Expression of the methyl-CpG-binding protein MeCP2 in rat brain. An ontogenetic study

Abstract

Rett syndrome (RS) is caused by mutations in the gene encoding methyl-CpG-binding protein 2 (MeCP2) and is characterized by arrested postnatal neurodevelopment. We followed the expression of MeCP2 protein in various brain structures of normal rat from birth to 2 years of age. By measuring the amount of protein using the Western blot technique, or by determining the percentage of immunoreactive cells, significant heterogeneity in MeCP2 distribution among various brain areas was observed. Highest expression was found in olfactory bulb and in frontal cortex. In contrast, little expression was detected in caudate-putamen, septum and hippocampus. Except in the olfactive nuclei, very few cells showed detectable MeCP2 protein at birth. The number increased during the first week of age, especially in cortex and nucleus accumbens. Rather than playing a global role in gene transcription, the heterogeneous distribution of MeCP2 transcription factor favors the idea that it has a specialized function in neurons.

Keywords

• Rett syndrome
• Gene silencing
• MeCP2 protein
• Rat brain
• Ontogenetic study
• Cerebral cortex