Keynote Lectures - speaker bios & abstracts Print E-mail

Denis Duboule

University of Geneva, CH
Denis Duboule studied biology at the University of Geneva, CH and then earned his doctorate of sciences in 1984 at the same institution. His career next led him to work at the University of Strasbourg, FR, then at the European Molecular Biology Laboratory (EMBL) in Heidelberg, DE, before he returned to the University of Geneva as a full Professor in 1992. In Geneva, he has directed the Department of Zoology and Animal Biology since 1997 and the Frontiers in Genetics NCCR since 2001.  He was awarded the Louis-Jeantet Prize for Medicine in 1998 and is a world-renowned specialist in developmental genetics. He was one of the first to take an interest in the Hox genes, revealing their essential role in limb formation and the basic mechanisms of how they work. His findings on this topic launched a line of research that has since become extraordinarily active, with important implications for understanding the evolution of species.

Tuesday 7 September 09:00 - 10:00 - The Auditorium

Title & synopsis
Hox genes & the specification of the body axis


During vertebrate development, Hox genes follow a time sequence in their transcriptional activation, which progresses in cis along their respective genomic clusters. While the importance of this ‘Hox clock’ to secure and coordinate body patterning has been recognized, the underlying mechanism are still elusive. We have designed and used genetic approaches to produce large allelic series in mice, including deletions, duplications and inversions at the HoxD locus, to try and understand the relationship between gene topography and transcriptional onset.


By using ChIP and Chromosome Configuration Capture on micro-dissected embryonic material, we show that successive Hox gene activation in the embryo is closely associated with both a directional transition in chromatin status, as judged by the dynamic replacement of repressive marks by transcription-competent modifications, and a spatial re-organisation of the locus, suggesting that the Hox clock may be regulated by an epigenetic mechanism, leading to the progressive accessibility of Hox clusters to the transcription machinery (open for business). I will discuss both the impact, in term of ontogenetic and phylogenetic constraint, of such a cis-acting regulatory system upon the stability of the animal body plan, and its potential to produce morphological flexibility via heterochronic modifications, as exemplified with some vertebrate species.

Elizabeth Blackburn

University of California, US

Elizabeth Blackburn is a leader in the area of telomere and telomerase research. She discovered the molecular nature of telomeres-the ends of eukaryotic chromosomes that serve as protective caps essential for preserving the genetic information - and discovered the enzyme telomerase, which replenishes telomeres. Blackburn is currently the Morris Herzstein Endowed Professor in Biology and Physiology in the Department of Biochemistry and Biophysics at University of California, San Francisco, where she is working with various cells including human cells, with the goal of understanding telomerase and telomere biology. She is also a Non-Resident Fellow of the Salk Institute. Throughout her career, Blackburn has been honored by her peers as the recipient of many prestigious awards, including The Albert Lasker Medical Research Award in Basic Medical Research (2006), and she was selected as the 2008 North American Laureate for L'Oreal-UNESCO For Women in Science. In 2007 she was named one of TIME Magazine's 100 Most influential People. Winner of The Nobel Prize for Physiology or Medicine 2009.

Sunday 5 September 09:00 - 10:00 - The Auditorium

Title & synopsis
Roles of telomeres & telomerase in human health & disease

Telomerase, a specialized ribonucleprotein reverse transcriptase complex, is essential for long-term proliferation of eukaryotic cells and for stability of their genomes. By replenishing the DNA at telomeres, telomerase can counteract telomere shortening. The telomerase RNA component provides a short template that is copied to make telomeric DNA. In addition to its telomere-elongating role, recent findings suggest that telomerase may also play other roles in cells: cells lacking or overexpressing telomerase show a variety of responses even in the absence of detectable effects on telomere integrity or functionality.   

Telomerase is highly active in many human malignancies. Thus the telomere maintenance system is a possible avenue to potential cancer therapeutic approaches. Telomerase functions in cancer maintenance include replenishing telomeric DNA and maintaining cell immortality. Also, human cancer cells responded rapidly to abrupt depletion of telomerase RNA by rapid and distinctive cellular/transcriptional responses, despite no obvious bulk telomere shortening or loss of telomere integrity.

Although telomerase activity is normally regulated to low levels in many adult human cells, a minimal threshold level of telomerase is required for replenishment of tissues, such as those of the immune system, throughout human life. In collaborative studies (Epel, et al, 2004; 2006; unpublished work) we have found that low telomerase in unstimulated normal white blood cells is associated with six of the known major risk factors, including chronic psychological stress, for cardiovascular disease in people. This work adds to the growing evidence implicating normal-cell telomere maintenance in protection from common diseases of human aging. We are now analyzing whether improvements in risk profiles for various age-related diseases can be associated with perturbations of telomere maintenance in humans.

