Final Meeting Booklet
Update 20 January 2017: Please find the final Meeting Booklet here:
Download final Meeting Booklet
This booklet will be printed and handed out at the meeting to all participants.
Abstract Booklet
Please find all abstracts below with the numbering for the poster session. The organizing committee takes no responsability for the way the authors and titles were listed by the poster presenters during registration.
Download final Abstract Booklet
Please note that for space reasons (and to save trees), the printed Meeting Booklet on-site (see above) will NOT contain the abstract texts, but only poster number/title/authors/affiliations and that the Abstract Booklet will NOT be printed.
| Thursday | 02.02.2017 |
| 08:00 – 09:00 | Registration, Welcome Coffee, Mounting of Posters |
| 09:00 – 09:10 | Welcome Address Jean Gruenberg (UNIGE, President of LS2) |
| 09:10 – 09:15 | "10 years SystemsX.ch: What did we do? What did we learn?" Daniel Vonder Mühll (Managing Director SystemsX.ch) |
| 09:15 – 10:00 | Plenary Lecture I The Pervasiveness of Host-Microbial Mutualism If we view mammals as host-microbial super-organisms, non-pathogenic microbes at body surfaces comprise 90% of the cellular load and 99% of the genetic diversity. Host and microbial metabolism are intimately integrated and the profound biological influences on almost every host organ system stem not only from signalling at mucosal surfaces and the penetration of a small proportion of live organisms into host tissues, but also the promiscuous circulation of microbial metabolic products. In this talk I shall discuss how these effects start in utero, even before the successive waves of endogenous microbial colonisation take place after birth. The functional consequences of host microbial mutualism are critical throughout the trajectory of life including shaping the innate and adaptive arms of the immune system and preparing host metabolism for the challenges of xenobiotic exposure. Despite this intimate arrangement of prokaryotic and eukaryotic metabolism, the two components are physically compartmentalised in health: I shall show how anatomic and immune firewalls set these boundaries. Hide text… |
| 10:00 – 10:30 | Coffee Break @ Lichthof, Industry Exhibition, Poster Viewing |
| 10:30 – 12:30 | Parallel Symposia I |
Virology Viruses, Microbes and Their Hosts
Session chairs: Urs Greber (UZH) and Stefan Kunz (UNIL)
Jason Mercer (University College London) Caroline Tapparel Vu (University of Geneva)
Emilio Yángüez (University of Zurich) Nikolaos Tsolakos (University of Zurich) Nikolas Friedrich (University of Zurich) Fanny Georgi (University of Zurich) | |
Swiss Personalized Health Network Personalized Medicine
Session chair: Torsten Schwede (UNIBAS & SIB Swiss Institute of Bioinformatics) Peter Meier-Abt (Past president Swiss Academy of Medical Sciences, Zurich, Chairman of the National Steering Board SPHN) Russ B. Altman (Stanford University) Cisca Wijmenga (University Medical Center Groningen) Linda Sundermann (ETH Zurich/Bielefeld University) Kathrin Oehl (University Hospital Zurich)
Sandra Goetze (ETH Zurich) Adithi Varadarajan (ETH Zurich) | |
Lemanic Animal Facility Network (RESAL) Alternative Animal Experimentation
Session Chairs: Fabienne Chabaud (UNIL/RESAL), Marcel Gyger (EPFL) Aaron Voigt (University Medical Centre , Jülich Aachen Research Alliance (JARA)) Martin Schwarzer (Institute of Functional Genomics of Lyon (IGFL)) Federico Miozzo (University of Geneva) Samuel Rommelaere (EPF Lausanne) Louise Lefrançois (University of Geneva) | |
Tomorrow's PIs: The Future of Swiss research
We're proud to have with us (selected from 72 applications!):
Abstract: Protein abundance is set by four rates: transcription, translation, mRNA decay and protein decay. A given protein abundance can be obtained from infinitely many combinations of these rates. This raises the question of whether the natural rates for each gene result from historical accidents, or are there rules that give certain combinations a selective advantage? We address this question using high-throughput measurements in diverse organisms to find that about half of the rate combinations do not exist: genes that combine high transcription with low translation are strongly depleted. We show that this depletion is due to a trade-off between precision and economy: high transcription decreases stochastic fluctuations but increases transcription costs. Our theory quantitatively explains which rate combinations are missing, and predicts the curvature of the fitness function for each gene. It can guide the design of synthetic gene circuits with optimal transcription and translation rates.
