Journal
NEUROBIOLOGY OF DISEASE
Volume 8, Issue 5, Pages 784-791Publisher
ACADEMIC PRESS INC
DOI: 10.1006/nbdi.2001.0420
Keywords
transcriptional repression; gene silencing; DNA methylation; Old World monkey; Macaca mulatta; frontal lobe; autism
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Funding
- NCI NIH HHS [CA 44339] Funding Source: Medline
- NINDS NIH HHS [NS21377] Funding Source: Medline
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Dysfunction of the prefrontal cortex may contribute to the autistic features and mental retardation of Rett syndrome, a neuropsychiatric condition caused by mutations of the gene encoding methyl-CpG-binding protein 2 (MeCP2). Because nothing is known about the expression of MeCP2 and other chromatin-associated factors in primate brain, we studied in monkey prefrontal cortex and murine cerebral cortex expression patterns of MeCP2 and of macrohistone H2A (MacroH2A), which like MeCP2 is associated with transcriptionally silent chromatin. In both species, MeCP2 and MacroH2A appeared to be ubiquitously expressed by cortical neurons, including projection neurons and GABAergic interneurons. In the adult monkey, MeCP2 expression was robust throughout all layers of the prefrontal cortex but it was limited in fetal monkeys at embryonic day 110 to the deeper cortical layers and the subplate. These results suggest that MeCP2 may be important for neuronal maintenance in the developing and in the mature primate prefrontal cortex, consistent with the previously reported phenotype of MeCP2-null mutant mice. (C) 2001 Academic Press.
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