LS² Annual Meeting 2027

Bio: Luiggi Cavalcanti Pessôa is an Assistant Professor and Researcher at SENAI CIMATEC University (Brazil). His research focuses on circular bioeconomy, microalgae biotechnology, waste-to-value systems, biorefineries, and biogas and biomethane development. He holds an M.Sc. in Energy and Environment from Universidad Adolfo Ibáñez (Chile) and a Ph.D. in Chemical Engineering from the Federal University of Bahia (Brazil), including a visiting doctoral appointment at the University of Almería (Spain). Dr. Pessôa combines academic, industrial, and applied R&D experience, including leadership roles in manufacturing operations. He develops research grant proposals and leads collaborative research and innovation projects involving industry, government, and international partners, advancing resource recovery, circular economy, and energy transition solutions. He is the Technical Coordinator of the MBI in Circular Economy at SENAI CIMATEC and was recognized for his doctoral research with the 2024 UFBA Best Engineering Ph.D. Thesis Award and the 2025 UFBA Polytechnic School Recognition Award. 

Title: From the Factory Floor to the Lecture Hall: An Unconventional Journey to Becoming a Young Professor 

Abstract: More than once, I found myself standing on a factory floor, in different countries, convinced that industry would define my professional future. Yet one thing never went away: a persistent curiosity to keep growing, challenge myself, and better understand the world around me, even when I could not fully explain why. What followed was anything but a linear career path. A planned Ph.D. in Canada never materialized after scholarship funding was cut. I left industry to start over in a country whose language I did not speak. Personal losses and the passing of mentors forced me to rethink my priorities and sense of purpose. And when I finally secured a faculty position, a new international opportunity emerged, tempting me to change directions once again. This is not a talk about career planning. It is a story about uncertainty, curiosity, perhaps resilience, and how some of the most important decisions in life are often the ones we never intended to make. There was no roadmap. Looking back, many of the best decisions of my career were never part of the original plan. If these stories spark curiosity in even one person in the audience, then the journey will have been worthwhile. Hope you enjoy it! 

Bio: Prof. Felix Randow is Professor of Molecular Immunity at the University of Cambridge and Programme Leader at the MRC Laboratory of Molecular Biology, where he leads a research programme investigating cell-autonomous and innate immunity. His research focuses on how host cells detect and eliminate intracellular bacterial pathogens, with particular emphasis on ubiquitin signalling, antibacterial autophagy, membrane damage sensing, and host–pathogen interactions. Over the past two decades, Prof. Randow has made several landmark discoveries that have transformed our understanding of innate immune defence mechanisms, including the identification of key pathways linking ubiquitin signalling and selective autophagy to antibacterial immunity. He is an elected EMBO Member and Fellow of the Academy of Medical Sciences, and has received numerous prestigious awards, including a Wellcome Trust Senior Investigator Award. His work has been published in leading journals such as Nature, Science, Cell, Nature Immunology and Molecular Cell.

Talk title: Ubiquitylation of non-protein substrates: Mechanisms and consequences

Abstract: Ubiquitylation is essential for eukaryotic life. Historically, proteins were thought to be the exclusive targets of ubiquitylation. Our discovery of lipopolysaccharide ubiquitylation during bacterial infection revealed non-protein ubiquitylation as an 'eat-me' signal for selective autophagy. In searching for endogenous substrates of non-protein ubiquitylation, we recently discovered the ubiquitylation of aberrant glycogen as an essential mechanism of glycogen quality control that prevents polyglucosan disease. I will discuss the mechanisms and biological significance of non-protein ubiquitylation in immunity and organismal homeostasis.

