This webinar discusses the role of a newly discovered, brain-enriched form of non-CpG DNA methylation in neural development and disease.
Neurons in the brain must express diverse complements of genes in order to form synaptic connections and execute physiological responses to stimulation. But how is this complex neuronal transcriptome regulated? Do unique mechanisms exist in neurons to control this process?
During the webinar, Harrison Gabel of Washington University describes a study that used chromatin immunoprecipitation-sequencing, RNA-sequencing, and whole-genome bisulfite-sequencing to demonstrate that uniquely high levels of non-CpG methylation in the brain play a critical role in regulating neuron-specific transcriptional programs.
Dr. Gabel and colleagues have further uncovered evidence that this non-CpG DNA methylation is an important binding site for MeCP2, the protein disrupted in the neurological disorder Rett syndrome.
Dr. Gabel describes these and other studies that have used genomic methods to define how methylated CA (mCA) accumulates in neurons, determine the molecular mechanism of transcriptional regulation mediated by mCA and MeCP2, and understand how disruption of this gene-regulatory pathway contributes to neurodevelopmental disease.