Fig. 3
During embryonic development, homozygous CBP knockout in NPCs induces apoptosis and leads to reduced proliferation in the ventricular zone. a1–10 Overview of ventricular zone and the emerging neocortex at E16.5 in H&E staining of frontal sections with confirmation of CBP knockout in transgenic animals. Sox2 marks stem cells, pHH3 proliferating cells and Caspase3 apoptotic cells in high-power magnifications of the ventricular zone at E16.5. b1–3 Ventricular zone thickness significantly reduced at E16.5 in transgenic mice. A significant rise in apoptosis rate and a significantly diminished proliferation rate was measured within the ventricular zone of transgenic mice. c1–8 Overview of hippocampal formation at E16.5 in H&E staining of frontal sections. Displaying the Cornu ammonis (CA1 and CA3), hippocampal neuroepithelium (HNE), dentate neuroepithelium (DNE, 1ry) and 2ry & 3ry matrix, with a complete CBP depletion in both the DNE and in migrating cells in knockout animals. High power magnifications of the 2ry & 3ry matrix of the developing dentate gyrus at E16.5 with Caspase3 apoptosis staining and EdU proliferation with DAPI nucleus staining (EdU injection at E16.5). Black arrows mark Caspase3+ apoptotic cells and white arrows EdU+ proliferating cells. d1–2 1ry matrix (DNE), significantly thinner and area sizes of 2ry & 3ry matrix, significantly reduced in hGFAP-cre::CBPFl/Fl animals at E16.5. d3–4 Significant increase in apoptosis rates and significant decrease in proliferation in the 2ry and 3ry matrix of hGFAP-cre::CBPFl/Fl mice at E16.5 c. Scale bar: 80 μm (a1,3) 50 μm (a2,4–10, c3–8), 100 μm (c1,2); *p < 0.05, **p < 0.01, ***p < 0.001