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. 1999 Jan 5;96(1):145–150. doi: 10.1073/pnas.96.1.145

Figure 1.

Figure 1

(A–F) The phenotypes of GMRced-4 transgenic flies are partially blocked by p35. (A and D) Wild-type compound eye. (B and E) Ectopic expression of one copy of GMRced-4 causes a reduction of eye size and disordered cell arrangement in the eye. (C and F) The size of the GMRced-4-expressing eye was partially rescued by the coexpression of p35. (A–C) Scanning electron microscope images. (D–F) Thin sections of adult eyes. Scale bar, 10 μm. (G–O) Ectopic expression of GMRced-4 induces cell death and caspase activation in eye discs from third-instar larvae. In this figure, anterior is to the right and posterior is to the left. (G, J, M) Wild-type. (H, K, M) Third-instar eye disc from GMRced-4 larvae. (I, L, O) GMR-p35; GMRced-4. (G–I) Acridine orange staining (AO) to detect dead cells. Scale bar, 100 μm. (J–L) Immunostaining by using anti-ELAV antibody. Scale bars, 100 μm. (M–O) In situ affinity labeling (IAL) of active caspases in third-instar larval eye discs. The dotted line indicates the outer shape of the eye disc. Scale bars, 80 μm. In each experiment, immunohistochemical analysis revealed the expression of CED-4 in larval eye discs, and CED-4-positive cells were distributed in the posterior of the morphogenetic furrow (data not shown).