral views of larval cuticle preparations of wild-type (D), bicoid (E) and oskar (F) mutants. (G-I) Lateral views of TUNEL-labeled embryos of wild-type (G), bicoid (H) and oskar (I) mutants. (H,I) Brackets indicate areas of increased cell death; arrows indicate the presumptive telson (Te) areas, which are TUNEL negative. (J-L) CM1 labeling to detect active DrICE in wild-type (J), bicoid (K) and oskar (L) mutants. Lateral views. (K,L) Brackets highlight areas of increased caspase activation; arrows indicate the presumptive telson (Te) areas, which lack caspase activation. (M-O) Expression of the caspase inhibitor P35 blocks TUNEL-positive cell death in wild-type (M), bicoid (N) and oskar (O) mutants.