Andrea Esposito

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 uses polymer physics models and simulations to show how chimeric proteins cause aberrant chromatin looping, and proposes strategies to inhibit this process.

The paper uses polymer physics models to simulate and analyze the 3D structure of the LTN1 gene region, comparing results with Hi-C data to predict structural features for microscopy experiments.

The paper investigates how ecDNA clusters form through phase separation, creating regulatory contacts that boost MYC expression, and shows how JQ1 disrupts this process.

The paper compares loop-extrusion and polymer phase-separation models against chromatin data, finding they can co-exist in shaping single-cell chromatin architecture.

The paper uses machine learning and polymer physics to infer 3D chromatin architecture from Hi-C data and shows how 1D epigenetic patterns encode this structure through combinatorial binding site arrangements.

The paper shows that divergent gene expression within TADs is resolved through TAD restructuring and DNA methylation, not enhancer-promoter compatibility or position.

The paper uses polymer physics models to show that chromatin folding variability in single cells arises from phase separation driven by chromatin factor interactions.

The paper shows that preformed chromatin topology supports robust Shh transcription during limb development, with CTCF and ZRS alleles influencing enhancer-promoter communication.