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Fig. 1 | Molecular Autism

Fig. 1

From: RNA sequencing and proteomics approaches reveal novel deficits in the cortex of Mecp2-deficient mice, a model for Rett syndrome

Fig. 1

Transcriptome-wide expression in Mecp2 Jae/y cortex. a. Heat map of 391 significant, differentially expressed (DE) genes. Each genotype has 4 biological replicates, where each column represents 1 biological replicate and each row represents the Log10-transformed FPKM of a significant DE gene. Biological replicates are listed in the order of how they cluster, which is indicated by the cluster dendrogram above the heat map. Genes with a false discovery rate (q-value or FDR) of < 0.05 were considered to be significantly, differentially expressed. b. Volcano plot of all the detected genes’ expression (Log2 fold change) in the Mecp2 Jae/y whole cortex transcriptome. Significant DE genes previously identified as RTT hits are highlighted in red crosses and arrows. Due to space constraints, additional genes identified in supplemental material from Chahrour et al. [4] and Veeraragavan et al. [34] were not highlighted in this volcano plot; for information on these genes, see Table 1. Dotted line indicates a q-value of 0.05, where anything above the line indicates a significant DE gene. c. Venn diagram comparing our transcriptome data to previously published microarray studies (Urdinguio et al. [24] and Tudor et al. [20]) on Mecp2 Jae/y mouse cortex. Note that in the Urdinguio study, the fold change expression was not differentiated between cortex, midbrain, and cerebellum due to their finding that there were no differences in gene expression between the 3 brain regions [24]; rather, fold change values represent combined tissue expression. Six genes were shared between the Mecp2 Jae/y transcriptome data and the Urdinguio et al. study, while 5 genes from the Tudor et al. study were shared in common with the transcriptome data. One of the targets (Fabp7) from the Tudor et al. study was also overlapped with the Urdinguio et al. study

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