Speakers

Felix RANDOW
MRC Laboratory of Molecular Biology, Cambridge, UK
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Ubiquitylation of non-protein substrates: Mechanisms and consequences
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.
Astrid Katharina Maria STUBBUSCH
Monash University, Clayton, Australia
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Prix Schläfli Award Ceremony and Lecture
Bio: Dr. Astrid Stubbusch is a microbial systems ecologist who joined Monash University in October 2024. Her research explores microbial processes that drive ecosystem functions, crucial to human and planetary health. Astrid obtained a B.Sc. in Biological Sciences and a M.Sc. in Systems Biology from the University of Heidelberg (Germany), during which she spent time as an exchange student in Leicester (UK) and worked as research assistant in Cambridge (UK) and Singapore. She then conducted her PhD at ETH Zürich and Eawag (Swiss Federal Institute of Aquatic Science and Technology) in Switzerland. Here, she focused on nutrient acquisition strategies and trophic interactions of bacteria. To dive more into microbial metabolism and its significance for ecosystems, Astrid joined the Climate Microbiology group at Monash University as postdoctoral researcher. Here, she studied microbial hydrogen metabolism in the human gut in health and disease, and now, as an SNSF fellow, explores the role of metabolic versatility in microorganisms for ecosystem resistance to environmental changes.
Talk title: How Microorganisms Feed - and Why It Matters for Climate and Health
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Georg Erich WINTER
AITHYRA – Research Institute for Biomedical Artificial Intelligence
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Chemical Rewiring of Biological Circuits for Cancer Therapy
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.
Magdalena GÖTZ
Institute of Stem Cell Research, Helmholtz Zentrum München and Physiological Genomics, Biomedical Center, Ludwig Maximilian University of Munich
Novel mechanisms of neurogenesis and neural repair
Bio: Prof. Dr. Magdalena Götz studied Biology and did her PhD at the FMI in Tübingen on the mechanisms of how input connections to the cerebral cortex form during development and how specific neuronal subtypes are specified. She then moved to the National Institute for Medical Research to use retroviral vectors for clonal analysis and identified mechanisms delineating neighboring forebrain regions. Afterwards she started her own lab at the Max-Planck Institute for Neurobiology and made the breakthrough discovery that radial glial cells are neural stem cells. This inspired her to attempt turning also mature glial cells into neurons already in 2002 in vitro and in 2005 in vivo. In order to determine which glial cells best to convert to neurons after traumatic brain injury, she systematically examined the roles of distinct glial subtypes after traumatic brain injury when she was appointed Director of the Institute of Stem Cell Research at the Helmholtz Center Munich in 2004 and Chair of Physiological Genomics, now at the Biomedical Center of the Ludwig-Maximilians University in Martinsried Munich. Since then she identified key hurdles in the glia-to-neuron reprogramming reprogramming which led to high efficiency in vivo reactive glia-to-neuron conversion as well as human glia-to-neuron conversion in vitro. As one of the hurdles she identified was metabolic conversion, this led her to identify the new concept of organelle heterogeneity in different cell types – from mitochondria to even centrosomes. This is exciting because protein localization at a specific organelle can explain how mutation of ubiquitous proteins can cause an organ-specific disease when mutated. Thus, she combines deep cell biological analysis with fate conversion mechanisms aiming to repair.
Talk title: Novel mechanisms of neurogenesis and neural repair
Abstract: Organelles such as centrosomes, nucleoli or mitochondria perform well-known common functions in all cell types. However, we found a surprisingly large degree of differences in composition in the context of development, disease and direct reprogramming. For example, the centrosome of human neural stem cells differs by more than half of its proteome from the one in neurons (O’Neill et al., Science 2022). Such cell type-specific composition also explains why some ubiquitous proteins have organ-specific defects, when mutated in patients, as they are only at a specific organelle in specific cell types. I will explain this for the splicing protein PRPF6 that plays specific roles at the centrosome in neural stem cells which is relevant for the disease periventricular heterotopia. I will then turn to organellar heterogeneity in direct neuronal reprogramming and discuss the role of mitochondria heterogeneity in this process and how to overcome hurdles in this conversion process due to late change of the mitochondrial proteome to a neuronal identity. I will then talk briefly about nucleolar heterogeneity, before turning to the cytoskeleton in the nucleus. I will talk about the discovery of a large number of microtubule-associated proteins in the nucleus, and discuss how the nuclear role of one of them affects neural stem cell fate and causes disease when mutated in patients. Taken together, these data highlight the concept of multiplying protein function with different roles at different organelles or cell compartments with relevance in development, disease and repair.


