Background

Over the past two decades, technological advances have revealed that the three-dimensional organization of chromatin plays a crucial role in regulating gene expression.

During interphase, the genome is arranged into a hierarchy of structural domains within the nucleus. At the largest scale, chromosomes occupy distinct regions known as chromosome territories, where gene activity is influenced by their proximity to nuclear structures associated with either gene repression or activation. At finer levels of organization, chromatin is divided into A and B compartments, representing transcriptionally active and inactive genomic environments. Within these compartments, the genome further organizes into topologically associating domains (TADs), regions that promote interactions between regulatory elements such as enhancers and promoters, enabling coordinated gene regulation. At the most local scale, chromatin loops create microenvironments that directly facilitate enhancer–promoter interactions and fine-tune gene expression.

Our research aims to understand how these structural and epigenetic features shape both normal and disease-associated transcriptional programs, particularly in the context of cardiac disease. To achieve this, we combine high-throughput genomic techniques (including Hi-C, ATAC-seq, ChIP-seq, RRBS, and RNA-seq) with advanced microscopy and animal models that replicate human heart disease.