Speakers & Round Table

I am a geneticist with an Associate Professor position at the Department of Genetics of the Universitat de Barcelona. 

I work on the genetic basis of different neuropsychiatric disorders, trying to understand the mechanisms involved in these disorders and the shared genetic factors that underlie the comorbidity between them.

My research is focused on the genetic analysis of neuropsychiatric disorders (addiction, autism, aggressive behavior, and ADHD) using different methodological approaches that include genomics, transcriptomics, methylomics, association studies, functional studies, animal/cellular models and neuroimaging techniques.

In the last years I have lead research projects using both genomic data in humans and animal models (mouse and zebrafish) to identify and characterize genes with a pleiotropic effect in different psychiatric disorders. One of these genes is RBFOX1, with a wide pleiotropic effect on many different psychiatric disorders. In the last years we have been working on characterizing its role using animal models (both mouse and zebrafish), observing alterations in many different behavioural tests, as well as neurotransmitter alterations and brain activity. On the other hand, one of our last projects have identified shared genetic risk factors between addiction and aggression and related behavioural traits, such as risk-taking behaviour, neuroticism and irritability, showing positive genetic correlations. 

Our research contributes to the understanding of these complex disorders, their high comorbidity and the underlying mechanisms and circuits involved and may help to design new medications that could be more effective for the treatment of these disorders.

I am Bernardo Rodríguez-Martín, an independent fellow and team leader at the Centre for Genomic Regulation (CRG). My team, the Repetitive DNA Biology (REPBIO) laboratory, investigates the impact of repetitive DNA on genome function, evolution, and disease. To do so, we utilize cutting-edge sequencing technologies, including long-read multiomic approaches, combined with the development of innovative computational methods.

In this presentation, I will provide an overview of our research efforts to understand the role of repetitive DNA in generating structural variation—a class of large genetic changes, such as deletions or insertions of DNA sequences. Using long-read genome sequencing, we identify up to three times more polymorphic structural variants per human genome compared to traditional short-read approaches, many of which involve repetitive DNA elements. This includes inversions, a particularly challenging variant class often flanked by segmental duplication repeats. Additionally, in a separate study of cancer genomes using long-read sequencing, we uncovered novel mechanisms for the formation of genomic rearrangements driven by LINE-1 repeats.

Overall, these findings highlight the significant role of repetitive DNAs in generating both germline and somatic structural variation, as well as the potential of long-read sequencing to investigate DNA repeats and repeat-rich genomic regions, which have historically been difficult to analyze.

Hi, I'm Victoria Neguembor. I recently started my group "Chromatin Folding and Nanoscopy at IBMB, CSIC Institute of Molecular Biology of Barcelona. 

Our research group focuses on understanding the interplay between genome organization and gene function. We employ cutting-edge techniques such as super-resolution microscopy and we develop tools to investigate chromatin topology and its impact on cellular processes like transcription, as well as on differentiation and disease. 

We are located at the PCB. For more information please visit our website https://ibmb.csic.es/en/department-of-structural-and-molecular-biology/chromatin-folding-and-nanoscopy/ and follow us on X @Vickyneguembor

I am a researcher interested in understanding how epigenetic mechanisms safeguard genome integrity and maintain cellular homeostasis. I have received training and conducted research at world-class institutions, including the University of Barcelona, INSERM, Duke University, Rutgers University, and the Josep Carreras Leukemia Research Institute. During the past five years, I have held a senior postdoctoral researcher at the Josep Carreras Leukemia Research Institute and, currently, I am starting my research group at the Autonomous University of Barcelona, in the Cell Biology, Physiology and Immunology Department. During my graduate work (University of Barcelona; Duke University), I studied early transcriptional induction upon cellular stress. As a postdoctoral researcher (Rutgers University), I focused on genome integrity pathways, particularly in transposable element repression, DNA damage repair, and chromosome segregation. Among my accomplishments is the discovery of novel epigenetic programs critical for organismal and reproductive aging. Since I joined the Josep Carreras Leukemia Research Institute, I have pioneered studies investigating how genome integrity pathways regulate immune cell differentiation, providing new insights into immune cell aging and leukemia formation. As an independent researcher (UAB), my goal is to continue unraveling epigenetic mechanisms governing genome maintenance, with a particular focus on germ cell aging and fertility preservation. My research employs cutting-edge transcriptomic and genomic approaches, high-resolution microscopy, biochemistry, and both animal and cellular models.

