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. 2020 Jul 31;11:3839. doi: 10.1038/s41467-020-17551-4

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© The Author(s) 2020

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 1 — a Dorsal view of whole-mount P0 control (ctrl) and Ino80 conditional mutant (cKO) brains. Nuclear (n)GFP (green) was expressed Cre-dependently from ROSA^nT-nG. Emx1^Cre-mediated Ino80 deletion from cortical NPCs (cKO-E) led to microcephaly, whereas Neurod6^Cre-mediated Ino80 deletion from postmitotic excitatory neurons (cKO-N) did not. Sample measurements of cortical area (red) quantified in c are indicated (ctrl: n = 4, cKO-E: n = 4, cKO-N: n = 3 animals). OB olfactory bulb, Nctx neocortex, Mb midbrain. b MAP2 (magenta) and nGFP (green) immunostaining of coronal P0 brain sections. cKO-E, but not cKO-N, was characterized by microcephaly and severe hippocampal hypoplasia. Sample measurements of cortical thickness (yellow) and mediolateral extent (blue) quantified in c are indicated (ctrl: n = 4, cKO-E: n = 3, cKO-N: n = 3 animals). CPu caudate putamen, Hp hippocampus, Th thalamus. c Cortical area (red), thickness (yellow), and mediolateral extent (blue) were each significantly decreased in cKO-E, but not cKO-N, compared with ctrl (data are mean, one-way ANOVA with Tukey’s post hoc test, Cortical area, ctrl: n = 4, cKO-E: n = 4, cKO-N: n = 3 animals, thickness and mediolateral extent, ctrl: n = 4, cKO-E: n = 3, cKO-N: n = 3 animals). d DAPI staining (cyan) of coronal P0 sections revealed altered lamination of medial neocortex and severe hypoplasia of hippocampus in cKO-E (n = 3 animals). Analyzed by marker immunostaining (insets), the lamination of LHX2 + (L2-5, green), BCL11B + (L5, blue), and TLE4 + (L6, red) neurons was correctly ordered in lateral (Lat) neocortex of cKO-E, but severely disrupted in medial (Med) neocortex. In cKO-N, normal lamination was present in medial and lateral neocortex. e, Analysis of cumulative distribution of layer marker-expressing neurons through thickness of cortex from white matter (WM) to marginal zone (MZ) revealed disrupted lamination in medial cKO-E cortex (n = 3 animals). Scale bar: 1 mm in a; 500 μm in b, d; 50 μm in d inset.