Plenary Lectures - speaker bios & abstracts Print E-mail

Evolution of animal forms

Detlev Arendt

Heidelberg DE

Detlev Arendt obtained his Ph.D. in zoology in 1998 from the University of Freiburg, DE, where he compared nervous system development of bilaterian animals. In 1999, he joined the lab of Joachim Wittbrodt at the European Molecular Biology Laboratory (EMBL) in Heidelberg, DE, where he worked on eye development. After 3 years of postdoctoral training, he set up his laboratory at the EMBL in 2003 as a Group Leader in the Developmental Biology Unit. The Arendt laboratory has established the marine annelid Platynereis dumerilii, a slow-evolving species, as a new marine molecular model for evolutionary and neurobiological research. It has also recently pioneered the comparison of cell types as a novel approach in the field of evolutionary developmental biology. In 2007, Detlev Arendt became Senior Scientist at the EMBL and was awarded an honorary professorship at the University of Heidelberg, DE.

Title & Synopsis

Evolution of the central nervous system in animals - a cell type perspective

Animal nervous systems are composed of neuron types specialized for functions as diverse as light perception or hormone secretion. Some animals such as cnidarians have few neuron types, while human neuron types count in hundreds. Understanding the evolution of neuron types is key to understanding the evolution of animal nervous systems. The use of molecular fingerprints for cell type comparisons sets the stage for the study of neuron type evolution. Each neuron type displays a unique profile of expressed genes, which encode transcription factors, microRNAs and differentiation gene batteries. Since many of these genes are deeply conserved in animal evolution, this allows the identification of homologous cell types over large evolutionary distances. Molecular fingerprint comparisons also allow identifying, within a given species, sister cell types that are related by evolutionary diversification. To determine the molecular fingerprints for the whole set of neuron types in the developing brain, we have developed a novel technique, the "wholemount in silico expression profiling". This technique determines co-expression of genes by image registration for all brain cells simulatenously. We have used this technique in the marine annelid Platynereis dumerlii to elucidate the evolutionary origin of neuron types that make up the vertebrate hypothalamus, eyes, pineal and telencephalon.

Alejandro Sánchez Alvarado

Howard Hughes Medical Institute, US

Alejandro Sánchez Alvarado received his Bachelor's Degree in Molecular Biology and Chemistry from Vanderbilt University in 1986.  In 1992, he received his Ph.D. in Pharmacology and Cell Biophysics at the University of Cincinnati School of Medicine, where he studied mouse ES cells and their in vitro differentiation under Dr. Jeffrey Robbins and Thomas Doetschman.  In 1994, he joined the laboratory of Dr. Donald D. Brown at the Carnegie Institution of Washington, Department of Embryology as a postdoctoral fellow and in 1995 was appointed Staff Associate. During this period, he began to explore systems in which to molecularly dissect the problem of regeneration.  In 2002 he became an Associate Professor at the Department of Neurobiology and Anatomy at the University of Utah School of Medicine, and in 2005 he was promoted to Professor and appointed a Howard Hughes Medical Institute Investigator.  His current efforts aim to elucidate the molecular basis of regeneration using the free-living flatworm Schmidtea mediterranea.

Title and synopsis

Stem cells, regeneration & the planarian Schmidtea mediterranea

Organisms possessing relatively long life spans have evolved a series of renewal and repair mechanisms to respond to both trauma and normal wear and tear.  For example, under normal physiological conditions, the functions of many organs depend on the continuous destruction and renewal of their cells, and in some cases the adult tissues and organs of many organisms can be fully restored after amputation. Numerous questions remain unanswered, including: How do organ systems maintain their order and function while in a state of cell flux? How do animals control and coordinate the size and cell number of multiple organ systems? Does regeneration invoke embryogenesis, generic patterning mechanisms, or unique circuitry comprised of well-established patterning genes? One approach to obtain molecular insights into these issues is to study simpler animals with extensive tissue turnover and regeneration capacities.  One such animal is the planarian, an organism known by generations of biologists to possess uncanny developmental plasticity. I will discuss how the molecular study of the planarian Schmidtea mediterranea is beginning to shed light on the way adult animals regulate tissue homeostasis and the replacement of body parts lost to injury.



