My research focuses upon different topics, in the fields of evolutionary and functional genomics.
Specifically, the following lines of research summarize my most recent research activity:
Evolution of gene regulation: Recent advances in High Throughput sequencing (NGS) revolutionized the field of genomics, opening tons of new possibilities towards a better understanding of how the metazoan genomes work. In this context, I focus on the evolution of cis-regulatory elements (CREs) in humans and other primates. Using techniques as ChIP-seq, ATAC-seq and RNA-seq, I am interested in unveiling how CREs evolved in the primate lineage, trying to address some of the following big picture questions: 1) what are the tempo and mode of cis-regulatory evolution in primates? 2) what determines whether a given CRE needs to be evolutionarily conserved across species? 3) To what extent transposable elements generate regulatory novelty in the primate gene regulation?
Enhancer dynamics in cell fate determination: Understanding how cell differentiate from a pluripotent progenitor is a key question in biology. Specifically, I am interested in how cis-regulatory elements, and in particular enhancers, are reprogrammed by transcription factors and protein complexes to fine-tune cell fate determination and organismal development. I take advantage of cutting-edge genomic techniques as GRO-seq, ATAC-seq, RNA-seq, and ChIP-seq to address these questions, in different biological systems, with a particular interest for the hematopoietic compartment.
Epigenomics and transcriptional regulation: Gene expression and RNA transcription are regulated by transcription factors and protein complexes that orchestrate the interplay between enhancers, promoters and RNA Polymerase II, to ultimately elicit transcription. Many of these mechanisms are evolutionary conserved, others are species specific. One of the most important regulators of transcription is the SWI/SNF complex, which is involved in chromatin remodeling, enhancer configuration, and RNA processing. Importantly, this complex is evolutionarily conserved across Metazoans, and many of its subunits are among the most commonly mutated epigenetic regulators across all cancers. In this context, I investigate how this complex regulates transcription and gene expression, mostly focusing on ARID1A and ARID1B, representing the mutually exclusive DNA binding subunits of the complex. Notably, ARID1A is the most frequently mutated epigenomic modifier in cancer, and its role as master transcriptional regulator has recently emerged.