Figure - PMC

Skip to main content

An official website of the United States government

Here's how you know

Here's how you know

Official websites use .gov
A .gov website belongs to an official government organization in the United States.

Secure .gov websites use HTTPS
A lock ( ) or https:// means you've safely connected to the .gov website. Share sensitive information only on official, secure websites.

View full-text article in PMC

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

Search in PMC
Search in PubMed
View in NLM Catalog
Add to search

© 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/.

PMC Copyright notice

Fig. 5 — a Dorsal view of P0 whole-mount brains and BCL11B immunostaining (black) of P0 coronal sections. Co-deletion of Trp53 with Ino80 (dKO-E) rescued major Ino80 deletion (cKO-E) phenotypes, including microcephaly, severe hippocampal hypoplasia, and disrupted neocortical lamination. Sample measurements quantified in b are indicated (ctrl cortical area: n = 6, all other measurements: n = 4 animals). b Cortical area (red), thickness (yellow), and mediolateral extent (blue) were restored in dKO-E and not significantly different compared with ctrl (data are mean, one-way ANOVA with Tukey’s post hoc test, ctrl cortical area: n = 6, all other measurements: n = 4 animals). c CC3 immunostaining (magenta) revealed no increase in apoptosis in dKO-E E13.5 neocortex (n = 3 animals). d The number of SOX2 + (red) and EOMES + (cyan) NPCs in E15.5 dKO-E cortex were restored to levels not significantly different compared with ctrl (data are mean, one-way ANOVA with Tukey’s post hoc test, ctrl: n = 4, cKO-E: n = 4, dKO-E: n = 3 animals). e UMI RNA-seq volcano plots comparing cKO-E with ctrl, and dKO-E (n = 7 animals) with ctrl E13.5 cortex. In the cKO-E versus ctrl comparison (left panel), differentially regulated genes are indicated (upregulated, red dots; downregulated, blue dots). The same genes are labeled in the dKO-E versus ctrl comparison (right panel). Genes that remained differentially regulated (FDR < 0.001) following Trp53 co-deletion are indicated by dots of the same color. Genes that lost differential expression (FDR ≥ 0.001) are indicated by black dots. The vast majority of cKO-E-upregulated genes (202/205) were rescued by Trp53 co-deletion, indicating that their upregulation was p53-dependent. About one-third of cKO-E-downregulated genes (134/418), however, remained significantly downregulated in dKO-E, consistent with p53-independent gene regulation by Ino80. f Intersectional analysis of the 134 p53-independent downregulated genes with published ChIP-seq data from mouse neural stem cells (NSCs) revealed an enrichment of genes bound at their transcriptional start site (TSS) by transcription factor YY1, a known binding partner of INO80. This enrichment was absent from the 42 cKO-E downregulated genes that were reversed by Trp53 co-deletion. Scale bar: 500 μm in a; 100 μm in c, d.