Marie-Anne Félix

Institut Jacques Monod, FR

Marie-Anne Félix started her scientific career in cell biology by a PhD in Eric Karsenti's lab at EMBL (Heidelberg, DE). She later turned to development and evolution in a postdoc in the lab of Paul Sternberg (Caltech). In the last years, her laboratory focused on evolution of vulva development in the nematode Caenorhabditis elegans and other Caenorhabditis species and on studies of natural populations of these species. Marie-Anne Félix is a Research Director at the CNRS (Centre National de la Recherche Scientifique, FR) and a Principal Investigator at the Institut Jacques Monod in Paris.

Title & Synopsis
Robustness and evolution of the Caenorhabditis vulva development

Most biological processes are studied in the laboratory under one standard condition in one reference genetic background. We study the impact of environmental and genetic variation on vulva development, as an example of a biological system that is robust to stochastic noise and environmental change. The observed buffering of the system's output to environmental variation may further result in buffering of some genetic variation, thus allowing for evolution in the process without change in its output. Consistent with this scenario, we reveal such cryptic evolution within C. elegans and among different Caenorhabditis species using various experimental approaches combined with quantitative modeling of the cell fate patterning events.


Shigeru Kuratani

RIKEN Center for Developmental Biology, JP

Shigeru Kuratani graduated from Department of Zoology, Kyoto University, JP in 1981, obtained his PhD in Zoology in 1986, and moved to Okinawa to work as an instructor of Anatomy Department in the University of the Ryukyus, School of Medicine. From 1988, he studied abroad in the US as a postdoc and an Assistant Professor at the Medical College of Georgia and Baylor College of Medicine, respectively, and returned to Japan in 1994. After working as an Associate Professor in Kumamoto University School of Medicine and Professor in Okayama University Department of Biology, he moved to RIKEN Center for Developmental Biology, in Kobe, JP to be engaged in evolutionary developmental biology of vertebrates. Throughout his career, his main interest has been, and still is, evolutionary morphology and embryology of the vertebrate head, since he saw a pseudosegmental pattern in the developing skull base in mice.

Title & Synopsis
Origins of the turtle body plan

The turtle body plan is characterized by the possession of the shell that develops outside the shoulder girdle. Since the dorsal part of the shell, or the carapace, is derived from the ribs, the tutle skeletal system exhibits a reversed topography as to the relative positions of the scapula and ribs. By examining developmental morphology of the shoulder region among amniote embryos, turtle-specific developmental factors to generate the shell are identified.




Systems biology & functional genomics

Marc Vidal

Dana-Farber Cancer Institute, US

Marc Vidal is Professor of Genetics at Harvard Medical School and Director of the Center for Cancer Systems Biology (CCSB) at the Dana-Farber Cancer Institute. Dr. Vidal received his PhD in 1991 from Gembloux University (Belgium) for work performed at Northwestern University (Evanston, IL, USA) where he identified the yeast genes RPD3 and SIN3, and demonstrated that they encode global transcriptional regulators. These genes were subsequently found to encode Histone Deacetylase (HDAC) and its main recruiting factor, respectively. During postdoctoral training at the Massachusetts General Hospital Cancer Center, he developed the reverse two-hybrid system, a widely applicable method used to genetically characterize protein-protein interactions. Having developed interdisciplinary strategies together with collaborators from the fields of physics, computer science, mathematics, genomics and human genetics, he and his team have been charting protein-protein and other "interactome" networks for 15 years and are developing ways to integrate interactome maps with other large-scale functional genomic and proteomic maps, with the ultimate objective to discover novel network properties from a systems point-of-view.  Dr. Vidal was elected Associate Member of the Royal Academy for Science and the Arts of Belgium and has received several awards, including a Chair from the Francqui Foundation (Belgium) and an Abbott Bioresearch Award.