My scientific career has been devoted to tackling different biological problems from a proteomics point of view using mass-spectrometry (MS) tools. In my PhD I studied changes of the natural protein isotopic composition as indicators of growth and health status in fish using isotope-ratio MS and characterized the response to continuous swimming in the muscle proteome. Then, during my first postdoc I implemented SILAC-based protein turnover assays to uncover the major determinants of protein turnover in eukaryotes using yeast as a model and applied phosphoproteomics to find novel therapeutic targets for mitochondrial disease and characterize the impairment of the muscle signaling network during aging in mice. During my second postdoc I set up novel methods for studying protein lipidation and its implication in metastasis. Now as a junior group leader at UB I aim to study lipid-mediated cell signaling network associated with cancer by combining proteomics together with genetic tools.

I did my Ph.D. in the university of Granada on protein design and evolution. Then later I move as a postdoc to the Weizmann Institute of Science to study how proteins self-assemble into high-order structures from a physical and cellular perspective. I obtained a Ramon y Cajal grant and joined the Structural Biology Department of the IBMB in 2022 to start my group on protein assembly and evolution.  

The cellular interior is not a mere Brownian soup of molecules; it is rather an exquisitely structured entity organized into hierarchical levels. Knowing how proteins assemble into different layers of organization, is thus fundamental to understanding the functioning of the cell. 

We recently demonstrated that proteins are a few mutations, sometimes even one mutation away, to form infinite polymers –aka supramolecular assemblies– (Garcia-Seisdedos, et al. Nature 2017, Empereur-Mot, Garcia-Seisdedos, et al Sci Data 2019, Garcia-Seisdedos, et al PNAS 2022). They are amorphous or ordered structures resulting from the self-assembly of folded proteins. 

In recent years a growing number of studies have identified proteins that naturally (often in a condition-dependent manner, e.g. membrane-less organelles), or as a result of mutation, form supramolecular assemblies, suggesting important implications in cellular adaptation and disease. 

Although it is a widespread phenomenon that is shifting the way we see the proteome organization, supramolecular assembly remains poorly understood. Its characterization will bring about important advances with implications in evolution, disease, and protein design.

The research of the lab is at the interface of Structural, Cell, and Systems Biology and aims to understand the process by which proteins form supramolecular assemblies in the cell, as well as its role in cellular organization, adaptation, and disease. To address these aims, we combine the power of yeast genetics and high-content microscopy with biophysical and structural techniques.

Dr. Maus's research focuses on uncovering shared tissue remodeling patterns in aging and cancer, using in vitro genetic and pharmacological screens to reveal the molecular links between the two. His lab translates these discoveries from bench to bedside, modeling findings in mice and applying them clinically.

Before joining VHIO, Dr. Maus completed postdocs at NYU, studying immunometabolism with Dr. Stefan Feske, and at IRB Barcelona with Dr. Manuel Serrano, investigating the metabolic ties between senescence and fibrosis. He holds a PhD in Immunology from Eotvos Lorand University.

Dr. Maus has received prestigious awards, including the Lady Tata Award, Alex's Lemonade Stand Young Investigator Award, Marie Curie Fellowship, and Ramon y Cajal Award.

Regulation of cellular metabolism is a fundamental trait of all living organisms. For long considered a housekeeping process mainly aimed to convert nutrients into energy and biomass, it is becoming increasingly evident that metabolism is actively involved in the control of many physiological and pathological processes, including cancer development. By focusing on colorectal cancer, the overarching goal of the Sebastián laboratory is to understand the role of metabolism as a regulator of stem cell fate, tissue homeostasis and tumorigenesis, and the functional interplay between metabolic reprogramming and other genetic and epigenetic programs involved in these processes. Our main research lines include:

1. Metabolic regulation of stem cell fate during intestinal regeneration and tumorigenesis.

2. Metabolic heterogeneity, plasticity and evolution of colorectal cancer

3. Metabolic crosstalk in the tumor microenvironment

To carry on these objectives, we employ stem cell cultures, 3D-organoids systems, genetically modified mouse models, tumor samples, patient-derived organoids and unique genetically encoded metabolic reporters. Results derived from our research could potentially provide valuable information to improve current therapeutic approaches to treat colorectal cancer patients by targeting specific metabolic pathways. 