Abstract: The diversity of animal behaviours we observe today is a product of evolution, yet we know little about how random mutations, drift and natural selection shape nervous systems. Harnessing the rich ecological diversity found within the Drosophila species complex, my current and future research focuses on the evolution of olfactory sensory systems because they provide a great entry point into these questions. During my postdoc I studied the evolution of the olfactory acid sensing system of D. sechellia, a species with evolved olfactory behaviours. D. sechellia is attracted towards its novel host, Morinda fruit, which is toxic to other Drosophila species and contains high quantities of long chain carboxylic acids, prominently hexanoic acid. We found that a single amino acid change in a receptor (IR75b) is sufficient to confer novel hexanoic acid sensitivity, and further studied how the downstream attraction-mediated circuit evolved. In addition, we found that another receptor, presumed to be a pseudogene in D. sechellia, is unexpectedly functional and has evolved sensitivity towards longer chain carboxylic acids through the same mechanism as IR75b. Importantly, we extended this discovery to other species, showing that olfactory receptor pseudogenes - classically thought of as non-functional relics of once useful receptors – are still functional thanks to a premature stop codon read-through process that is active in neurons, but not in other cell types, including glia. For my future research programme, I propose to investigate the evolution of neural circuits by using different Drosophila species, as well as tsetse flies (insect vectors of African Sleeping Sickness). We will combine neuroscience, genetics and functional studies of olfactory receptors to gain a broad understanding of how evolution sculpts nervous systems, and how this knowledge may increase our ability to cure diseases and control insect pest species.
Abstract: Neurogenesis involves a complex interplay between morphogens and transcription factors to initiate genetic programs that promote neuronal differentiation and subtype specification. However, at the same time unwanted genetic programs have to be shut down including signaling pathways such as Notch that repress proneural transcription factors and neuronal differentiation. This raised the intriguing question how differentiating neurons can escape this inhibition and turn of unwanted transcription programs to enable neuronal commitment? Studying the induced conversion of fibroblasts to neurons we found that the neuronal reprogramming factor Myt1l accessed most of its physiologic targets in fibroblasts and acted predominantly as repressor through recruitment of the Sin3/HDAC complex to silence many non-neuronal programs including the fibroblast-specific transcriptome. One of the repressed pathways is Notch by silencing of several members, explaining how newborn neurons can escape Notch activation during normal development. Strikingly, depletion of Myt1l in differentiated primary neurons induced loss of neuronal function and gene expression, suggesting that continuous repression of unwanted programs safeguards neuronal cell fate. Based on our findings, we propose that active and sequence-specific repression mechanisms exist to generally suppress many unrelated lineage programs, enabling cell fate choice and stability during development and disease.
Abstract: Phagocytosis, the process by which immune cells ingest and degrade or process foreign material to produce antigens, is paramount for both innate and adaptive immunity. It also represents an enormous intracellular signalling and trafficking challenge for the cell as a new organelle is formed. Various pathogens subvert signals generated during phagocytosis in order to elude the immune system. Identifying the molecules that generate and decode these signals may thus provide novel targets for therapeutic interventions, but can also provide unprecedented insights into the general and specialized functioning of cells. Using the latest high-resolution imaging techniques, I have studied how Ca2+, pH and ROS are regulated during phagocytosis and identified novel determinants of phagosomal pH such as the Hv1 channel. I also discovered that the ER-resident proteins STIM1 and junctate promote the formation of membrane contact sites (MCS) between the ER and phagosome, highlighting a mechanism by which the cell can spatially restrict signalling events to a discrete location. I have shown that localized Ca2+ signals and MCS correlate with phagocytic efficiency in neutrophils, and are critical for the cross-presentation of ingested antigens by dendritic cells, a process central to adaptive immunity against intracellular pathogens and cancer cells. My current efforts are aimed at identifying new MCS components through a proteomic screen, and to define whether the ERGIC SNARE protein Sec22b is involved in MCS formation. In the future, I propose to further investigate MCS formation and function in intracellular trafficking and signalling in the context of immune cells. As MCS also form between the ER and mitochondria, Golgi, endosomes and lysosomes, this line of research may lend insight into the biology of other MCS not only in immune cells but in other cell types.