Bio: Georg Winter performed his graduate studies at CeMM in Vienna, working on elucidating the mechanism of action of cancer drugs with a specific emphasis on proteomics- as well as chemical genetics approaches. He continued his training in chemical biology, working as a postdoctoral fellow with Dr. James Bradner the Dana Farber Cancer Institute where he published the first paper reporting on in vivo target protein degradation and co-developed degron-tagging approaches that leverage the E3 ligase CRBN (dTAG approach) to understand the mechanistic involvement of gene control factors in oncogenic transcriptional circuits. He was recruited as a CeMM Principal Investigator in June 2016, continuing his work on targeted protein degradation with a particular emphasis on the phenotypic identification and mechanistic characterization of molecular glue degraders. In April 2025, Georg has been appointed as the Life Science Director at AITHYRA. The Winter lab has been funded via several national and international third-party grants, including two ERC Grants (Starting and Consolidator), an Aspire Award (Mark Foundation) and a Cancer Grand Challenge Award. Georg has authored more than 70 peer-reviewed papers and his contributions to the field of chemical biology in general, as well as targeted protein in particular, have been recognized via several international awards including the Eppendorf Award for Young European Investigators, the Wilson S. Stone Memorial Award from the MD Anderson, the Tetrahedron Young Investigator Award and the EFMC Price for Young Chemical Biologists.

Talk title: Chemical Rewiring of Biological Circuits for Cancer Therapy

Abstract: Cancer therapies have traditionally focused on inhibiting disease-driving proteins. An emerging alternative is to reprogram cellular circuitry by chemically rewiring protein function, interactions, localization, and fate. In this lecture, I will discuss recent advances in induced-proximity pharmacology and chemical biology that enable the rational manipulation of biological networks beyond conventional inhibition. Drawing on examples from targeted protein degradation, molecular glue discovery, transcriptional reprogramming, and chemically induced post-translational modifications, I will illustrate how small molecules can redirect endogenous cellular machinery to create new therapeutic mechanisms. These studies reveal opportunities to convert previously undruggable cancer dependencies into tractable therapeutic targets and suggest a broader framework in which medicines act not merely as inhibitors, but as programmable agents that rewire biological circuits. Together, these approaches point towards the possibility of re-imagining cancer therapy.

Bio: As an undergraduate at Ohio State University and graduate student at Duke University, my research focused on understanding protein function at a molecular level with biophysical techniques. During my postdoc at MIT, I uncovered an unexpected relationship between protein folding and MHC antigen presentation. As a Damon Runyon Postdoctoral Fellow in Tyler Jacks’ Lab, I integrated my protein biochemistry background with mouse model engineering and developed tools for lineage restricted analysis of antigen presentation in vivo. My independent lab has continued to expand our immunopeptidomics toolkit and have applied our unique approach to isolate MHC-I and MHC-II peptides from numerous in vivo contexts including healthy tissues and preclinical models of lung cancer, pancreas cancer, head and neck cancer, colorectal cancer, and melanoma. These efforts have yielded insights not only into the mechanisms that shape the antigen landscape of cancer but also identified therapeutically actionable targets for antigen-specific immunotherapy. Additionally, we have applied our MHC-I and MHC-II toolkit to isolate antigens from professional and non-professional antigen presenting cells including dendritic cells, macrophages, B cells, and fibroblasts. Finally, we have leveraged our interactions with clinical colleagues at Moffitt Cancer Center to analyze patient samples. These cross-species, integrated approaches have provided a holistic view of antigen presentation and revealed cell type specific programs of antigen processing and presentation that can be used to engineer antigen specific immunotherapies in cancer.