I am a results-oriented Immuno-Oncology Project Leader with a strong scientific background and a proven track record in immune-oncology research. My academic journey began with a Bachelor's degree in Biotechnology (2010), followed by a Master's in Biomedicine (2011) and a PhD in Immunology (2016). Continuously pursuing excellence, I have enhanced my skill set through targeted project management courses, including a post-graduate course in Project Management (2020); a Pharma and Biotech Project Management course (2021); Leadership and Development of Managing Skills Course (L2022). 

As the Immuno-Oncology Project Leader at Peptomyc, I leverage my extensive knowledge of the immune system to coordinate, monitor, and supervise projects. My focus is on elucidating how MYC inhibition modulates the anti-tumor immune response in various cancer models. Additionally, I explore the interaction of Omomyc with the host immune system at both preclinical and clinical levels. In addition to leading the project focused on the predictive and pharmacodynamic circulating biomarker signatures, I oversee the development of companion diagnostic stratification and real-time response monitoring tests for Omomyc. Furthermore, I leverage my experience in drug development projects to manage studies involving drug combinations with MYC inhibitors, unlocking new avenues for enhanced therapeutic efficacy for cancer treatment. I'm also interested in pushing MYC inhibition outside oncology, specially for the treatment of autoimmune diseases. Additionally, I actively contribute to the advancement of Omomyc into the clinical phase by ensuring seamless integration of preclinical and clinical efforts.

My research focuses on the role of the exposome in shaping the epigenetic landscape and its link to cancer. The exposome encompasses exposure over a lifetime to environmental and lifestyle factors, such as diet, smoking, air pollution, and chemical exposures. The complexity of measuring all such factors makes it challenging to comprehensively study their implications on health. To address this, I explore DNA methylation as an epigenetic marker to indirectly assess the impact of these exposures on disease development.

Through our study, we utilized DNA methylation data measured in tumors of patients with early-onset colorectal cancer (eoCRC, aged < 50) and those with later-onset colorectal cancer (loCRC, aged ≥70). We developed methylation risk scores (MRS) to quantify exposure levels for various exposome traits, including lifestyle factors, air pollution, and pesticide exposure. These scores allowed us to compare eoCRC patients with loCRC patients, revealing specific exposome factors—such as increased smoking exposure and certain pesticides, like picloram—significantly associated with eoCRC incidence. Employing meta-analyses, we validated our findings across multiple independent datasets.

Our analysis emphasizes the value of utilizing epigenetic alterations as a proxy for exposome exposure, offering a powerful approach to assess their contribution to cancer development. The potential of exposome-driven epigenetic research provides a pathway for prevention strategies through personalized interventions and policy changes.

I joined the CRG as a Group Leader less than a year ago. Our Group's research focuses on understanding how the cytoskeleton impacts RNA processing in the nucleus of different cell types in health and disease.

My undergraduate degree in biotechnology provided a broad understanding of how contemporary technology can be used to unravel biological conundrums, with a focus on human physiology. Then I pursued a PhD with Prof. Monserrat and Dr. Moreno at the University of Barcelona focused on autoimmunity and cancer biology, specifically related to chronic lymphocytic leukemia (CLL). In 2013, I started as a postdoctoral researcher in training at The Feinstein Institute for Medical Research (USA), working with Prof. Chiorazzi, one of the world leaders on a CLL xenograft model using immune-deficient mice; to understand better the interaction of CLL cells with other cells of the microenvironment, especially T cells. In addition, I started a new area of investigation the ménage à trois between CLL cells, myeloid suppressor cells and T cells. On December 2019 I joined the Josep Carreras Leukaemia Research Institute to develop my line of research on immunology and epigenetics to better understand leukemogenesis, immune evasion and transformation.

I have done my PhD in Germany on cell motility in 3D spheroids and human cancer samples. I found that cells (and also nuclei) deform when they move through dense tissues, which indicates a fluidized tissue. This finding is an example of an active phase transition in biology, and particularly, cancer. It connects clinical histology (the cancer diagnosis criterion known as pleomorphism) with modern soft matter physics (active phase transitions and (un-)jamming).

