James O. J. Davies

This study identifies the transcriptional regulatory mechanisms governing ERFE expression in human erythroblasts using genomic approaches.

The paper investigates Menin's role in enhancer-promoter interactions in MLL-rearranged and NPM1c leukemia models, finding context-dependent effects on transcriptional regulation and enhancer function.

This study shows FACT maintains promoter topology by preserving nucleosomes and preventing chromatin factor spreading into gene bodies.

This study uses CRISPR-Cas genome editing to selectively inactivate JAK2 V617F mutations in patient cells, showing that heterozygous cells are not oncogene addicted while homozygous cells are eradicated, suggesting genome editing as a potential treatment for MPNs.

The paper shows enhancers mediate euchromatin hopping, spreading euchromatin features to distal regions through chromatin looping, redefining enhancer identification using chromatin features.

This study identifies enhancer heterogeneity as a driver of transcriptional differences in KMT2A::AFF1 ALL patients, revealing patient-specific enhancer activity at oncogenes.

This study shows that MYB activity sustains enhancer-promoter interactions and transcription by maintaining enhancer function in leukemia.

The paper identifies a novel mechanism where focal deletions of an intronic element in FTO lead to IRX3 activation in T-ALL through enhancer hijacking.

The paper identifies that SOX2 maintains chromatin accessibility at regulatory sites that drive gene expression, distinguishing them from non-activating binding sites.

This study identifies PAF1 and FACT as essential for enhancer activity in MLL-AF4-driven leukemia by maintaining histone acetylation and enhancer-promoter interactions.

The paper analyzes sub-kilobase chromatin topology to show that nano-scale regulatory interactions depend on CTCF but not cohesin, and that cohesin affects longer-range enhancer-promoter interactions.

The paper shows BET inhibition reduces transcription but not enhancer-promoter contacts, suggesting these processes are separable.

The paper introduces a new method, NuTi Capture-C, that improves high-resolution chromosome conformation capture by reducing noise and increasing sequencing content, enabling reproducible genome-wide interaction profiles.

CaptureCompendium provides software tools to simplify the design, analysis, and visualization of 3C experiments, addressing the need for specialized bioinformatics skills in genome folding studies.

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