RNA-Seq of wild-type murine primary cortical neurons co-cultured in a transwell-based system with Mecp2 knock-out or wild-type cortical murine astrocytes

ABSTRACT: Rett syndrome (RTT; OMIM#312750) is a rare devastating neurodevelopmental disorder that represents the most common genetic cause of severe intellectual disability in girls. Mutations in the X-linked methyl-CpG-binding protein 2 (MECP2) gene have been reported in over 95% cases of classical forms of RTT. Although initial studies supported a role for MeCP2 exclusively in neurons, recent data indicate a function also in astrocytes, which emerged as critical players involved in RTT pathogenesis through non-cell autonomous effects. Indeed, Mecp2 knock-out (KO) astrocytes cannot properly support neuronal maturation of wilt-type (WT) neurons and our data demonstrated a detrimental effect also on synaptogenesis and synaptic maintainence. Nevertheless, the molecular mechanisms by which RTT astrocyt

INSTRUMENT(S): Illumina NovaSeq 6000

ORGANISM(S): Mus musculus

SUBMITTER:  

PROVIDER: E-MTAB-12393 | biostudies-arrayexpress |

SECONDARY ACCESSION(S): ERP142796

REPOSITORIES: biostudies-arrayexpress