Wouter L. de Laat

The paper shows that deleting intervening DNA can bring enhancers closer to silenced genes, reactivating their expression in adult cells.

The paper identifies causal SNPs near ERAP2 that regulate its expression through long-range chromatin interactions, linking autoimmune disease risk variants to enhancer activity.

This study uses TACL to analyze individual cohesin loop extrusion trajectories in vivo, revealing new roles for cohesin subunits and their interactions with CTCF and chromatin structure.

This study shows enhancers recruit cohesin to form chromatin domains, engage CTCF sites, and activate distant genes, with transcription factors and mediator required for all distances but cohesin specifically for long-range activation.

This study shows CTCF regulates BLV transcription and 3D chromatin structure, affecting viral latency and host cell organization.

The paper generates Hi-C data from human cardiac tissue and develops a method to identify regulatory interactions, showing how disease variants intersect with these interactions to prioritize causative genes.

The paper introduces damC, a method to measure chromatin structure in vivo without crosslinking or ligation, confirming TADs and CTCF loops and showing chromatin rigidity below 5 kilobases.

The paper introduces a new 3C method, MC-4C, to study multi-way DNA conformations and reveals cooperative and competitive chromatin interactions, including enhancer hubs and loop collisions.