Douglas R. Higgs

The paper shows that active enhancers recruit cohesin to form cell-specific chromatin domains, using the alpha globin cluster as a model.

This study identifies CTCF binding sequences that effectively block enhancer-promoter activity, showing that their function is not correlated with CTCF/cohesin levels, conservation, or sequence similarity to consensus motifs.

This study identifies conserved and species-specific cis-regulatory elements in human and mouse blood cells using integrative epigenomic analysis and clustering.

The paper investigates the role of cohesin-mediated loop extrusion in enhancer-promoter proximity and gene expression during mouse erythropoiesis, finding that it is important but not exclusive for gene activation.

This study shows that SUPT5H mutations disrupt RNA polymerase II pausing, delaying erythroid differentiation and cell cycle progression in human cells.

The paper uses live-cell imaging to study transcriptional bursting dynamics during mouse erythropoiesis, finding changes in burst patterns associated with differentiation stages.

The paper shows that super-enhancers function directionally and orientation-dependently, unlike regular enhancers, by analyzing the β-globin super-enhancer.

The paper investigates the functional interdependence of super-enhancer elements in erythroid -globin gene regulation, revealing the necessity of facilitator elements for optimal activity.

This paper establishes a scalable protocol to isolate primitive-like erythroid cells from in vitro differentiated mESCs, showing they recapitulate normal erythropoiesis and mutation effects seen in primary cells.

The paper shows that actively transcribed genes can function as chromatin boundary elements, similar to CTCF-bound sites, by stalling chromatin loop extrusion.

The paper studies chromatin architecture changes during mouse erythroid differentiation using Tiled-C and shows enhancer-promoter interactions form during differentiation, not before gene expression.

The paper integrates epigenomic and transcriptomic data from mouse hematopoiesis to identify regulatory elements and their dynamics across cell types.

This study investigates ATR-16 syndrome, finding that deletion size correlates with severity but no critical region defines the phenotype, and genetic background significantly affects outcomes.

The paper develops a platform combining ATAC-seq, DNaseI footprints, NG Capture-C, and machine learning to identify causal variants and genes for polygenic human traits.

The paper investigates promoter competition in the -globin domain using chromatin interaction data, finding that promoters interact simultaneously with a super-enhancer rather than competing.

The paper integrates GATA transcription factors and epigenomes in mouse hematopoietic cells using IDEAS to map regulatory landscapes and identify candidate cis-regulatory elements.

This study shows that enhancers primarily regulate gene expression by promoting transcription initiation rather than by affecting RNA polymerase II pausing.

This study models erythropoiesis in CDA-I by analyzing patient-derived erythroblasts, identifying abnormalities in DNA accessibility, proliferation, and enucleation, with genotype-phenotype correlations.

The paper develops Tri-C, a single-cell 3C method, to reveal dynamic chromatin interactions and regulatory hubs in mammalian cells.