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. 2019 Jul 9;11(7):962. doi: 10.3390/cancers11070962

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© 2019 by the authors.

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).

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Specific blockage of the p300/β-catenin interaction in wild-type mouse embryos increases the proportions of post-mitotic neurons and neurogenic precursors. To assess the consequences of direct perturbation of the mode of division in NSCs on the rate of neurogenesis, we investigated NeuN and Ngn2 expression by immunostaining. Treatment with small-molecule p300/β-catenin antagonists, YH249 or IQ-1, increased the percentage of post-mitotic neurons (A), as well as the percentage of neurogenic precursors (B) in wild-type mouse embryos (E12.5), similarly to KO of p73. The effects of YH249 were reversed by ICG-001 treatment (Rescue YH in A-B). One-way ANOVA followed by a Newman–Keuls multiple comparison test showing a significant difference of IQ-1 and YH249 treatments from the other three treatments. vz, ventricular zone. n ≥ 6. ** p < 0.01, *** p < 0.001.