Synopsis: 

Elongated Cells May Unjam Cancers - https://physics.aps.org/articles/v14/s19. Here in Barcelona, I work on dynamics, i.e. forces of cells and cell clusters. In collective cell motility in development and disease, not much is known about the force patterns that cells use (and need) to move, be it alone or collectively. At IBEC, I use traction force microscopy to measure these forces, and I use optogenetics to control cell motility in tissues, i.e. to make cells move on-demand. 

With my colleagues, we have recently discovered a force-velocity relation for 1D-cell motion, in very small groups of cells. Somewhat surprisingly, although "force-velocity relation" sounds like very basic physics, this has not been known before for cells! I intend to extend this knowledge to clusters of cells, which can swirl, move collectively in fascinating patterns, and invade other tissues.

https://www.nature.com/articles/s41567-024-02600-2 

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I am a postdoctoral researcher in the Bigas lab at the Hospital del Mar Research Institute with expertise in embryology, stem cells, stem cell-based embryo models, and haematopoiesis. In 2012, during my Master’s internship in the Martinez Arias laboratory (Cambridge University, UK), I pioneered the first stem cell-based embryo model (van den Brink et al, Development, 2014). This embryo model, named ‘3D mouse gastruloids’, is generated by aggregating embryonic stem cells into embryonic organoids. During their culture, these embryonic organoids spontaneously elongate and self-organize into embryo-like structures that recapitulate key aspects of post-implantation mouse embryos. During my Ph.D. (van Oudenaarden laboratory, Hubrecht Institute, The Netherlands), we characterized mouse gastruloids in detail using single-cell and spatial transcriptomics. In addition, we discovered that physical somites (blocks of tissue giving rise to skeletal muscles) can be generated in vitro by adding a small amount of Matrigel to the gastruloid culture protocol (van den Brink et al, Nature, 2020). During my PhD, we also collaborated with the Martinez Arias lab to establish and characterize a first human version of the 3D gastruloids embryo model (Moris et al, Nature, 2020). In November 2021, I started a postdoc that aims to develop modified versions of gastruloid models that can be used to study healthy and leukemogenic haematopoiesis in vitro. In this project, we are using a combination of microscopy-based screenings, flow cytometry, whole-mount immunohistochemistry, and whole-mount HCRv3.0 spatial transcriptomics technologies to screen for conditions that allow in vitro formation of the embryonic and adult haematopoietic niches.

During my second postdoc in Barcelona, I have been focused on the regulation of circadian rhythms in the context of muscle stem cells. These cells, also known as satellite cells, are a small but powerful subpopulation of the cells of the muscle and are the main effector of muscle repair. Circadian rhythms are essential for our physiology, they regulate organisms’ behavior according to time-of-the-day. A key regulator of these rhythms is the suprachiasmatic nucleus (SCN) in the brain, which is synchronized by light and synchronizes peripheral tissues. Nevertheless, every cell in our body has a clock, that is represented by a group of oscillating transcription factors that regulate the oscillations of a subset of genes that constitute the circadian output. What is the role of peripheral clocks and whether they are autonomous from the central clock in the SCN are actual questions in the field and at the basis of my work on satellite cells.

Briefly, we found that central rhythms are necessary and sufficient for the oscillation of metabolic transcripts in satellite cells and that these oscillations need a functional autophagy machinery to occur. Autophagy is a homeostatic pathway impaired in many diseases and as such it has been the subject of my previous works in Paris on cancer and metabolism. As a subject of my lab in the future, I am interested in further elucidating the interplay between autophagy and circadian rhythms and their role in inter-organ crosstalk and disease.