Abstract: My long-term research goals are to understand how chromatin integrates information for cellular decision making and to translate this knowledge into strategies for treating human disease. Progress in chromatin research is limited in the identification and reliable quantification of relevant components of this molecular network. To mitigate this technical obstacle, we developed quantitative proteomic methods for measuring histone modifications and sequence isoforms with improved comprehensiveness, sensitivity, and accuracy. By comparing histone signatures during physiological transitions, such as during aging and cancer progression, we derive general design principles and identify specific regulators of chromatin structure and function. As a proof-of-concept, we applied the chromatin systems biology platform to two aging models. Studying fly aging, we uncovered the acetyltransferase dHBO1, whose ablation prolongs life and health span in D. melanogaster, validating our strategy. By comparing trajectories of histone signatures during muscle stem cell activation between young and aged mice, we observed a global re-organization of the epigenome and identified and validated ten murine genes that regulate stem cell aging. Integrating histone signatures with complementary datasets, we have started to define common principles that underlie the chromatin basis of aging, which emerges as an important factor contributing to many diseases including cancer. In future research, I aim to develop quantitative models for chromatin-mediated regulation of cellular communication and memory. I will test these models by investigating how the cellular (disease) context affects a drug’s potential to modulate chromatin networks that contribute to disease progression or prevention. Because cancer is a multifactorial disease, we will refine the models by accounting for chromatin signatures caused by age, lifestyle and environmental factors. Finally, we will verify our models by predicting and validating solitary and combinatorial (epigenetic) drugs with the goal of delaying cancer progression.
Abstract: Personalized medicine entails a vision where biomedical data is used to generate static individual risk profiles (through personalized genomes) and to track patients' health longitudinally using dynamic molecular and physiological data. Mass spectrometry (MS) plays a critical role in providing quantitative molecular profiles of patients over time, allowing early detection of disease and monitoring of interventions. While MS-based proteomics and metabolomics technologies capture crucial dynamic information on the molecular level, they currently lag behind sequencing-based technologies due to lack of throughput, reproducibility and coverage. Recently, SWATH-MS has emerged as a technology that allows researchers to perform accurate targeted proteomics measurements in high throughput. Targeted data analysis implemented in the OpenSWATH software allows quantification of thousands of proteins in human samples, while the reference-free, graph-based targeted alignment software TRIC enables consistent quantification of analytes across hundreds of samples. We have successfully applied SWATH-MS to study the dynamic interaction network of 14-3-3 beta, to classify cancer tissue samples and to investigate the blood plasma proteome variation in twins. More recently, we used MS to profile 23 prediabetic adults during a weight gain perturbation where our data provides novel insights into the dynamics of diabetes progression, combining genomics, microbiome, transcriptomics, proteomics and metabolomics data. These examples highlight how MS-based methods employed in a personalized multiomics context can capture the dynamics of complex diseases. I will discuss how further improvements in computational methods could allow SWATH-MS to be applied for profiling of post-translational modifications, protein isoforms and metabolites. Also, I will discuss the need for new analysis tools that can fully exploit longitudinal personal omics data and combine static risk analysis (from genomics data) with dynamic molecular data for the study complex disease risk and progression. | |
