Harrison Gabel received his A.B. in molecular biology from Princeton University and a Ph.D. in genetics from Harvard Medical School, where he studied the mechanisms of small-RNA mediated gene silencing in the laboratory of Gary Ruvkun. During his postdoctoral fellowship with Michael Greenberg at Harvard Medical School, Gabel utilized a combination of biochemical and genomic approaches to study gene regulation in the mammalian brain. Through this work, he identified a new mechanism of gene regulation mediated by a recently discovered form of non-CpG DNA methylation in neurons and the Rett syndrome protein MeCP2. These studies have shed light on the unique complexity of gene expression programs that are used during mammalian brain development and provided new insight into the molecular etiology of Rett syndrome and related disorders.

Gabel established his independent laboratory at Washington University in St. Louis in 2015. Positioned at the intersection of the accelerating fields of human neurological disease genetics and epigenomics, his research group is applying next-generation sequencing technology in mouse models to dissect the molecular functions of transcriptional regulatory proteins that are disrupted in autism. A major focus of his work is to define the functions of neuronal non-CpG DNA methylation in neural development and understand how its disruption can contribute to autism and related disorders. The goal of these studies is to identify molecular pathways that are points of convergence for disruption in autism, uncovering commonalities of cellular dysfunction that can be targeted for the development of therapeutics for these disorders.