Talk title: Decoding antigen presentation in the tumor microenvironment

Abstract: Adaptive immunity to cancer requires effective antigen presentation on Major Histocompatibility Complexes (MHC). While recent advances in computational prediction of cancer-specific MHC antigens have ushered in a new era of antigen-specific immunotherapies, including cancer vaccines, there is widespread recognition that these approaches misidentify most actionable antigenic targets. To address this, many groups have employed liquid chromatography-tandem mass spectrometry (LC-MS/MS) based empirical measurement of peptides presented by MHC-I and MHC-II, also known as “immunopeptidomics”. These efforts have greatly expanded our understanding of antigen presentation across various cells and tissues. However, these analyses are typically performed with cultured cells or bulk tissues, limiting our understanding of cell-type specific patterns of antigen presentation in the tumor microenvironment (TME). Our group has pioneered a new approach, based on engineered Cre-inducible affinity-tagged mouse MHC-I or MHC-II (H2-K1, “KbStrep”; H2-Ab1, “AbStrep”), enabling lineage-restricted immunopeptidomics in vivo. We applied these tools to immunocompetent models of lung adenocarcinoma (LUAD) and pancreatic ductal adenocarcinoma (PDAC), enabling precise purification of MHC peptides from either malignant cells or various stromal cell lineages in the TME. Integrating immunopeptidomics data with single cell RNA sequencing facilitated the deconvolution of the cellular origin of various tumor associated antigens. Also, we applied next generation proteomics search strategies to capture highly complex landscapes of post-translationally modified MHC peptides, revealing additional peptide binding modes and reflecting intracellular oncogenic signaling throughout tumor evolution. Our data suggests that the antigen landscape is dependent on physiological context and is highly dynamic throughout tumor evolution, highlighting an ever-evolving landscape of MHC targets for T cells that may underlie the success or failure of immunotherapy. Understanding these patterns across cell types in the TME will likely yield more precise and effective antigen-specific immunotherapies. Beyond cancer, the application of lineage-restricted immunopeptidomics to models of infectious disease and autoimmunity has great potential for basic immunology discovery.

Bio: Carolin Lerchenmüller is Professor and Chair of Gender Medicine at the University of Zurich and a cardiologist at the University Hospital Zurich, where she leads the Women’s Heart Health Program within the Department of Cardiology.Following her medical studies and specialist training in Heidelberg, she conducted research at Massachusetts General Hospital and Harvard Medical School. Her research combines molecular cardiology and gender medicine, focusing on sex and gender differences in cardiac adaptation, disease, and injury, as well as cardioprotective mechanisms of the heart.In addition, her work addresses the role of gender medicine in global health, as well as issues of equity, diversity, and inclusion in medicine and science.

Talk title: From Mechanisms to Medicines: Integrating Sex and Gender in Biomedical Research

Abstract: Sex- and gender-sensitive medicine recognizes biological sex and sociocultural gender as distinct but interacting determinants of health and disease. It examines how sex-related biology influences molecular pathways, disease mechanisms, and responses to drugs, while gender shapes exposures, health behaviours, access to care, and treatment.Integrating these dimensions across the research continuum - from cells and animal models to clinical trials and clinical practice - is essential for reproducible science and more precise, effective therapeutics. In this talk, I will provide an overview of the current state of the field and discuss how sex and gender can be appropriately incorporated at different stages of biomedical discovery. Drawing on our research in cardiovascular medicine, clinical trials, and the distribution of research efforts, I will illustrate how sex- and gender-informed approaches can reveal biological mechanisms, identify persistent blind spots, and improve the translation of biomedical research into better care for everyone.

Bio: My group’s focus is on investigating the dynamics of biomolecular assemblies and trying to design them from the ground up using computational protein design.

Talk title: Accurate design of protein binders

Abstract: Protein-protein interactions are central to biology and drug discovery, yet traditional antibody generation is slow and costly. BindCraft is an open-source, automated computational pipeline for de novo protein binder design that routinely yields nanomolar binders with 10-100% experimental success, without high-throughput screening or maturation. We illustrate their different biological and biochemical applications and outline how deep learning workflows can accelerate next-generation therapeutics, diagnostics, and bioprocessing.

