3/20/2024 0 Comments Sandra orlow nude early![]() ![]() Our results suggest that i reduced neuronal size is an important in vitro cellular phenotype of Mecp2 mutation in mice, and ii MeCP2 might play a critical role in the maintenance of neuronal structure by modulation of the mTOR pathway. We also found that Mecp2 mutation leads to down-regulation of the mTOR signaling pathway, known to be involved in neuronal size regulation. IGF-1 (insulin growth factor-1 treatment of neuronal cells from Mecp2 mutant mice rescued the soma size phenotype. In cultures from such doubly heterozygous female mice, the size of neurons expressing the mutant ( A 140 V allele also showed a significant reduction compared to neurons expressing wild type MeCP2, supporting a cell-autonomous role for MeCP2 in neuronal development. ![]() We also examined soma size in hippocampus neurons from individual female transgenic mice that express both a mutant (maternal allele and a wild type Mecp2 gene linked to an eGFP transgene (paternal allele. ![]() Cultured hippocampus and cerebellar granule neurons from mutant animals were significantly smaller than neurons from wild type animals. Morphological analyses focused on quantifying soma and nucleus size were performed on primary hippocampus and cerebellum granule neuron (CGN cultures from mutant (Mecp2 A 140 V/y and wild type (Mecp2+/y male mice. We have created a mouse model (Mecp2 A 140 V “knock-in†mutant expressing the recurrent human MECP2 A 140 V mutation linked to an X-linked mental retardation/Rett syndrome phenotype. Reduced neuronal size and mTOR pathway activity in the Mecp2 A 140 V Rett syndrome mouse model [version 1 referees: 2 approvedĭirectory of Open Access Journals (Sweden)įull Text Available Rett syndrome (RTT is a neurodevelopmental disorder caused by mutation in the X-linked MECP2 gene, encoding methyl-CpG-binding protein 2. ![]()
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