Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation

Damina Balmer, Jared Goldstine, Y. Manjula Rao, Janine M LaSalle

Research output: Contribution to journalArticle

85 Citations (Scopus)

Abstract

Rett syndrome is caused by mutations in MECP2 and characterized by arrested postnatal neurodevelopment. MECP2 is ubiquitously expressed, but its protein product, methyl-CpG-binding protein 2 (MeCP2), is highly expressed in a subpopulation of cells in the adult brain. Automated quantitation of MeCP2 expression on a human developmental tissue microarray was performed by laser scanning cytometry. A significant correlation between age and MeCP2 level, population heterogeneity, and percentage of MeCP2 high-expressing cells was specifically observed in cerebral but not renal samples. In contrast, an inverse correlation between use of the long 3′ UTR of MECP2 and age was observed, suggesting that an acquired switch in polyadenylation is responsible for the elevated MeCP2. Acquired elevated MeCP2 expression in neurons beginning in infancy and progressing through childhood may explain the delayed onset and developmental arrest of Rett syndrome.

Original languageEnglish (US)
Pages (from-to)61-68
Number of pages8
JournalJournal of Molecular Medicine
Volume81
Issue number1
StatePublished - Jan 1 2003

Fingerprint

Methyl-CpG-Binding Protein 2
Polyadenylation
Human Development
Brain
Rett Syndrome
Laser Scanning Cytometry
3' Untranslated Regions
Population Characteristics
Kidney
Neurons
Mutation

Keywords

  • Brain development
  • MECP2 mutation
  • Methyl-CpG-binding protein 2
  • Rett syndrome

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Elevated methyl-CpG-binding protein 2 expression is acquired during postnatal human brain development and is correlated with alternative polyadenylation. / Balmer, Damina; Goldstine, Jared; Rao, Y. Manjula; LaSalle, Janine M.

In: Journal of Molecular Medicine, Vol. 81, No. 1, 01.01.2003, p. 61-68.

Research output: Contribution to journalArticle

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