Bio: Sabine Liebscher is a physician and neuroscientist, currently Professor of Systems Neurobiology and Director of the Institute of Systems Neuroscience at the Medical University of Innsbruck, a position she has held since February 2025. Before her appointment in Innsbruck, she served as W2 Professor of Cellular Neurophysiology at the Faculty of Medicine, University of Cologne, and previously led a Clinician Scientist research group while training in Neurology at the Institute of Clinical Neuroimmunology, at the University hospital Munich of the Ludwig Maximilians University (LMU) Munich, Germany. She studied medicine at the Technical University of Dresden, where she also completed her MD thesis. In 2007, she joined the laboratory of Nobel Laureate Paul Greengard at The Rockefeller University in New York. She later earned her PhD in Neuroscience with distinction from the Max Planck Institute of Neurobiology and the LMU Munich. In 2014, she established her independent junior research group through the prestigious Emmy Noether Programme of the German Research Foundation (DFG). Her research focuses on the pathophysiology of neurodegenerative diseases, particularly amyotrophic lateral sclerosis (ALS). She investigates how neural circuits and their components contribute to disease symptoms and drive the degenerative process. Her work integrates clinical insight with experimental neuroscience, combining in vivo two-photon imaging, single-cell transcriptomics, and viral circuit manipulation to uncover network-level mechanisms of neurodegeneration.

Talk title: Exciting complexity: Circuit mechanisms of cortical dysfunction in ALS / FTD

Abstract: Neurodegenerative diseases are increasingly recognized as disorders of neural circuits rather than the simple consequence of cell loss. Functional alterations in defined neuronal populations and networks often emerge before overt degeneration and can persist beyond it. Our work focuses on identifying these circuit-level dysfunctions to uncover early pathogenic mechanisms and therapeutic targets. I will present examples from amyotrophic lateral sclerosis (ALS), the most common adult-onset motor neuron disease, characterized by the loss of upper and lower motor neurons. A hallmark of ALS is cortical hyperexcitability, which appears early and plays a pivotal role in disease progression. Our studies show that this hyperexcitability is associated with early synaptic alterations and hyperresponsive layer 2/3 pyramidal neurons, which provide excessive glutamatergic drive to upper motor neurons and thereby promote aberrant feedforward excitation. In parallel, we find that noradrenergic input to the motor cortex is markedly reduced in both mouse models and ALS patients, suggesting a loss of neuromodulatory control that may further exacerbate cortical hyperexcitability. Together, these alterations arise before overt neuronal loss and contribute to abnormal motor output, indicating that network dysfunction, rather than degeneration alone, underlies selective vulnerability. Targeting compromised circuit elements delays disease onset and progression, underscoring their pathophysiological importance.

Bio: Andreas Dendorfer is Professor for Cellular Signal Transduction at the Walter-Brendel-Centre of the LMU Hospital. He studied electrical engineering and medicine, and received his professional education at the Institute of Physiology of the LMU München, and the Institute of Pharmacology and Toxicology of the Medical University of Lübeck. His research interests are focused on cardiovascular physiology and pharmacology, covering hypertension, autonomic innervation, and cardiac metabolism and preconditioning. More recently, he established the use of myocardial living slices for his research, and developed a bioreactor for the biomimetic cultivation of this tissue preparation. To promote tissue culture technology in general, he co-founded the start-up company InVitroSys.

Talk title: Biomimetic culture of human myocardium: A versatile in vitro model

Abstract: Living myocardial slices (LMS) are thin, vibratome-cut sections of authentic myocardium which can be prepared from hearts of various species, and particularly, from explanted human myocardium of heart transplant recipients. Since O2 demands are covered by diffusion, the viability and functional state of LMS can be maintained under biomimetic conditions (preload, pacing, compliance) for many weeks. As such, LMS form a medium complexity experimental platform which provides a 3-dimensional, multicellular, biomechanical model of adult myocardium, but excludes exogeneous factors such as perfusion, metabolism, and neuro-hormonal regulation. The experimental benefits of the model comprise long-term interventions, sequential functional readouts, and free end-point analyses.LMS have been used for studies on drug effects, cardiac plasticity, cellular interactions, and genetic cardiomyopathies. They exclusively enable such investigations in human adult myocardium. However, the model presents limitations due to the low availability and pathologic state of human myocardial samples, and to the artificial conditions of tissue culture. The vision to meet these challenges includes strict definition of suitable study protocols, highly specific interventions, and high content analyses. Perspectively, a standardized experimental and analytical workflow needs to be established in order to develop the full potential of the cardiac slice culture in between cellular models and in vivo experiments.

