Our research focuses on identifying genes associated with psychiatric disorders. We use genomic techniques like sequencing to study the genetic basis of conditions like autism, bipolar disorder, and schizophrenia. We analyze both common and rare genetic variants to understand their roles in these disorders. Our work has led to the discovery of several susceptibility genes and pathways related to bipolar disorder. We also collaborate with international efforts to study the genetics of psychiatric disorders and their response to treatments.

Our lab focuses on studying the metabolic features of aggressive lymphomas with poor outcomes, specifically those involving MYC and BCL2 alterations. We aim to identify new metabolic vulnerabilities in these tumors using advanced tools and patient samples, potentially leading to targeted therapies beyond current options.

Meiosis is an essential process during gametogenesis, giving sexually reproducing organisms the ability to adapt to the environment through evolution. Our research focuses on the ability of cells to correctly perform the processes of homologous recombination (HR) of the DNA during meiosis, and to identify the response of those same cells when recombination is defective or absent. When these defects occur, problems during recombination could have a major impact on gamete quality.

Our research line is focused on elucidating the molecular mechanisms involved in the development of giant cell arteritis. Specifically, the main objective of our research group is to determine the genetic and epigenetic contribution to the pathogenesis of this disease by using genomic (genome-wide association studies, GWAS), epigenomic (DNA methylation and chromatin conformation analysis by ATAC-seq and ChIP-seq) and transcriptomic (RNA sequencing and single-cell RNA sequencing) approaches in cell types with a relevant role in giant cell arteritis.

Our lab studies genome protection using the BRCA2 protein as a model, exploring its role in breast cancer susceptibility. We found new partners of BRCA2 through interaction studies, including RNA helicases. BRCA2 deficiency leads to DNA-RNA hybrids accumulation, which we addressed with the RNA helicase DDX5 collaboration (Sessa et al EMBOJ 2021).

Our research focuses on understanding the immune response's intricacies during infection, particularly the activation of B lymphocytes that produce antibodies and memory cells. We study the metabolic changes in these cells, known as Germinal Centers (GC), during their initiation, progression, and termination. We have discovered the role of mitochondria in GC reactions and how B cell metabolism influences both B and T cells' functions, which we term "metabolic communication." We use advanced techniques to analyze B cell metabolism and aim to identify molecular mediators of this process.

This research group is focused in the replicative sequences that have colonised and multiply within the human genome, known as mobile genetic elements (MGEs) or mobile DNA. MGEs’ replicative activity led to an accumulation of copies that accounts for ~50% of the human genome. They cause insertional mutagenesis, leading to an increase of genetic diversity and occasionally responsible of spontaneous genetic disease and cancer. Epigenetic silencing is known to minimise their deleterious impact, although the mechanism responsible for driving this silencing to active MGEs is largely unknown.

Our research team focuses on the study of the tissue remodelling that occurs during the development, progression and resolution of chronic diseases, with a special emphasis on fibrosis and cancer. Tissue remodelling involves both the cellular components of the tissue and the extracellular matrix (ECM) in a complex interplay where both send signals to each other, triggering important biological events such as cell death/proliferation, ECM synthesis/degradation, regeneration and inflammation among others.

At the Pathogen Gene Regulation Unit, we combine cutting-edge techniques and bioinformatic analyses to understand how microbial pathogens infect, survive, cause disease, and develop antibiotic resistance, both at the molecular and cellular levels. Our main research focus is centred on understanding how translational regulation and alternative initiation mechanisms contribute to phenotypic adaptation and antibiotic resistance in bacteria. We have a special focus on Mycobacterium tuberculosis, the causative agent of human tuberculosis.

The genetic information in eukaryotic cells is tightly wrapped around histone proteins to form chromatin, which is highly repressive to processes occurring on DNA. However, we know since pioneering studies by Vincent Allfrey in the early 1960s that histones are subjected to a wide variety of covalent post-translational modifications (PTMs) that can modulate DNA accessibility, thereby playing key roles in many biological processes.