Title & Synopsis
Interactome networks & human disease

For over half a century it has been conjectured that macromolecules form complex networks of functionally interacting components, and that the molecular mechanisms underlying most biological processes correspond to particular steady states adopted by such cellular networks. However, until recently, systems-level theoretical conjectures remained largely unappreciated, mainly because of lack of supporting experimental data. To generate the information necessary to eventually address how complex cellular networks relate to biology, we initiated, at the scale of the whole proteome, an integrated approach for modeling protein-protein interaction or "interactome" networks. Our main questions are: How are interactome networks organized at the scale of the whole cell? How can we uncover local and global features underlying this organization, and how are interactome networks modified in human disease, such as cancer?



Edward Rubin


Edward (Eddy) Rubin has served since 2002 as Director of the U.S. Department of Energy Joint Genome Institute (JGI), and Director of the Genomics Division at Lawrence Berkeley National Laboratory (LBNL).  With more than 200 peer-reviewed publications, his research focuses on the development of computational and biological approaches for studying genomes. Under his leadership, the JGI, one of the world's five leading institutions responsible for sequencing the human genome, completed and published the DNA sequence of human chromosomes 5, 16, 19.  He has played a major role both nationally and internationally advancing genome sciences.  Completing DOE's commitment to the Human Genome Project in 2004, He redirected the JGI's focus to the sequencing and analysis of organisms of relevance to bioenergy, carbon cycling, and bioremediation.  This scientific focus of the JGI is described in his review, "Genomics of cellulosic biofuels," published in the journal Nature on 14 August 2008.

Title & Synopsis
Genomic approaches for enhancer identification

Despite their anticipated importance in human biology and disease, transcriptional enhancers remain challenging to both identify as well as predict their associated in vivo gene regulatory activities.  I will describe two whole genome strategies for the identification of Mendelian enhancers, comparative genomics and Chromatin Immunoparticipation coupled with massively parallel next generation sequencing (ChiP-Seq).  Both of these enhancer prediction approaches have been linked to large scale in vivo validation where ~1500 putative enhancers have been tested in a transgenic mouse enhancer assay system.  Summaries of the results and insights will be presented.


Ron Weiss

Princeton University, US

Ron Weiss is an Associate Professor in the Department of Biological Engineering and in the Department of Electrical Engineering and Computer Science at the Massachusetts Institute of Technology. He received his PhD from MIT in 2001 and held a faculty appointment at Princeton University between 2001 and 2009. His research focuses primarily on synthetic biology, where he programs cell behavior by constructing and modeling biochemical and cellular computing systems. A major thrust of his work is the synthesis of gene networks that are engineered to perform in vivo analog and digital logic computation. He is also interested in programming cell aggregates to perform coordinated tasks using cell-cell communication with chemical diffusion mechanisms such as quorum sensing. He has constructed and tested several novel in vivo biochemical logic circuits and intercellular communication systems. Weiss is interested in both hands-on experimental work and in implementing software infrastructures for simulation and design work. For his work in synthetic biology, Weiss has received MIT's Technology Review Magazine's TR100 Award ("top 100 young innovators", 2003), was selected as a speaker for the National Academy of Engineering's Frontiers of Engineering Symposium (2003), received the E. Lawrence Keyes, Jr./Emerson Electric Company Faculty Advancement Award at Princeton University (2003), his research in Synthetic Biology was named by MIT's Technology Review Magazine as one of "10 emerging technologies that will change your world" (2004), was chosen as a finalist for the World Technology Network's Biotechnology Award (2004), and was selected as a speaker for the National Academy of Sciences Frontiers of Science Symposium (2005).
Title & Synopsis
Synthetic biology: from modules to systems