Bio: Dr. Zanou is an M.D., Ph.D., and Senior Lecturer - Group Leader at the University of Lausanne. She received her medical degree in Benin in 2006 and then completed master's and Ph.D training in biomedical sciences at the Catholic University of Louvain in Belgium, earning her Ph.D. in 2012. During her Ph.D, Dr Zanou's research focused on the role of plasma membrane calcium channels in skeletal muscle development and function, as well as in the pathophysiology of Duchenne muscular dystrophy. In 2013, she received a research associate fellowship from the Belgian National Fund for Scientific Research to continue her research on the activation mechanisms of those channels in normal and pathological cells. In 2015, her work received an award from the Académie Royale de Médecine de Belgique. She then moved to Switzerland to broaden her international experience. In Lausanne, Dr Zanou’s research focused on intracellular calcium channels, especially the role of the ryanodine receptor type 1 (RyR1) channels in muscle health and disease. She developed the Institute of Sport Sciences' first molecular laboratory at the University of Lausanne, enabling her to conduct translational research on muscle adaptations to exercise and disease and the role of intracellular calcium channels including the RyR1. She also completed research internships at the University of Barcelona in Spain (2017) and at Columbia University in the United States (2017 and 2018). Her success is reflected in her numerous high-impact publications and robust collaborations forged locally in Lausanne (UNIL, EPFL, Nestlé Research, and CHUV) and abroad. She received several competitive grants (Swiss National Science Foundation grant, UNIL-CHUV Interdisciplinary grant, Swiss Foundation for Research on Muscle Diseases grant…) to support her different research projects.

Talk title: The ryanodine receptor at the hub of skeletal muscle plasticity to exercise and disease

Abstract: The ryanodine receptor type 1 (RyR1) is the primary intracellular calcium release channel in skeletal muscle cells. It is located at the endoplasmic/sarcoplasmic reticulum (ER/SR) and is involved in excitation-contraction coupling (ECC). RyR1 is stabilized by a protein called calstabin1 (calcium channel stabilizing binding protein 1), which is encoded by FKBP12. RyR1 function can be modulated by post-translational modifications, such as oxidation, phosphorylation, or nitrosylation, which lead to calstabin1 dissociation and leaky RyR1. Alternatively, mutations can alter RyR1 configuration or expression. Prolonged leaky RyR1 has been shown to play a detrimental role in several diseases.Using a translational approach that combined experiments in human and mouse models, as well as in vitro models of simulated exercise, we showed that a single session of sprint interval training (SIT) triggers acute Ca²⁺ leak through RyR1, whereas moderate-intensity continuous training (MICT) does not. The mitochondria take up this Ca²⁺ to dephosphorylate and activate pyruvate dehydrogenase (PDH), thus enhancing NADH-linked mitochondrial bioenergetics.

Bio: David Brückner is an Assistant Professor of Theoretical Biophysics at the Biozentrum and Department of Physics of the University of Basel, Switzerland. His research focusses on theoretical physics approaches to uncover how interactions of cells and molecules control the behavior of multicellular systems. Previously, he was Postdoc at the Institute of Science and Technology Austria and obtained his PhD from the Ludwig Maximilian University in Munich. He has been awarded with the Gustav-Hertz-Prize of the German Physical Society, and received an ERC Starting Grant.

