FIGURE 2.
The absence of α6 integrin in the developing lens leads to low expression of NFκB and its target survival proteins resulting in high levels of caspase-3 activity and cell death by apoptosis. A–E, E18.5 lens cryosections from α6+/+ (upper panels) and α6−/− (lower panels) mice were co-labeled for: A, cleaved caspase-3 (red), F-actin (blue), α6 integrin (green); B, TUNEL (red), nuclei (blue); C, NFκB p65 (red), nuclei (blue), F-actin (green); D, Bcl-2 (red), nuclei (blue), F-actin (green); and E, survivin (red), nuclei (blue), and F-actin (green). All images were obtained by confocal microscopy. A–E are single optical slices of 1 μm thickness, selected from an acquired z-stack. D is a projection image (5 μm thickness), acquired from a z-stack of 1-μm thick optical slices. Scale bar = 20 μm in all images. Results show that in the absence of α6 integrin, expression of the transcription factor NFκB (C, red), and its downstream effectors Bcl-2 (D, red) and survivin (E, red), were significantly diminished, inducing a high level of caspase-3 activity and cell death by apoptosis. Whole eye cryosections were examined from a minimum of three different embryos taken from each of the α6+/+ and α6−/− mice groups and are thus representative of three independent studies.