During the past 13 years, the group has studied two DNA polymerases implicated in DNA double strand break (DSB) repair in humans: Pol lambda and Pol mu, which were identified in our laboratory. Given their role in DSB repair by non-homologous end joining (NHEJ), these two enzymes are essential to maintain genomic stability and also to generate the variability needed in certain genes, such as antigen receptors.

Our research interests are Genome Biology, DNA replication, transcription and Epigenetics. We focus our investigation in trying to understand how chromatin structure modulates the expression and maintenance of the information encoded in eukaryotic genomes, and how these processes take place within the context of a highly complex and compacted genomic chromatin environment. This knowledge is of fundamental importance to understand the complex role of chromatin in regulating the versatility and stability of our genome both in physiological and pathological conditions.

The role playing by RNA-binding proteins in physiological situations as development, or pathophysiological situations as the interface of the apoptosis regulation and the development and/or establishment of the program of cell proliferation/transformation or cancer, as well as aging-associated diseases/pathologies such as Welander distal myopathy.

Functional and structural analysis of RNA regions involved in translation control. RNA-binding proteins involved in postrancriptional control of gene expression

The research activity of our group has been focused on molecular aspects of the protist Leishmania and the immune-pathology that the infection of this parasite causes. On the one hand, we are studying molecular processes associated with the peculiar mechanisms of gene expression in an organism in which transcriptional regulation is almost absent.

The group belongs to the Biomedical Network Research Centre for Rare Diseases (CIBERER) and to Hospital La Paz Institute for Health Research (IdiPaz). Our work is focused on rare neurometabolic diseases, performing translational studies by the generation and charactetrization of cellular and animal models of disease, as research tools to understand underlying molecular and physiopathological mechanismsm, to identify biomarkers and novel therapeutical targets.

Our group is interested in understanding how eukaryotic cells maintain genome stability during chromosome replication, especially under conditions that cause DNA damage or replicative stress

Structural Bioinformatics: Analysis and prediction of conformation changes in proteins with the torsional elastic network model. Changes of structure and function in the evolution of proteins. Prediction of thermodynamic stability of proteins and models of protein evolution with selection on unfolding and misfolding stability. Evolutionary analysis of structural disorder in proteomes. Theoretical ecology: Dynamics of ecological systems with mutualism and competition. Detection of ecological interactions between bacteria from ecological samples.

Our group studies the involvement of thioredoxins (Trxs) and thioredoxin reductases (NTRs) in mechanisms of redox regulation in plants, focusing on the function of NTRC, an enzyme first described by our group (Serrato et al. (2004) J. Biol. Chem. 279:43821-43827). Recently, we have proposed a novel model for chloroplast redox regulation according to which, the reductive activation of biosynthetic enzymes in this organelle depends of the redox state of 2-Cys peroxiredoxin, an enzyme that reduces hydrogen peroxide to water (Pérez-Ruiz et al. (2017) PNAS 114:12069-12074).

The main goal of our research is to elucidate the molecular mechanisms underlying cellular adaptation to changing conditions and stress. To this aim, we use the model photosynthetic organisms Chlamydomonas reinhardtii and Arabidopsis thaliana. Our group has been pioneer in the study of the TOR signaling pathway, a master regulator of cell growth, and autophagy, a degradative process by which cells maintain cellular homeostasis and cope with limiting conditions and stress that is negatively controlled by TOR.