Harrison W. Gabel

This study shows that DNMT3A mutations in TBRS disrupt cortical interneuron differentiation, leading to neuronal network dysfunction and contributing to intellectual disability and autism.

This study identifies microglial subpopulations and shows their origin and transitions through transcriptomic and epigenomic analysis.

The paper shows that non-CG DNA methylation and MeCP2 regulate long genes to maintain neuron type-specific gene programs at high resolution.

This study identifies a functional interaction between MeCP2 and TOP2β in neurons, showing MeCP2 inhibits TOP2β activity at long genes, which may contribute to neurodevelopmental disorders.

This study examines how different DNMT3A mutations cause varied behavioral, epigenetic, and transcriptional issues in neurodevelopmental disorders.

The paper shows NSD1 deposits H3K36me2 to pattern non-CG DNA methylation in neurons, linking this to neurodevelopmental disorders.

This paper develops a MYT1L syndrome mouse model that recapitulates human phenotypes, revealing disrupted brain development and neuronal maturation as underlying mechanisms.

This study shows that DNMT3A mutations cause behavioral and epigenomic changes in mice, similar to human neurodevelopmental disorders, by disrupting non-CG DNA methylation.

This study identifies genomic binding sites of Gtf2i and Gtf2ird1 in the developing brain and assesses their combined effects on transcription and behavior in knockout mice.