Robert S. Porter

The paper identifies neuron-specific microexon splicing in chromatin regulators, showing that PHF21A loses DNA-binding function in neurons while retaining H3K4me0 recognition, contributing to brain development.

The paper shows that PHF21A microexon expression precedes LSD1 microexon expression during neurodevelopment, leading to stepwise deactivation of the LSD1-PHF21A complex and unique gene-regulatory roles in neurons.

This study shows LSD1/KDM1A suppresses primed enhancers in mESC by maintaining H3K4me1 levels and preventing aberrant enhancer activity.

This study shows that KMT2A and KDM5C, which have opposing enzymatic activities, work together to regulate neuronal structure, behavior, and H3K4 methylation, with their combined loss reversing some phenotypes.

The paper develops SEMpl, a pipeline that predicts SNP effects on transcription factor binding affinity using ChIP-seq data to identify disease-causing regulatory loci.

This study shows that SMCX/KDM5C, a histone demethylase, is required for X-inactivation in female mammals by inducing Xist RNA and silencing X-linked genes.