The Journal of Neuroscience, June 8, 2005, ():
Phosphorylation of c-Jun in Avian and Mammalian Motoneurons In Vivo during Programmed Cell Death: An Early Reversible Event in the Apoptotic Cascade
J. Neurosci. Sun et al.
25: 5595
Supplemental Material
Files in this Data Supplement:
- Supplementary Fig. 1
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Figure S1. Heterogeneity of the expression level of MN markers among P-Jun+ cells. Several MN specific markers including Lim2, Hoxc10, and Islet1/2 (green) were co-labeled with P-Jun (red). Nuclei were counter-stained with Hoechst 33342 (blue). Note that a subset of P-Jun+ MNs failed to express MN markers (arrows).
- Supplementary Fig. 2
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Figure S2. Schematic illustration of changes in c-Jun phosphorylation in MNs in vivo. Before the onset of PCD, all MNs form provisional contacts with targets and receive some trophic support. A. At the onset of PCD in normal animals, a subset of MNs exhibit c-Jun phosphorylation (red nucleus), and a subset of P-Jun+ MNs die. As a result of the death of a sub-set of MNs, the remaining MNs can obtain more trophic support, which rescues some of these remaining P-Jun+ MNs from death. The size of the green arrows indicates the relative amount of trophic support. B. In Bax-KO mice, because the excess Bax-KO-rescued MNs remain in the competitive pool, more MNs exhibit c-Jun phosphorylation. However, following the atrophy and axonal retraction of the Bax-KO-rescued MNs, the remaining MNs can obtain more trophic support and thus they lose P-Jun-IR. C. By contrast, because activity blockade increases the availability of trophic support, the excess rescued MNs do not exhibit c-Jun phosphorylation. D. Following the cessation of activity blockade, a transient imbalance in the number of competing MNs vs. available trophic support increases the number of P-Jun+ MNs. However, as the delayed degeneration of the excess MNs occurs, the number of P-Jun+ MNs is reduced to control values.
