Mecp2-Null Mice Provide New Neuronal Targets for Rett Syndrome

摘要: Background Rett syndrome (RTT) is a complex neurological disorder that one of the most frequent causes mental retardation in women. A great landmark research this field was discovery relationship between disease and presence mutations gene codes for methyl-CpG binding protein 2 (MeCP2). Currently, MeCP2 thought to act as transcriptional repressor couples DNA methylation silencing. The present study aimed identify new target genes regulated by Mecp2 mouse model RTT. Methodology/Principal Findings We have compared expression profiles wild type (WT) Mecp2-null (KO) mice three regions brain (cortex, midbrain, cerebellum) using cDNA microarrays. results obtained were confirmed quantitative real-time PCR. Subsequent chromatin immunoprecipitation assays revealed seven direct bound vivo (Fkbp5, Mobp, Plagl1, Ddc, Mllt2h, Eya2, S100a9), overexpressed due an indirect effect lack (Irak1, Prodh Dlk1). always methylated, suggesting involvement domain mechanism interaction. Conclusions identified are Mecp2-KO excellent candidate various features disease. Our demonstrate targets provide us with better understanding underlying mechanisms RTT.