The EMBO Meeting

The EMBO Meeting 2012





Monday, 18 Nov 2013




The Francis Crick Institute & Rockefeller University

Saturday, 22 September, 17:45-18:30, Apollon Auditorium

Controlling the cell cycle -

Both S-phase and mitosis are common to all cell cycles and both are necessary for the two newly divided cells to receive a full complement of genes.  In fission yeast the onset of S-phase and mitosis can be controlled by a single cyclin dependent kinase (CDK) with different levels of CDK activity bringing about progression through the cell cycle in an orderly fashion.  A low CDK activity is sufficient to bring about S-phase whilst a high activity blocks a further S-phase and is needed for onset of mitosis.  A G2 cell can be programmed to undergo either S-phase or mitosis simply by modifying CDK activity indicating there is no inherent direction in the cell cycle.  Activation of CDK activity is determined by growth rate and cell size, with cell size determined in part by a gradient mechanism.  A genomic wide screen for small sized mutants has identified new genes that act in previously unidentified pathways to regulate CDK activity at mitotic onset.

Biography -

Paul Nurse is a geneticist and cell biologist who has worked on how the eukaryotic cell cycle is controlled and how cell shape and cell dimensions are determined.  His major work has been on the cyclin dependent protein kinases and how they regulate cell reproduction.  He is President of the Royal Society and Director of the Francis Crick Institute in London and has served as Chief Executive of Cancer Research UK and President of Rockefeller University.  He shared the 2001 Nobel Prize in Physiology or Medicine and has received the Albert Lasker Award and the Royal Society's Royal and Copley Medals.  He was knighted in 1999 and received the Legion d'honneur in 2003.

Max Planck Institute for Biology of Ageing & University College London

Monday, 24 September, 09:00-9:45, Apollon Auditorium

Nutrient-sensing pathways and ageing -

Research into ageing has been rejuvenated by the discovery that mutations in single genes can increase healthy lifespan in laboratory model organisms. The nutrient-sensing insulin/insulin-like growth factor/TOR signalling network has thus been found to have a role in ageing that is conserved from yeast to mammals, possibly including humans. Extension of lifespan is accompanied by an increase in health and function at later ages, and manipulation of this signalling network can also reduce the pathology associated with genetic models of human ageing-related diseases. This talk will discuss the mechanisms at work and their potential relevance to humans.

Biography -

Professor Linda Partridge works on the biology of ageing. Her research is directed to understanding both how the rate of ageing evolves in nature and the mechanisms by which healthy lifespan can be extended in laboratory model organisms. Her work has focussed in particular on the role of nutrient- sensing pathways, such as the insulin/insulin-like growth factor signalling pathway, and on dietary restriction. Her current work is directed to developing pharmacological treatments that ameliorate the human ageing process to produce a broad-spectrum improvement in health during ageing.
She is the recipient of numerous awards, including giving the Royal Society Croonian Lecture in 2009 and a DBE for services to science. She is a Fellow of the Royal Society, the Academy of Medical Sciences, the European Academy of Sciences and the American Academy of Arts and Sciences. She is the Director of the UCL Institute of Healthy Ageing, as well as founding director of the new Max Planck Institute for Biology of Ageing in Cologne.

Nuffield Department of Clinical Medicine, University of Oxford

Louis-Jeantet Prize Lectures
Monday, 24 September, 09:45-10:15, Apollon Auditorium

Gut reactions: Immune pathways in the intestine in health and disease -

The gastrointestinal (GI) tract is home to a large number and vast array of bacteria that play an important role in nutrition, immune system development and host defense. In inflammatory bowel disease (IBD) there is a breakdown in this mutualistic relationship resulting in aberrant inflammatory responses to intestinal bacteria. Studies in model systems indicate that intestinal homeostasis is an active process involving a delicate balance between effector and immune suppressive pathways. The cytokine IL-23 plays a pivotal role in orchestrating intestinal inflammation and several genes in the IL-23/Th17 pathway confer risk to IBD. We have recently shown that IL-23 acts directly on T cells to promote pathological Th17 type responses at the expense of immune suppressive regulatory T cells. In addition IL-23 drives a novel population of innate lymphoid cells (ILC) that mediate colitis through the production of Th17 associated cytokines. Like Th17 cells, IL-23 driven ILC are dependent on the transcription factor RORγt indicating striking functional parallels between innate and adaptive lymphoid populations in the gut. In this presentation I will review our recent data that highlight the multiple activities of IL-23 that mediate tissue inflammatory responses and in some cases tumourigenesis.

