Figures & data
Figure 1 miRNAs upregulated and downregulated in the brain of a mouse model for Rett syndrome. Validation by quantitative RT-PCR provided the most commonly disrupted miRNAs. Example of the expression of the miR-29b in pairs wild-type/Mecp2 null brain showing upregulation of the transcript in the disease-associated tissue.
Figure 2 DNA methylation and Mecp2 occupancy analysis for the 5′-end CpG islands of miR-29b, miR-199b, miR-146a and miR-146b. (A) Bisulfite genomic sequencing of multiple clones. Black squares, methylated cytosines; white squares, unmethylated cystosines. Vertical black arrow, transcription start sites of the miRNA. Black arrows, bisulfite genomic sequencing primers; white arrows, chromatin immunoprecipitation primers. (B) Quantitative chromatin immunoprecipitation (ChIP) assays. Mecp2 occupancy is shown in the wild-type brain for the miR-29b-1, miR-146a and miR-146b CpG islands. IgG and H3 are used as negative and positive controls for the ChIP assay.
Figure 3 Downstream targets upon miRNA deregulation in Rett syndrome. Transfection of the precursor molecules of miR-146a and miR-146b downregulates IL-1 receptor-associated kinase 1 (Irak1) expression in the mice neuroblastoma cell line Neuro-2a.
