Our group is interested in deciphering at a molecular and cellular level the mechanisms involved in infectious processes caused by intracellular bacterial pathogens as Salmonella enterica and Listeria monocytogenes. We put special emphasis in the study of non-productive infection models in which both the pathogen and the host coexist. These models can provide insights into teh basis of asymptomatic or peristent infections as well as chronic pathologies linked to microbial infections.

Nosocomial infections due to opportunistic pathogens are an important health problem. In our laboratory we are using Pseudomonas aeruginosa and Stenotrophomonas maltophilia as models to study the mechanisms underlying the pathology caused by organisms remains. Our research is aimed at understanding the biology of the opportunistic pathogens, especially the regulatory networks that connect their resistance to antibiotics and their virulence . We are currently addressing this problem studying insertion mutants in P.

Our research is aimed to engineer E. coli bacteria for biomedical applications, including the selection of small recombinant antibodies and the design of bacteria for diagnostic and therapeutic use in vivo. We study protein secretion systems found in pathogenic E. coli strains and engineer them to develop protein nanomachines that can be applied for selection of recombinant antibodies and the delivery of therapeutic proteins by non-pathogenic E. coli strains. Among the recombinant antibodies, we employ single-domain antibodies (sdAbs) or nanobodies.

The goals of the research group are to characterize the role of the repair (which are required for error-free DNA repair), and genetic recombination functions (which are required to adquire genetic material through horizontal gene transfer); and their contribution to chromosomal segregation. We are studying these function that are essential to promote genetic stability and the relationship among them and the role that they play in the reversion of the resistance and/or persistence to antibiotics in bacteria of the Firmicutes phylum.

The major interest of the group is to understand the bacterial responses to stress. We specifically study hypermutation and hyperrecombination as bacterial “strategies” to speed adaptation to environmental stresses. One of the models used here is antibiotic stress and the development of antibiotic resistance. Our work is focused on both stable and inducible hypermutation/hyperrecombination in E. coli, P. aeruginosa and M. smegmatis/tuberculosis.

To describe the rules of assembly of microbial communities. To achieve predictive capacity on the function of such communities, given their composition. This will allow determination of the conditions that favor particular combinations of species able to fulfill specific goals in biotechnological, clinical, and ecological scenarios.

Our laboratory is committed to understanding how bacteria that inhabit natural niches sense and process multiple environmental signals into distinct responses –both at the level of single cells and as a community. Unlike laboratory settings, in which growth conditions can be controlled and changed one at a time, bacteria in the environment must perpetually make decisions between activating metabolic genes for available, frequently mixed C-sources and those for escaping or adapting to physicochemical stress.

Our group is interested in different aspects of Bioinformatics, Computational Biology and Systems Biology. Our goal is to obtain new biological knowledge with an "in-silico" approach which complements the "in-vivo" and "in-vitro" methodologies of Biology. This mainly involves mining the massive amounts of information stored in biological databases. Besides our lines of scientific research, we also collaborate with experimental groups providing them with bioinformatics support for their specific needs, and participate in different teaching projects.

Our group is interested in the relationship between virus and cancer

Study of diseases associated with disruption of actin filaments. The assembly and disassembly of filamentous actin structures provides a driving force of dynamic processes such as cell motility and growth cone and tumor invasion, and therefore require special control and precise temporal. The reorganization of the actin cytoskeleton is regulated by actin-binding proteins such as WASP (Wiskott Aldrich syndrome protein) and WIP (WASP interacting protein). WIP stabilizes actin filaments and regulates the location and WASP degradation.