Fig. 5: The dysregulated genes and pathways in Q84Pfs-Het cortex at P1. | Nature Communications

Fig. 5: The dysregulated genes and pathways in Q84Pfs-Het cortex at P1.

From: The patient-specific mouse model with Foxg1 frameshift mutation provides insights into the pathophysiology of FOXG1 syndrome

Fig. 5

a Differentially expressed genes (DEGs) in the RNA-seq analyses of P1 cortices of Q84Pfs-Het and WT mice as shown by the volcano plot (n = 3 for Q84Pfs-Het mice; n = 2 for WT). The posterior probability of being equally expressed (PPEE) was used as P-value. b Cortical upper layer and interneuron genes were downregulated, whereas the deep layer genes were upregulated. c The integration of DEGs of Q84Pfs-Het cortex and FOXG1 ChIP-seq data revealed the fraction of the DEGs that directly recruit FOXG1, as marked by orange. d The motif analysis (HOMER) of FOXG1 ChIP-seq peaks associated with up- or down-regulated genes in Q84Pfs-Het cortex reveals the potential partner TFs that work with FOXG1 in cortex development. TF, transcription factor. P values are adjusted for multiple testing using the Benjamini-Hochberg false discovery rate (FDR) correction and the tests were two-sided. e–h, Gene set enrichment analysis (GSEA) of DEGs. The tissue (e) and cell type (f) analyses show the tissue types and cell types that are associated with up- and down-regulated DEGs. Analyses of biological process (BP) and cellular component (CC) terms for up-regulated (g) and down-regulated (h) DEGs. Benjamini-Hochberg FDR was applied to adjust for multiple comparisons and the tests were two-sided.

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