Tom van Schaik

This study shows that transcription inhibition rapidly and reversibly rewires chromatin-nuclear lamina contacts through distinct Lamin A and LBR tethering mechanisms.

The paper integrates 4D Nucleome data to analyze 3D genome structure and function in human cells, revealing chromatin domains, loops, and interactions, and showing how genetic variants affect genome folding.

The paper identifies TOP2B as a regulator of genome-nuclear lamina interactions, showing its role in partitioning genomic regions between the nuclear lamina and interior, with LBR playing a complementary role.

The paper investigates how genomic regions called LADs interact with the nuclear lamina, finding that these interactions are multivalent and cooperative, with some subregions having stronger affinity and influencing neighboring sequences.

The paper shows that DSBs in LADs cause megabase-scale detachment from the nuclear lamina, which is necessary for efficient repair.

This study shows that cohesin accumulates at CTCF-bound loop anchors after WAPL depletion, and active genes form long-range clusters independent of cohesin.

The paper examines genome organization in human cells relative to nuclear locales, finding that gene expression and replication timing correlate with different nuclear structures and that LADs and iLADs compete for lamina attachment.

The paper identifies chromatin regulators involved in gene repression in lamina-associated domains (LADs) through genetic screens, showing that transcription elongation and chromatin remodeling factors, not nuclear lamina proteins, mediate repression.

The paper shows that disrupting nuclear lamina association promotes ABCB1 gene derepression and taxol resistance in RPE cells.

The paper investigates Ki67's role in chromatin organization by analyzing its genomic interactions and dynamics during the cell cycle in human cells.

The paper investigates the role of CTCF and cohesin in LAD positioning, finding they reinforce borders but do not position LADs, and mediate fine-tuning of nuclear lamina interactions.

The paper measures how chromatin context influences the balance between DNA repair pathways after Cas9-induced breaks in over 1,000 genomic locations.

The paper introduces SPIN, a method to identify genome-wide nuclear spatial localization patterns by integrating nuclear compartment mapping and chromatin interaction data.

The paper develops pA-DamID to study LAD-NL contacts during interphase, finding rapid early G1 establishment and differential dynamics between distal and centromere-proximal LADs.

The paper investigates how gene activation affects nuclear lamina interactions and shows that transcription can locally rewire these interactions without broadly altering chromosomal regions.

The paper shows that LADs create a repressive chromatin environment that affects promoter activity and transcription elongation, with variability in promoter sensitivity to LAD repression.