Mario Nicodemi

The paper develops a polymer physics model of ecDNA condensates showing that structural variability scales with copy number, stabilizing oncogene regulatory contacts.

The paper identifies essential cardiac enhancer modules and regulatory mechanisms governing heart development, revealing resilience in cis-regulatory architectures and the role of Hand2 upstream regulatory intervals.

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 compares super-enhancer networks in embryonic stem cells and dopaminergic neurons, revealing their structural differences and functional roles in transcriptional regulation.

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 GAM to study haplotype-specific 3D chromatin structures in mESCs, finding extensive allelic differences in chromatin architecture and gene expression mediated by Polycomb repression.

The paper shows that genome-lamina interactions are reconfigured during limb development to prime regulatory domains for gene activation and support cell-fate decisions.

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.

This study shows that a single cocaine exposure causes long-lasting 3D genome structure changes in midbrain dopamine neurons, affecting gene regulation and synaptic plasticity.

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 introduces multiplex-GAM, a ligation-free method for genome-wide chromatin contact mapping, showing it detects different strong contacts compared to Hi-C, particularly involving active genomic regions.

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.

This study shows that chromatin organization remains largely intact in mouse embryonic stem cells after acute CTCF depletion, despite reduced cell growth and changes in chromatin loop interactions and cohesin occupancy.

This study investigates how CTCF binding sites mediate transcriptional insulation in mouse embryonic stem cells, showing that insulation depends on CTCF site number, sequence context, and TAD boundary location.

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 investigates cell-type specific 3D chromatin structures in the brain using immunoGAM, finding TAD melting, neuron-specific contacts, and compartmentalization patterns related to gene expression and neurodegenerative diseases.

This study shows that CTCF depletion in mESCs weakens TAD boundaries and INs but only affects a small subset of enhancer-promoter contacts, highlighting CTCF's role in promoting long-range gene regulation.

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

The paper develops Tri-C, a single-cell 3C method, to reveal dynamic chromatin interactions and regulatory hubs in mammalian cells.

The paper investigates how promoter activation states influence the 3D folding of the HoxB locus in mouse ES cells using simulations and single-cell imaging.