Talk title: Information flow in self-organized developmental systems

Abstract: Embryonic development relies on multi-cellular systems self-organizing into precise spatial patterns of cell fates. An inevitable obstacle is intrinsic noise at the single-cell level, which constrains the information available to cells for fate decisions. This information is often considered to be encoded in extracellular morphogen concentrations, but cells respond to a much broader set of inputs, including dynamical and combinatorial signaling as well as mechanosensitive pathways that sense tissue mechanics. Yet we lack principled frameworks to quantify and predict how cells obtain sufficient information to reliably differentiate into the right fate at the right time and place. I will discuss how combining biochemical and mechanical models of patterning and morphogenesis with information theory provides a mathematical language for analyzing biological self-organization across diverse systems. First, I will demonstrate how the coupling between mechanosensitive YAP1 signaling and lateral inhibition governs diverse epithelial organoids, from intestinal to mammary. We develop a unifying model for these systems and analyze it using information theory. Second, I will discuss how richer inputs, from mechanical gradients to combinatorial signaling, can be incorporated into this framework. This opens an avenue toward unifying the zoo of chemical and mechanical signaling processes that orchestrate embryonic development.

Bio: Amy Gladfelter is a quantitative cell biologist interested in fundamental mechanisms of cell organization. She is currently a Distinguished Duke Health Science and Technology Professor in the Cell Biology and Biomedical Engineering Departments at Duke University. Previously she was Professor of Biology and Associate chair at the University of North Carolina at Chapel Hill from 2016- 2023. She remains a longstanding fellow of the Marine Biological Laboratory in Woods Hole, MA and is currently the course director of the Physiology Course. In her research program, she uses microscopy, biophysical and genetic approaches to study syncytial cells and how these large cells spatially organize the cytoplasm via biomolecular condensates and sense their shape. 
She has been honored with the 2014 Graduate Mentoring Award from Dartmouth, the 2015 Mid-Career Award for Excellence in Research from the American Society of Cell Biology, the 2020 Graduate school mentoring award from UNC and was a Howard Hughes Medical Institute Faculty Scholar. She is an elected fellow of AAAS, the America Academy of Microbiology and the American Academy for Arts and Sciences and member of the National Academy of Sciences. 

Talk title: Cellular computing using condensates 

Abstract: Syncytia are found throughout the biosphere from free-living fungi to the human placenta and malignant tumors. These cells contain many nuclei in a shared cytoplasm raising the possibility of genome cooperation and competition even within a shared cytoplasm. Work in our lab focuses on understanding the emergent functions that arise from having multiple genomes in the same cell in both filamentous fungi and in the human placenta. One area of work is focused on how the cytoplasm is structured to support different nuclear identities using condensed assemblies of RNA and proteins. Biomolecular condensates are vessels to spatially and temporally control biochemistry in cells for a variety of processes. Despite their ubiquitous roles in the entire lifecycle of RNA, how RNA impacts the composition, properties and functions of condensates remains poorly understood. The chemical properties and sequence of RNAs are generally considered in light of housing or regulating the genetic code. However, most amino acids are encoded by multiple codons, making the genetic code degenerate. Synonymous mutations in RNA sequences affect protein translation and folding, but their impact on RNA itself is often neglected. We developed a genetic algorithm that introduces synonymous mutations to control the conformational heterogeneity of structures sampled by an mRNA. The behavior of the designed mRNAs reveals physical information layered in the genetic code. We find that mRNA conformational heterogeneity impacts the physical properties and functional outputs of RNA-protein complexes and biomolecular condensates. The role of structure and disorder of proteins in biomolecular condensates is well appreciated, but we find that RNA conformational heterogeneity is a major contributor to condensate properties. This feature of RNA enables both evolution and engineers to build cellular structures with specific material and responsive properties. This talk will examine how syncytial cell organization leads to distinct kinds of cell functions and how RNA in condensates is used to spatially pattern functions in these giant cells.