These questions are addressed in the lab through the following projects, which are a combination of ongoing research as well as of novel research interests:

1. Escaping from pluripotency and the acquisition of cell fate. We study the mechanisms by which cells change their transcriptional programs in order to follow specific developmental trajectories that result in differentiated cell types. We focus on different contexts during mouse development such as the first lineage choice that takes place in the preimplantation embryo and the specification of blood cells or cardiomyocytes.

Escaping from pluripotency and the acquisition of cell fate


2. The role of 3D genome structure in development and disease. The 3D organization of the chromatin has emerged in recent years as a major player in the regulation of the genome. We address how this is necessary for the development of the cardiovascular system, as well as how its disruption can underlie human cardiovascular and hematological diseases.

The role of 3D genome structure in development and disease


3. Deciphering the genetic and genomic contribution to human atrial fibrillation (AF). We aim to understand the function and mechanisms behind GWAS related to CVD, by focusing on genetic loci related to AF in humans, most of which lie in non-coding intergenic regions. By means of functional genomic approaches in mice, we aim to understand the regulatory nature of variants linked to the disease and identify upstream inputs altered between healthy and diseased status. In a complementary approach, we aim to chart the transcriptomic and epigenomic changes that occur during progression of AF in large animal models, such as sheep and pig, in collaboration with clinical and translational groups at CNIC.

Deciphering the genetic and genomic contribution to human atrial fibrillation (AF)