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. Author manuscript; available in PMC: 2018 Mar 1.
Published in final edited form as: J Comp Neurol. 2016 Sep 27;525(4):1034–1054. doi: 10.1002/cne.24105

Figure 7.

Figure 7

Death of Sus cells (as a result of the Cyp2G1-driven expression of diphtheria toxin A) causes downregulation of ΔNp63 in HBCs and, thereby, HBC proliferation and activation to multipotency (Herrick and Schwob, 2015). The effect on ΔNp63 is mediated, at least in part, by changes in Notch signaling. HBCs express both Notch1 and Notch2 receptors as well as the Delta-like1 ligand, whereas Sus cells express the Jagged1 ligand as well as the Notch2 receptor. Constitutive activation of Notch signaling by overexpression of the Notch1 intracellular domain selectively in HBCs elevates the downstream factor Hes1 as well as the levels of ΔNp63 expression. Conversely, excision of Notch1 from HBCs decreases their expression of ΔNp63 and enhances the rate of HBC spontaneous activation (Herrick and Schwob, 2015).