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My long-term research goal is to understand the dynamics of neuronal degeneration in Alzheimer’s Disease (AD), and Tau contribution to it, using a live-cell imaging approach. I am a Ramón y Cajal Researcher at IBEC. I did my PhD in morphogenesis and biomechanics. For my postdoctoral work, I decided to continue working at the interphase between physics and biology and I moved to the laboratory of Anthony Hyman at the Max Planck Institute of Molecular Cell Biology and Genetics where the concept of phase separation was just emerging. There, I investigated Tau molecular condensates and their possible contribution to: Tau function, as a Microtubule-Associated Protein; or Tau pathological solid transition, in neurodegenerative diseases. During this work, I realized that we have a knowledge gap in understanding Tau initial solid transition in axons and its immediate consequences for axonal function. Therefore, I decided to focus my independent research on this. A dynamic understanding of neuronal degeneration in AD is missing. Neurons are highly specialized cells with long and thin protrusions essential for neuronal function. Due to this morphology, they are particularly susceptible to traffic jams or any other mechanical perturbation that alters cargo supply to synapses. Axonal swellings and dystrophic neurites are observed early in the disease but how these structures form, or resolve is unclear. Using CRISPR-cas9 technology, we generated hPSCs and mice with endogenous Tau meGFP-tagged. We are using neurons derived from both models to understand the dynamics of axonal degeneration upon Tau or amyloid beta aggregation. 

In 2019, I joined the IBMB-CSIC in Barcelona through the Beatriu de Pinos MSCA COFUND program, and since 2022, I have been a Ramon y Cajal Research Investigator and Group Leader at the interface of structural biochemistry, proteolytic enzymes, and synthetic microbiology. My research group focuses on two main areas: the role of proteases in health and disease and the redesign of proteolytic flagellins to harness flagellar display for biotechnology and biomedicine. During my PhD at the University of Salzburg, Austria (2007-2011), I focused on clostridial collagenases, key pathogenicity factors (Eckhard et al. 2011, Nature Structural & Molecular Biology), while during my postdoc at the University of British Columbia in Vancouver, Canada (2011-2016), I comprehensively characterized the human matrix metalloprotease family, which are key signaling scissors during inflammation and tumor development (Eckhard et al. 2016, Matrix Biology). Moreover, I spearheaded the discovery and characterization of flagella-embedded proteolysis, nature's proof of flagellar display (Eckhard et al. 2017, Nature Communications). I then joined Uppsala University (2016-17), where I tackled the overarching question of how protein structure and function are intertwined during evolution and ecological adaptation, before returning to the University of Salzburg (2017-2019; 2 publications) to focus on the biochemistry and role of proteolytic flagellins in bacterial lifestyle. These studies allowed me to develop my current two key research lines in the lab: (1) structure-guided synthetic microbiology, where we functionalize bacterial flagella, and (2) structural biochemistry of pathogenicity factors, aiming to both address them during disease and repurpose them for BioMedTec.

I am a biologist (University of São Paulo/University of Tübingen) with more than 10 years of academic research experience in the field of hypothalamic development, maternal programming, metabolism and neurobiology of female feeding behaviours. I hold a PhD in Neuroscience from the University of Heidelberg. After a postdoc in the laboratory of Prof. Dr. Licio A. Velloso (University of Campinas) and in the laboratory of Dr. Marc Claret (IDIBAPS) I became a Principal Investigator with a Ramon y Cajal contract at the IDIBAPS in Barcelona.

Our team aims to understand how the female brain reshapes its activity during physiological states (e.g. menstrual cycle, pregnancy and lactation) and drive distinctive feeding, reproductive and social behaviours, as well as its transgenerational neuropsychological and metabolic impact. Our group combines neuroscience and metabolism, and employs a wide range of cutting-edge technology (mouse intersectional genetics, fiber photometry, chemogenetics, optogenetics, snRNAseq, etc.) and fields (endocrinology, behaviour, physiology, etc). 

My name is Júlia Domingo and I am the CEO and co-founder of ALLOX, a recent spin-off of the Centre for Genomic Regulation (CRG) that draws on the expertise and technology developed in the lab of Ben Lehner. The company was born out of the realisation that combining systematic mutagenesis, high-throughput phenotyping and biophysical modelling has the potential to revolutionise drug development but also transform biotechnology in general. Our most immediate goal is to identify allosteric switches in all proteins and then leverage this unprecedented resource to rapidly develop novel medicines to treat human diseases. The long-term vision of ALLOX is to become a leader in programmable biology, building the next generation of tools to predict, design and engineer new protein functions. At ALLOX we believe in a future where humanity will be able to harness the power of biology to solve our most pressing issues.

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