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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.
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