Alex M. JAEGER
Moffitt Cancer Center
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Parallel Symposia Session I – From Proteome to Mechanism: In Vivo Insights into Cellular Biology
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.
Celia BERKERS
Utrecht University, Faculty of Veterinary Medicine
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Parallel Symposia Session I – From Proteome to Mechanism: In Vivo Insights into Cellular Biology
Bio: Celia Berkers is Full Professor of Metabolomics and Vice Dean of Research at Utrecht University’s Faculty of Veterinary Medicine. Research in her team focusses on understanding metabolic re-wiring in the tumour microenvironment. Her aim is to leverage the power of metabolomics to identify novel metabolic targets with potential for exploitation by novel therapies. She is an expert in isotope tracing metabolomics (also known as fluxomics) and cross-omics data analysis, which she applies on complex in vitro model systems such as organoids and co-culture models, that her team develops for this purpose. Celia Berkers studied chemistry at Utrecht University, where she graduated with honours in 2003. She started her PhD at the Harvard Medical School in Boston, continued her research at the Netherlands Cancer Institute in Amsterdam, and received her PhD degree with honors in 2010. She then moved to the Beatson Institute for Cancer Research in Glasgow, where she did a post-doc in the laboratory of Prof. Karen Vousden. In 2013, Dr Berkers joined the Biomolecular Mass Spectrometry and Proteomics Department at Utrecht University as an independent group leader. She was appointed full professor at the Faculties of Veterinary Medicine and Science in 2018. She was awarded with the Antoni van Leeuwenhoek Prize, the Heineken Young Scientists Award for Biochemistry and Biophysics, and was elected member of the Young Academy of the Royal Society. She is an Associate Editor for Cancer & Metabolism and an Editorial Board Member for Molecular Omics.
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Carolin LERCHENMÜLLER
Chair for Gender Medicine, University of Zürich and University Hospital Zürich
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Parallel Symposia Session I – Gender Health in Biomedical Research: Advancing Precision Therapeutics
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.
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Martin PACESA
University of Zurich
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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.


Ludovic MURE
Inselspital and University of Bern
Parallel Symposia Session II – Neuronal Circuit Vulnerability Underlying Neurodegeneration
Bio: Ludovic Mure completed his MS in Neuroscience at the University of Lyon, France, and his Ph.D. in the laboratory of Dr. Howard Cooper at the SRBI (INSERM) where he investigated the recently discovered melanopsin, a photopigment expressed by a subset of retinal ganglion cells and rendering them intrinsically photosensitive (ipRGCs). He pursued in this very exciting and fast-moving field by joining the lab of Satchin Panda (The Salk Institute, San Diego, US). As a postdoc, he explored the non-visual responses to light in particular the relationship between the circadian clock and light. He found that melanopsin unique properties relied on both its structure and its binding partners. Then, in an exceptional collaborative project between INSERM, the Salk Institute, and the Institute of Primate Research (Kenya), he established the first rhythmic transcriptome of a diurnal primate. This study unveiled the unique features of primate rhythmic gene expression and unveiled the importance of the natural light-dark cycles for gene expression. Recently, together with F. Vinberg (U. of Utah) and A. Hanneken (Scripps Institute), he developed a human retina preparation that preserves the function of each photoreceptive system for several hours after the death of the donors and was able to record for the first time human ipRGCs and to characterize their responses, sensitivity, spectra, and functional diversity. Finally, in 2021, to transition to an independent research position in Europe, he joined the labs of Profs. Kleinlogel (U. of Bern) and Adamantidis (Department for Neurology, Inselspital) as a Velux Stiftung fellow to dissect ipRGCs circuits in the retina and the brain, in health and disease. In 2023, he joined the Department of Ophthalmology of the Inselspital in Bern (Switzerland) as a group leader.
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Sabine LIEBSCHER
Institute of Systems Neuroscience, Medical University Innsbruck, Innsbruck, Austria
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Parallel Symposia Session II – Neuronal Circuit Vulnerability Underlying Neurodegeneration
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.


Lucas PAOLI
School of Life Sciences, EPFL
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Parallel Symposia Session II – Self-assembly Across Scales: from Cells to Ecosystems
Bio: Lucas Paoli is an ELISIR group leader at the School of Life Sciences of EPFL. His lab uses environmental genomics to study the diversity and ecology of microbiomes. Through large-scale, data-driven approaches, they aim to understand how ecology shapes microbial immunity across environments. Prior to that, Lucas was an EMBO Postdoctoral Fellow with Dr. Aude Bernheim at Institut Pasteur in Paris, where he worked on microbial immunity. He holds a MSc in Ecology and Evolution, a MPhil in Environmental Policy, and conducted his PhD at ETH Zürich under the guidance of Prof. Dr. Shinichi Sunagawa. His doctoral work helped decipher the genomic blueprint and biosynthetic potential of the global ocean microbiome.
Talk title: Ecological diversity of microbial immunity
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Andreas DENDORFER
Ludwig-Maximilians-University München, LMU Hospital, Walter-Brendel-Centre of Experimental medicine
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Bio: Born 1961 in Schwandorf, Germany. Married, 2 children. Studies of Electrical Engineering and Medicine, 1989 licence as physician. Post-Doc at Med. Univ. Lübeck in Pharmacology and Toxicology. Prof. and group leader at the WBC, LMU-München.
Talk title: Biomimetic culture of human myocardium: A versatile in vitro model
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Olivier GUENAT
University of Bern, ARTORG Center
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Bio: Olivier T. Guenat is Professor in Biomedical Engineering at the University of Bern in Switzerland and Head of the Organs-on-Chip Technologies Group at the ARTORG Center. He is associated with the Pulmonary Medicine and the Thoracic Surgery Divisions of the University Hospital of Bern. His research focuses on the development of organs-on-chip, in particular lung-on-chip models that mimic the healthy and diseased in-vivo cellular microenvironments of the lung parenchyma. Prior to his position at the University of Bern, he worked at the Swiss Centre for Electronics and Microelectronics (CSEM), was an assistant professor at Ecole Polytechnique de Montréal (QC, Canada), and did postdoctoral work at Harvard Medical School in Boston and at the University of Neuchâtel in Switzerland. He is the founder of AlveoliX and co-founder of Vitronco, two biotech start-ups that spun out of his lab.
Talk title: From capillaries to arterioles on chip: multicellular vascular platforms with functional read-outs
Abstract: We present a suite of multicellular vascular platforms capturing distinct aspects of human microcirculation. Self‑assembled microvessels formed by vasculogenesis generate perfusable capillary‑like networks with physiological endothelial barrier and transport functions. A second platform applies cyclic mechanical stress to these vessels, revealing strain‑dependent changes in permeability, alignment, and gene expression relevant to cardio‑pulmonary environments. Finally, preliminary results of an arteriole‑on‑chip with circumferentially aligned smooth muscle cells enabling controlled vasoactive responses will be presented. Together, these complementary systems provide functional vascular readouts across multiple scales of the human microvasculature.


