Mus musculus strain:129S8 Transcriptome or Gene expression

Mental retardation is the main clinical manifestation of Down syndrome (DS), and neural abnormalities occur during the early embryonic period and continue throughout life. Tc1, a model mouse for DS, carries the majority part of the human chromosome 21 and has multiple neuropathy phenotypes similar to patients with DS. To explore the mechanism of early neural abnormalities of Tc1 mouse, induced pluripotent stem (iPS) cells from Tc1 were obtained, and genome-wide gene expression and methylation analysis were performed for Tc1 and wild type mouse iPS cells. Our results showed hyper-methylation profiles for Tc1 iPS cells, and the abnormal genes were shown to be related to neurodevelopment and distributed on multiple chromosomes. In addition, important genes involved in neurogenesis and neurodevelopment were shown to be down-regulated in Tc1 iPS cells. In short, our study indicated that genome-wide hyper-methylation leads to disordered expression of genes associated with neurodevelopmental in the early development in Tc1mouse. Overall, our work provided a useful reference for the study of molecular mechanism of nervous system abnormalities in DS.