Biography -

Fiona Powrie studied biochemistry at the University of Bath before a PhD in immunology in Don Masons lab in Oxford. Following postdoctoral studies in the US with Dr Robert Coffman, she returned to Oxford in 1996 to establish her own lab as a Wellcome Trust Senior Research Fellow. In 2009 she was appointed as the inaugural Sidney Truelove Professor of Gastroenterology within the Nuffield Department of Clinical Medicine in Oxford.

Fiona's work focuses on the role of immune pathways in the intestine in health and how these go awry in inflammatory bowel disease. She has identified a functionally specialised population of regulatory T cells (Treg) that play a key role in controlling the immune response in the intestine, preventing deleterious inflammatory responses to beneficial intestinal bacteria. She demonstrated that deficiencies in Treg number or function can result in chronic intestinal inflammation driven by the inflammatory cytokine IL-23. Her analysis of IL-23 functions in the intestine showed it acts directly on T cells to promote pathological Th17 type responses at the expense of immune suppressive regulatory T cells. In addition IL-23 drives a novel population of innate lymphoid cells (ILC) that mediate colitis through the production of Th17 associated cytokines. These results highlight the multiple activities of IL-23 that mediate tissue inflammatory responses. Together these results show that intestinal homeostasis is a delicate balance between effector T cells which drive inflammatory processes and regulatory T cells which can suppress them opening up new avenues for treatment of chronic inflammatory diseases. Fiona Powrie is a Fellow of the Royal Society and received the European Federation of Immunological Societies Ita Askonas Award in 2009 for her work on intestinal immune regulation.

Video -

Max Planck Institute of Biochemistry

Louis-Jeantet Prize Lectures
Monday, 24 September, 10:15-10:45, Apollon Auditorium

Near comprehensive proteome characterization and its applications in cell biology and cancer research -

The promise of proteomics as a component of systems wide investigation in biology has been obvious for a long time. However, it has only been in the last few years that mass spectrometry has successfully met the technological challenges associated with identifying and quantifying thousands of proteins in a relatively short time. Here I describe breakthroughs that now allow comprehensive quantification of the yeast model proteome in just a few hours. Mammalian proteomes can be mapped to a depth of more than 10,000 different species, enabling a first look at the features of the entire protein make-up of a specific cell type. We have already applied this technology to the problem of classification of cancer patients into subtypes. There have been corresponding advances in the ability of mass spectrometry to characterize thousands of post-translational modification sites in single projects and to efficiently determine protein interaction partners. A key challenge is now to assign functions to this bewildering universe of proteomic diversity. In conclusion, high resolution and quantitative mass spectrometry is now beginning to characterize the functional end point of gene expression – the proteome – in unprecedented depth, opening an entirely new view on cellular complexity.

Biography -

Matthias Mann studied physics and mathematics at Gottingen University and obtained his Ph.D. in chemical engineering at Yale University. Here he was decisively involved in the development of electrospray ionization, which has become a key technology of the life sciences. As a post-doctoral fellow and later as a professor for bioinformatics at the University of Southern Denmark in Odense, he developed, amongst others techniques, the first bioinformatic search algorithms for peptide fragmentation data and SILAC a new method of quantitative proteomics and a breakthrough in the mapping of protein interactions. Since 2005 Matthias Mann is director at the Max-Planck institute of biochemistry and since 2009 also the department head of proteomics at the Novo Nordisk Foundation Center for protein research in Copenhagen.

Dr. Mann has authored and co-authored more than 460 publications with a total citation count of more than 70,000, making him one of the most highly cited researchers worldwide according to the Institute for Scientific Information. He has been elected member of EMBO as well as the Royal Danish Academy of Arts and Sciences and also to a visiting professorship at Harvard Medical School. He has received two honorary degrees from Utrecht University and the University of Dundee, respectively.

Video -

The EMBO Meeting
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