The Louis-Jeantet keynote addresses are supported by a grant from the Louis-Jeantet Foundation and the journal EMBO Molecular Medicine (published by Wiley-Blackwell).


Michel Haïssaguerre

University Victor-Segalen
Bordeaux, FR

Michel Haïssaguerre was born 1955 in Bayonne, FR. He holds a Masters in human biology and earned his doctorate in medicine (1982) and his certificate in cardiology (1984). In that year he was named Senior Registrar at the Bordeaux University Hospital and medical assistant at the Bordeaux Hospitals. He is currently professor of cardiology at the University Victor-Segalen Bordeaux 2 and head of the Department of Cardiac Arrhythmias at the University Hospital of Bordeaux (Haut-Lévêque Cardiology Hospital).He has authored a very large number of publications and is a member of various scientific societies. He has received numerous distinctions, and notably the Best Scientist Grüntzig Award from the European Society of Cardiology, in 2003, the Pioneer Award from the North American Society of Pacing and Electrophysiology, in 2004, and the Mirowski Award for his excellent work in clinical cardiology and electrophysiology, in 2009. Winner of the 2010 Louis-Jeantet Prize for medicine.

Title & synopsis
Origin & treatment of atrial & ventricular fibrillation


Atrial and ventricular fibrillation are the most complex pathologies relating to cardiac rhythm. The former is the main cause of embolic cerebral vascular accidents. As for the latter, it is behind most cases of sudden death in adults, affecting 350’000 people every year in Europe. First of all, Michel Haïssaguerre studied the genesis of atrial fibrillation. In creating a «heart map» he was the first to notice that the electrical problems causing the illness were not occurring in the atrium, as had been thought for a long time, but further upstream in the cells situated in external wall of the pulmonary veins. This discovery was confirmed by numerous clinics across the world, and led to the development of a new treatment involving the ablation by cryotherapy or ultrasound of the cells causing atrial fibrillation. In 2009, 150'000 persons received this treatment, and the number of cases thus managed is growing constantly.
Michel Haïssaguerre and his team adopted this same original approach to look into the causes of ventricular fibrillation. Although in this case the heart mapping technique was more difficult due to the instantaneous nature of the disorder, which calls for immediate defibrillation using electric shocks, they achieved their goal. They demonstrated that these «electrical tornados» emanate from the tissue known as «de Purkinje», which only accounts for the tiniest fraction (2%) of the cardiac mass. The concept has since been validated in clinical trials on a few patients. Thermoablation focused on this tissue totally eliminated these patients' arrythmias.


Austin Smith
Centre for Stem Cell Research, University of Cambridge, UK
Austin Smith obtained his Ph.D. from the University of Edinburgh in 1986. Following postdoctoral research at the University of Oxford, he joined the Institute for Stem Cell Research at the University of Edinburgh (formerly Centre for Genome Research) in 1990 as a group leader. In 1996, he was appointed Director of the Centre. He was appointed MRC Research Professor in 2003. He took up the post of Director of the Wellcome Trust Centre for Stem Cell Research at the University of Cambridge in the autumn of 2006. His expertise is in the field of stem cell biology and he has pioneered key advances in the field of Embryonic Stem (ES) Cell research. His research focuses on the molecular and cellular controls of embryonic and somatic stem cells, and on interconversion between pluripotent and tissue-restricted states. Winner of the 2010 Louis-Jeantet Prize for medicine.

Title & synopsis
Design principles of pluripotency


Pluripotency is the capacity of an individual cell to initiate formation of all lineages of the mature organism plus the germline directed by extrinsic cues from the embryo. A pluripotent cell is a blank slate with no predetermined programme. In mice and rats this naïve state at the foundation of mammalian development can be captured in culture. Self-renewing embryonic stem (ES) cells are isolated by suppressing differentiation triggers. fibroblast growth factor activation of the, which is the trigger for differentiation. This can be efficiently achieved using selective small molecule inhibitors of the fibroblast growth factor/ extracellular signal regulated kinase (Erk) cascade and of glycogen synthase kinase-3 (Gsk3). The cytokine LIF also supports both the derivation and propagation of ES cells and molecular reprogramming through activation of Stat3. We are investigating how Erk antagonism, Gsk3 inhibition and Stat3 activation contribute to creating, maintaining and recreating authentic pluripotency.




Robert Bosch Stiftung