Language

English

Publication Date

6-12-2026

Journal

Science Advances

DOI

10.1126/sciadv.aeb4265

PMID

42268975

PMCID

PMC13251834

PubMedCentral® Posted Date

6-10-2026

PubMedCentral® Full Text Version

Post-print

Abstract

Rett syndrome (RTT) is an X-linked neurological disorder caused by MECP2 mutations, creating distinct cellular environments in females (mosaic) versus males (nonmosaic). Despite female patients representing most cases, how mosaicism contributes molecularly to RTT pathogenesis, particularly in presymptomatic stages, remains poorly understood. To address this question, we profiled hippocampal transcriptomes of young female and male RTT mice using bulk and single-nucleus RNA sequencing. We identified a core disease signature of consistently dysregulated genes only in MeCP2− cells across RTT models. Moreover, we uncovered non–cell autonomous effects exclusively in female MeCP2+ excitatory neurons, suggesting that these circuits are more vulnerable early in the mosaic RTT environment. The single-nuclei data also revealed an underappreciated MeCP2− interneuron subtype that had the most transcriptional dysregulation in both male and female RTT hippocampi. Together, these data highlight the different effects of MeCP2 loss on excitatory and inhibitory circuits between the mosaic and nonmosaic environments in early RTT pathogenesis.

Keywords

Rett Syndrome, Animals, Female, Methyl-CpG-Binding Protein 2, Male, Mice, Hippocampus, Transcriptome, Mosaicism, Disease Models, Animal, Gene Expression Profiling, Cell Nucleus, Mutation, Single-Cell Gene Expression Analysis

Published Open-Access

yes

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