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. Author manuscript; available in PMC: 2012 Sep 13.
Published in final edited form as: Dev Cell. 2011 Sep 13;21(3):492–505. doi: 10.1016/j.devcel.2011.07.012

Figure 7. p63 is required for apoptosis induced by a mutant Connexin 31 construct associated with human EKV disease.

Figure 7

(A) Overview of the Cx31 DNA constructs used in this study. (B–F) p53 mutant embryos were injected with wt or (C86S) mutant Cx31-EGFP constructs, then heat shocked at 24 hpf to induce Cx31-EGFP expression, fixed at 2 hrs later, and processed for anti-EGFP (green), anti-activated Caspase-3 (red) and phalloidin staining (blue) (See also Supplementary Figure 6). (B) (wt) Cx31-EGFP caused minimal apoptosis. (C) (C86S) Cx31-EGFP caused a higher level of epidermal apoptosis than (wt) Cx31-EGFP. (D) Zoomed region from (C). (E) Co-injection of p63 MO1 blocked the apoptosis induced by (C86S) Cx31-EGFP. (F) Quantification of apoptosis expressed as % Caspase-3 positive cells in an EGFP positive epidermal cluster. At least 8 embryos per condition were used for quantitation. (G) A model for the mechanism of ER stress-induced apoptosis in the developing epidermis.