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MeCP2's Role in Chromatin Structure and Stability

Autism spectrum disorders (ASDs) affect 1 in 110 children. Rett Syndrome (RTT) is one of the few ASDs that have a direct genetic link, which make it great model to understand some underlying causes of ASD. RTT is caused by mutation in the X‐linked Methyl CpG Binding Protein 2 (MeCP2). MeCP2 is associated with transcriptional repression and can act on naked DNA or, if found in high enough quantities, alters chromatin structure. Therefore understanding the functional implications on both specific genes and chromatin structure is critical in developing therapeutic strategies. After neural development MeCP2 is found in levels equivalent to H1 in neuronal cells and is believed to compete with H1. Like H1, MeCP2 binds at the entry/exit site of nucleosomal DNA, and could regulate the rate of wrapping and unwrapping around the nucleosome, thus being critical in target gene accessibility. Our goal is to understand how MeCP2 alters gene accessibility through dynamic changes to chromatin structure. We will use FRET measurements to determine the influence of MeCP2 on nucleosome stability, site accessibility, and higher order compaction; providing insight to the mechanistic functions of MeCP2 on gene expression.