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. Author manuscript; available in PMC: 2009 Aug 19.
Published in final edited form as: Nature. 2009 Feb 19;457(7232):981–989. doi: 10.1038/nature07767

Figure 3. Bax and Caspase-6 regulate axonal degeneration.

Figure 3

(a)Local sensory axon degeneration (TuJ1 immunostain) 48hr after NGF deprivation in Campenot chambers was blocked in neurons from Bax−/− mice.

(b)Dissociated sensory neurons double-labeled for pro-caspase-3 and TuJ1 (left), or pro-caspase-6 and TuJ1 (right). Caspase-3 is detected in cell bodies (arrowheads), caspase-6 in both cell bodies and axons.

(c)Local degeneration of sensory axons in Campenot chambers deprived of NGF for 24hr is inhibited by a caspase-6 inhibitor (zVEID-FMK) but not a caspase-3/7 inhibitor (zDEVD-FMK). Quantification in (c′).

(d)In dissociated sensory neuron cultures deprived of NGF for 24hr, siRNA knock-down of caspase-3 primarily rescues cell body death (TUNEL label), whereas caspase-6 knock-down primarily rescues axonal degeneration. Quantification in (d′). Extent of inhibition by individual siRNAs correlates with degree of target knock-down (Supplementary Fig. 6d).

(e)Detection of caspase-6 activation in sensory axons with a cleaved caspase-6-specific antibody (left; TuJ1 double-label on right). Punctate activation of caspase-6 following NGF deprivation (16 hr, middle) was reduced by anti-DR6.1 (bottom).

(f)Confocal section of a field from (e) shows that actived caspase-6 puncta correspond to sites of tubulin loss (fraction non-overlapping: 79 +/−5%).

Scale bar: (a), 250 μml (b): 100 μm; (c): 90 μm; (d): 75 μm; (g): 50 μm; (h): 25 μm.