| 12:30 – 13:30 | Lunch break @ Lichthof, Industry Exhibition, Poster Viewing |
| 12:30 – 13:30 | LS2 Section Molecular&Cellular Biosciences Board Meeting |
| 13:30 – 15:30 | Parallel Symposia II |
LS2 Section Physiology Nutrient Metabolism and Disease
Session chairs: François Verrey (UZH) and Zhihong Yang (UNIFR) Yibin Wang (University of California (UCLA)) Alaa S. Awad (Pennsylvania State University) Nourdine Faresse (NCCR Kidney.CH Junior Grant Awardee, UZH) Erika Tarasco (University of Zurich)
FLASH TALKS (5 min) Xu Wang (EPF Lausanne) Fabrizio Vacca (University of Geneva) Ji Huang (University of Fribourg) Ilaria Orlando (University of Zurich) | |
Swiss Plant Science Web (SPSW) Plant Genomics
Session chair: Kentaro Shimizu (UZH) This session is supported by the URPP Evolution in Action Hiroyuki Tsuji (Yokohama City University) Nils Stein (Leibniz Institute of Plant Genetics, Gatersleben) Thomas Wicker (URPP Evolution in Action, University of Zurich) Rie Shimizu-Inatsugi (URPP Evolution in Action, University of Zurich)
FLASH TALKS (5 min) Weihong Qi (ETH Zurich) Matthew Barbour (University of Zurich) Kinga Rutowicz (University of Zurich) | |
LS2 Section Proteomics Structural and Functional Proteomics
Session chair: Lydie Lane (Swiss Institute of Bioinformatics) Martin Beck (EMBL Heidelberg) Hui Zhang (Johns Hopkins University) Loïc Dayon (Nestlé Institute of Health Sciences) Yansheng Liu (ETH Zurich)
FLASH TALKS (5 min) Vera Bilan (University of Zurich) Yuehan Feng (ETH Zurich) Xavier Hernandez-Alias (ETH Zurich) Maik Müller (ETH Zurich) | |
| 15:30 – 16:00 | Coffee Break @ Lichthof, Industry Exhibition, Poster Viewing |
| 16:00 – 16:30 | Friedrich-Miescher-Award Lecture Petr Cejka (Institute for Research in Biomedicine (IRB), Bellinzona) To commemorate the 100-year anniversary of the discovery of nucleic acids the Molecular and Cellular Biosciences section of Life Sciences Switzerland (formerly Swiss Society for Molecular and Cellular Biosciences/Swiss Society for Biochemistry) has created the Friedrich-Miescher-Award. The prize is intended to honour young biochemists and is donated by the Friedrich-Miescher-Institute of the Novartis Research Foundation in Basel. |
| 16:30 – 17:20 | Plenary Lecture II Stem Cells in the Adult Brain: Identity and Niches http://www.biozentrum.unibas.ch/de/forschung/gruppen-plattformen/overview/unit/doetsch/ Hide text… |
| 17:20 – 17:30 | Crowdfunding Your Research: Test Ideas, Spread Knowledge
Speakers: Luc Henry and Mirko Bischofberger |
| 17:30 – 19:30 | Poster Session & Musical Apéro @ Lichthof Special poster session in the Industry Exhibition Area accompanied by an Apéro and the Soul Trio "Soul Potion". Poster Session A: odd numbers/sector A/B (17.30-18.30) Poster Session B: even numbers/sectors C/D (18.30-19.30) |
| 18:00 – 19:30 | LS2 Delegates Assembly |
| Friday | 03.02.2017 |
| 09:10 – 10:00 | The EMBO Keynote Lecture The Busy Life of Nascent Chains: Mechanisms of Folding and Assembly of Newly Synthesized Proteins The process of translation integrates multiple tightly regulated mechanisms ensuring that nascent polypeptide chains are correctly processed, targeted and folded into functional proteins. These include co-translationally acting factors, some of which associate transiently to ribosomes, which mediate spatially and temporally orchestrated protein maturation steps, and mRNA-encoded local translation speed variations which appear to guide these processes. Pro- and eukaryotes share basic principles but differ with respect to major features including the nature of the involved factors, indicating substantial evolutionary diversification. We report the dissection of the flux of newly synthesized proteins through the system of co-translationally engaged factors in E. coli and S. cerevisiae using ribosome profiling technology. In E. coli, the SRP targets almost exclusively inner membrane proteins to the membrane, whereas the chaperone trigger factor (TF) associates primarily with cytosolic, periplasmic and outer membrane proteins, indicating nascent chains are triaged between SRP and TF pathways. The Hsp70 chaperone DnaK interacts in concerted action with