Benjamin R. Doughty

The paper investigates chromatin state transitions during epigenetic memory formation by analyzing single-cell gene expression and chromatin structure changes after repressor recruitment and release.

The paper tests enhancer-promoter compatibility using improved assays, finding that promoter responsiveness, not enhancer rank order, determines activation sensitivity.

This study links in vitro transcription factor affinities to in vivo single-molecule chromatin states using thermodynamic models and experimental data for KLF1.

The paper introduces a high-resolution single-molecule chromatin accessibility mapping method to quantify transcription factor occupancy and co-accessibility in human cell lines.

The paper introduces Variant-FlowFISH to measure the effects of DNA sequence variants on gene expression, identifies regulatory mechanisms, and benchmarks predictive models.

This study uses CRUDO to show that cohesin and 3D contacts influence enhancer-promoter regulation, with distal enhancers showing stronger cohesin dependence.

This study links transcription factor binding to gene expression by analyzing chromatin configurations using single-molecule footprinting in human cells.

ENCODE-rE2G, a classifier trained on K562 CRISPR perturbations, maps 13,455,443 enhancer-gene interactions across 352 biosamples, matching or exceeding prior models on CRISPR, eQTL, and GWAS benchmarks.

This study maps chromatin accessibility, transcription, and 3D organization in Bdellovibrionota bacteria, revealing features similar to archaea and eukaryotes.

The paper reports 109 non-coding CRISPR screens analyzing 13.3Mb of the genome, identifies CRE-gene links, and provides guidelines and tools for screening non-coding regulatory elements.

HyPR-seq sensitively quantifies up to 100 chosen genes in single cells, achieving high sensitivity for individual transcripts and reducing costs compared to whole-transcriptome scRNA-seq.

The paper uses the ABC Model to map enhancer-gene regulation across 131 cell types and tissues, linking GWAS variants to disease genes, particularly in IBD.

The paper introduces CRISPRi-FlowFISH to perturb enhancers and an Activity-by-Contact model to predict enhancer-gene regulatory connections.