Bas van Steensel

This study identifies factors influencing Sleeping Beauty transposition, showing chromatin context, cargo size, and transcriptional activity affect efficiency and reintegration patterns.

This study compares ATAC-seq-based estimates of transcription factor activity with multiplexed reporter assays across perturbations, finding overlap but also discrepancies in their sensitivity to different TF types.

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

The paper investigates how CTCF binding sites affect the regulatory landscape of the mouse Sox2 locus by relocating them and measuring their impact on gene expression.

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 relocates promoter-reporter constructs to study the positional relationship between the Sox2 gene and its enhancer, revealing gene-mediated confinement of enhancer activity.

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.

This study uses sequence-based deep learning models to identify functional promoter mutations in cancer, finding enrichment in known and novel cancer genes.

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 manipulates transcription to show it can advance replication timing but is not required for the switch to early replication.

The paper systematically optimizes transcriptional reporters for 86 transcription factors and identifies 60 highly sensitive and specific reporters.

The paper tests how enhancer pairs combine to activate promoters in mouse cells, finding near-additive behavior with non-linear scaling depending on promoter strength.

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 uses TSA-seq to map genomic regions near nucleoli and pericentric heterochromatin in human cell lines, revealing variable heterochromatin localization and complex nuclear organization.

This paper introduces PARM, a deep learning model trained on MPRA data to predict human promoter activity and identify TF binding preferences, revealing positional and functional differences in regulatory grammar.

A multiplexed screen reveals how dozens of proteins sense the local chromatin context to tune the balance between two DNA repair pathways.

This study identifies 67 epigenetic drugs that modulate CRISPR-Cas9 editing efficiency and repair outcomes based on chromatin context in human cells.

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

The paper systematically examines how TP53 binding site architecture affects transcriptional output and develops a model to predict reporter activity.

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 systematically analyzes enhancer-promoter compatibility in the mouse genome using high-throughput assays, finding significant promoter selectivity and diverse compatibility patterns.

The paper quantifies how enhancer-promoter interactions influence transcription through nonlinear relationships and reveals mechanisms of transcriptional control via chromosome structure.

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.