Ivan MARTIN
Department of Biomedicine, University of Basel
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Bio: Prof. Dr. Ivan Martin studied Biomedical Engineering at the University of Genova where he obtained his PhD in 1996. Between 1996 and 1999 he was a postdoctoral associate at Harvard/MIT. He joined the Department of Biomedicine (DBM) at the University Hospital of Basel in 1999 as leader of the Tissue Engineering Research Group, in close coordination with the surgical units. In 2007 he was appointed Professor for Tissue Engineering at the University of Basel and from 2021 he is Director of the DBM. From 2004 to 2009 he was the first president of the European section of the Tissue Engineering Regenerative Medicine International Society (TERMIS), and later Chair of the TERMIS Strategic Alliance Committee. In 2018 he was elected as member of the Swiss Academy of Medical Sciences. He has been Chair of the ‘Mesenchymal stromal cell committee’ and is currently member of the ‘Orthopaedics and Musculoskeletal Committee’ of the International Society for Cellular and Gene Therapy (ISCT). He is part of the editorial boards of 6 international journals. His group includes scientists from the biological, engineering and clinical fields, dedicated to develop solid scientific basis for innovative translational strategies in regenerative surgery. In this field he is author of more than 300 peer-reviewed papers on international journals (H-index of 109), inventor on 12 patent applications and recipient of grants from the main funding bodies, including the prestigious European Research Council. The developed science and technology have been translated into different clinical trials for cell-based cartilage and bone repair, and into the founding of a spin-out company for the commercialization of bioreactors for 3D cell culture (Cellec Biotek AG).
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Elda BAUDA
University of Geneva
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Bio: My research aims to investigate the cellular envelope of unicellular organisms such as bacteria and yeast and to understand how the constraints of unicellular life necessitate rapid and robust adaptation to environmental stress. Despite their importance as protective barriers and as dynamic regulatory platforms, the native architecture of cellular envelopes remains poorly understood. To address this, I use and further develop in situ structural cell biology approaches, especially cryo-FIB-ET, which has recently opened a new frontier in exploratory imaging. By integrating cryo-FIB-ET with molecular cloning and live fluorescence microscopy, my long-term goal is to establish a structural cell biology framework that links membrane architecture to cellular decision-making in bacteria and yeast.
Talk title: Thekosomes: a new cellular strategy for membrane tension control
Abstract: The plasma membrane (PM) is the primary interface through which cells sense and respond to environmental stress, making its homeostasis essential for survival. Over the years, PM invaginations in S. cerevisiae have been reported across diverse experimental settings and under different names, particularly in conditions of reduced membrane tension. However, these observations have remained fragmented, lacking a coherent interpretation. Here, we integrate these seemingly disparate findings by demonstrating that membrane invaginations arising under low PM tension define a single, previously unrecognized cellular compartment, which we term thekosomes. Using cryo-focused ion beam electron tomography (cryo-FIB-ET), we reveal that thekosomes are membrane-bound compartments spanning hundreds of nanometers. Their lumen, containing organelles and proteins, is enclosed from the cytoplasm by two membranes incorporating cell wall material. Their formation is rapid and relies only on biophysical property change of the membrane. We demonstrate the recruitment of key membrane-associated proteins, including TORC2, Slm1, and septins, to thekosome upon their formation. Under conditions of chronic disruption of PM homeostasis, thekosomes are constitutively present at the PM. We further reveal thekosomes in the distantly related S. pombe, underlying a conserved membrane stress response mechanism. Together, these findings reveal highly dynamic, organelle-containing compartments that couple membrane remodeling and lipid homeostasis to maintain cellular integrity under stress.


Amy GLADFELTER
Duke University, USA
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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.