Non-cell autonomous influence of MeCP2-deficient glia on neuronal dendritic morphology

Nurit Ballas, Daniel T. Lioy, Christopher Grunseich, Gail Mandel

Research output: Contribution to journalArticlepeer-review

307 Scopus citations

Abstract

The neurodevelopmental disorder Rett syndrome (RTT) is caused by sporadic mutations in the transcriptional factor methyl-CpG-binding protein 2 (MeCP2). Although it is thought that the primary cause of RTT is cell autonomous, resulting from a lack of functional MeCP2 in neurons, whether non-cell autonomous factors contribute to the disease is unknown. We found that the loss of MeCP2 occurs not only in neurons but also in glial cells of RTT brains. Using an in vitro co-culture system, we found that mutant astrocytes from a RTT mouse model, and their conditioned medium, failed to support normal dendritic morphology of either wild-type or mutant hippocampal neurons. Our studies suggest that astrocytes in the RTT brain carrying MeCP2 mutations have a non-cell autonomous effect on neuronal properties, probably as a result of aberrant secretion of soluble factor(s).

Original languageEnglish (US)
Pages (from-to)311-317
Number of pages7
JournalNature Neuroscience
Volume12
Issue number3
DOIs
StatePublished - Mar 2009

ASJC Scopus subject areas

  • Neuroscience(all)

Fingerprint Dive into the research topics of 'Non-cell autonomous influence of MeCP2-deficient glia on neuronal dendritic morphology'. Together they form a unique fingerprint.

Cite this