TF, typically with longer nascent chains and and reflecting domain boundaries of the emerged nascent chains. We also find evidence that assembly of protein complexes initiates co-translationally once the domain interfaces of the interacting polypeptides are exposed. The organisation of the subunit-encoding genes in operons facilitates the assembly process. In S. cerevisiae the Hsp70 chaperone Ssb shows a different pattern of early nascent chain association as compared to its prokaryotic DnaK counterpart. Co-translational protein assembly is also observed, although operon organisation of genes is less common, pointing to differences in the principles governing protein assembly in pro- and eukaryotes. Hide text… |
| 10:00 – 10:05 | PACE PostDoc Association |
| 10:05 – 10:30 | Coffee Break @ Lichthof, Industry Exhibition, Poster Viewing |
| 10:30 – 12:30 | Parallel Symposia III |
LS2 Section Molecular and Cellular Biosciences From Cell Biology to Single Molecules
Session chair: Monica Gotta (UNIGE) Lori Passmore (University of Cambridge) Buzz Baum (University College London) Michael Elser (Takara Bio Europe) Sine Yaganoglu (ETH Zurich)
FLASH TALKS (5 min) Eric Durandau (University of Lausanne) Qian Feng (ETH Zurich) Ali Yasin Sonay (BSSE-ETH Zurich) | |
Cellular Immunology Cellular Processes in Host Defense and Inflammation
Session Chair: Salomé Leibundgut (UZH) Venizelos Papayannopoulos (The Francis Crick Institute, London) Lynn Wong (UZH) Tobias Junt (Novartis Institutes for Biomedical Research, Basel) Pierre-Yves Mantel (University of Fribourg)
FLASH TALKS (5 min) Ana Teresa Lopez Jimenez (University of Geneva) Eva Guiducci (University of Zurich ) Jesus Francisco Glaus Garzon (University of Zurich) | |
Satellite Workshop Non-Academic Careers in the Life Sciences
Session chair: Ulrike Rieder (Philochem AG) Starting with a Start-up Careers in Pharma Scientific Management
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| 12:30 – 14:00 | Lunch break @ Lichthof, Industry Exhibition, Poster viewing |
| 14:00 – 16:00 | Parallel Symposia IV |
Experimental Pharmacology New Drugs for Pain, Sleep, and Memory? From Basic Mechanisms to Clinical Implications
Session Chair: Hans-Peter Landolt (UZH) Hanns Ulrich Zeilhofer (University of Zurich) William Wisden (Imperial College London) Dominique de Quervain (University of Basel) Karthik Balakrishnan (University of Zurich) Konstantinos Kompotis (University of Lausanne) Aymeric Monteillier (University of Geneva) | |
Anatomy, Histology and Embryology Cellular Scissors- New Perspectives on Proteases
Session Chair: Franziska Theilig (University of Fribourg) Thomas Reinheckel (University of Freiburg) Edith Hummler (University of Lausanne) Diego Lopez Leon (University of Fribourg) Alexey Larionov (University of Fribourg) | |
SCNAT Forum for Genetic Research Misuse of Biological Research: Do We Need to be Concerned?
Session Chair: Ursula Jenal (Jenal & Partners Biosafety Consulting, Rheinfelden) | |
Satellite Workshop Academic Careers in the Life Sciences
Session chair: Ulrike Rieder (Philochem AG) Young Academia From Industry back to Academia Established Academia
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| 16:00 – 16:30 | Coffee Break @ Lichthof, Industry Exhibition, Poster viewing |
| 16:30 – 17:15 | Award Session |
Lelio Orci Award
Markus Aebi (ETH Zurich) | |
Poster Awards | |
Tomorrow's PI Award | |
| 17:15 – 18:10 | Plenary Lecture III Hox Genes Regulation During Vertebrate Development and Evolution Unlike in invertebrates, vertebrate Hox gene clusters are found in multiple copies and are tightly packed and organized, with all transcripts encoded by the same DNA strand. This vertebrate genomic synapomorphy has been largely verified by recent genome sequencing efforts and an exception to this rule has not been found thus far. This evolutionary conundrum can be tentatively explained when considering recent work on the various regulatory strategies implemented by these genomic loci. By using recent data addressing these issues, I will try and propose a model for this surprising observation. Hide text… |
| 18:10 – 18:15 | Closing Remarks Jean Gruenberg (UNIGE, President of LS2) |