Along the years our group has aim to understand the processes of signal transduction that let to changes in cell structure and function in physiology and diseases. We focus our attention on the signaling pathways regulated by G proteins and GPCRs. A novel localization of G proteins at the mitochondria and other endomembranes where they regulate morphology and physiology of these organelles has been recently demonstrated by our group. Mitochondria are dynamic organelles that produce most of the energy of the cell.

The goal of the lab is to examine novel levels of regulation of the proteasome pathway focusing on the mechanisms that control proteasome function and its interaction with protein substrates. Our ongoing studies pursue basic and applied research areas. Our objective is to characterize the regulatory interactions that control the proteasome and the impact cellular homeostasis. We also aim to identify novel ubiquitin pathway substrates by means of Omics approaches.

The connections in our brains are constantly changing. As we interact with the environment and each other, connections between our neurons are remodelled so that we can retain these interactions as learning and memory. At a molecular level, the brain accomplishes this remodelling in part by making new proteins at the specific sites where our neurons interact with each other (known as synapses). Abnormalities in synaptic plasticity contribute to a wide range of neurological and cognitive disorders, such as schizophrenia, autism, addiction and multiple sclerosis.

We aim at unveiling the molecular mechanisms supporting endocytic traffic, with a particular focus on the role that actin and lipids play in the process. We use S. cerevisiae as a model system to dissect the conserved molecular mechanisms involved. By combining the powerful yeast genetics with informative in vitro assays, life-cell fluorescence microscopy of single endocytic events and quantitative electron microscopy, we refine molecular models explaining membrane budding.

The main interest of our group is the control of proliferation and differentiation processes along nervous system development. Germ line and somatic mutations may cause an alteration of the mentioned processes, leading to an aberrant growth and in many cases prompting it to malignancies. Historically neoplastic growth has been associated to genes that either induce cell proliferation, or increase survival. Advanced tumours normally accumulate a large number of mutations, being difficult to discriminate which of those mutations were the founding ones.

The focus of my research has been to provide basic knowledge on the genetic regulation of developmental processes and I think that now we can say that the work of many laboratories has allowed to begin to understand the genetics logic behind development. Some years ago I decided to try to go a step forward in contributing to the understanding of how these mechanisms impinge on cell behavior and how changes in individual cells sum up to generate organs and the whole organism.

Our group was established in 2002 and at present consists of a PhD student, a master student, a technical assistant, a senior associate and the PI. Our research covers a range of topics related to Receptor Tyrosine Kinase (RTK) signaling and gene regulation in development, mainly using Drosophila as a model system. We are currently supported by research grants from the Spanish Government (BFU2017-87244-P) and AGAUR (Generalitat de Catalunya).

Development of the Spinal Cord in health and disease; The role of extracellular signals and the genetic networks that control cell numbers, cell identity and cell shape changes during the embryonic development of the neural tube.