Transgenic mice with Rett-causing mutations in MeCP2 reveal that a basic cluster in the C-terminus of the protein binds DNA and that both the methyl-CpG binding domain and the transcriptional repression domain are necessary to elicit toxicity in MECP2 duplication syndrome.

Individuals with deletions or duplications of the NUDT21 gene have altered levels of MeCP2 protein and intellectual disabilities.

In mouse models of Rett Syndrome, global loss of the Mecp2 gene induces microglia to engulf excess synapses, while microglia-specific loss or gain of Mecp2 has little impact on disease.

Global brain transduction of the instability-prone Mecp2 transgene by systemic AAV-PHP.eB administration is safe and effective in protecting male and female Mecp2 mutant mice from the Rett syndrome disease phenotype.

Excessive inflammation of the brain in early life predisposes individuals to neurodevelopmental disorders by preventing synapses from developing correctly.

The loss of Mecp2 results in cerebellar dysfunction that contributes to the motor deficits in Rett syndrome.

Loss of function of the Rett syndrome gene MeCP2 in a small but powerful interneuron population, the VIP cells, causes a unique combination of impairments in neural function and behavior.

Loss of MeCP2 function negatively impacts Tet1 and CTCF binding thereby negatively impacting learning-dependent DNA methylation and alternative splicing regulation.

Robust fear learning deficits and decreased tonic activity of NAc cholinergic interneurons caused by depletion of MeCP2 could be attributed to an elevation in α2-containing GABA_A receptors.

Single molecular imaging of MeCP2 at high spatial/temporal resolution identifies distinct structural domains contributing to its dynamic behaviors and chromatin interactions in live neurons.