Synthetic biology is revolutionizing how we conceptualize and approach the engineering of biological systems.  Recent advances in the field are allowing us to expand beyond the construction and analysis of small gene networks towards the implementation of complex multicellular systems with a variety of applications. In this talk I will describe our integrated computational / experimental approach to engineering complex behavior in living systems ranging from bacteria to stem cells.  In our research, we appropriate useful design principles from electrical engineering and other well established fields.  These principles include abstraction, standardization, modularity, and computer aided design. But we also spend considerable effort towards understanding what makes synthetic biology different from all other existing engineering disciplines and discovering new design and construction rules that are effective for this unique discipline. We will briefly describe the implementation of genetic circuits with finely-tuned digital and analog behavior and the use of artificial cell-cell communication to coordinate the behavior of cell populations for programmed pattern formation.  Recent results with implementing Turing patterns with engineering bacteria will be presented.  Arguably the most significant contribution of synthetic biology will be in medical applications such as tissue engineering.  We will discuss preliminary experimental results for obtaining precise spatiotemporal control over stem cell differentiation.  For this purpose, we couple elements for gene regulation, cell fate determination, signal processing, and artificial cell-cell communication.  We will conclude by discussing the design and preliminary results for creating an artificial tissue homeostasis system where genetically engineered stem cells maintain indefinitely a desired level of pancreatic beta cells despite attacks by the autoimmune response.  The system, which relies on artificial cell-cell communication, various regulatory network motifs, and programmed differentiation into beta cells, may one day be useful for the treatment (or cure) of diabetes.


Olivier Voinnet

CNRS Institute of Plant Molecular Biology, Strasbourg, FR

Olivier Voinnet graduated from the University of Paris VI and Grande Ecole AgroParisTech, FR in 1994 and 1995, respectively and then joined David Baulcombe’s laboratory (John Innes Center, Norwich, UK) in 1996 to obtain his PhD in 2001. His thesis work focused on deciphering the antiviral role played by gene silencing in plants, and the counter-defensive strategies deployed by viruses against this new form of defense. Olivier, now Research Director at the CNRS (Centre National de la Recherche Scientifique), was appointed in 2002 to establish his own laboratory in Strasbourg, FR, where he continued his investigations of the mechanisms and roles of RNA silencing, expanding his interests to mammalian model systems. Olivier has received several national and international awards and he was laureate of the 2009 EMBO Gold medal. From November 2010 he will take a full Professor position at the Federal Institute of Technology in Zürich, CH (ETH).
Title & Synopsis
Defense, counter-defense, counter-counter-defense: a never ending tale of antiviral RNA silencing

In plants and some invertebrates, RNA silencing, in the form of RNA interference (RNAi), plays an important role in containing viruses at the sites of their replication and, in some cases, in distant tissues. As a counter-defensive measure, viruses have evolved various strategies to circumvent the action of RNAi, which include the deployment of proteins known as Viral Suppressors of RNA silencing (VSR). The cellular targets and modes of operation of of VSRs are still largely elusive, as are the host mechanisms that sense the damages incurred by VSR to silencing pathways. These host mechanisms must exist to account for the constant and rapid evolution of VSR genes within viral genomes. Using a single example, I will illustrate an original mechanism of VSR action that targets the main effector protein in the plant antiviral silencing pathway, AGO1. I will then show how AGO1 suppression incurs profound changes to the various endogenous RNA silencing pathways of the host, and how these changes might contribute, unexpectedly, to strengthen the host defense responses to pathogens. I will finally illustrate how the continuous aggression of AGO1 by various parasites have led to the deployment, by the host, of a family of protein known as Resistance proteins (R proteins, analogous to the vertebrate NOD intracellular factors). One of these proteins, MAD1, seems to constantly monitor the status of the AGO1 protein complex and, under extreme circumstances, signals a form of cell death as an ultimate attempt to confine the aggressor. Strikingly, MAD1 activation is accompanied by an hormone-based, systemic reaction that apparently potentiates the antimicrobial action of AGO1. These findings unravel an exquisite degree of interconnection between silencing pathways and classical innate immune pathways in plants and, possibly, in invertebrates. They further illustrate the complexity and versatility of RNA silencing pathways at the system’s level.



Signalling in Development

Irma Thesleff

Institute of Biotechnology,
University of Helsinki
, FI

Irma Thesleff graduated from the Dental School of the University of Helsinki, FI in 1972, received her PhD  in 1975 on studies on the etiology of cleft lip and palate, and was a postdoctoral scientist at National Institute of Dental Research in Bethesda, US 1978-79. Since 1996 she is the Research Director of the Developmental Biology Programme at the Institute of Biotechnology, University of Helsinki. This programme has gained the status of a Center of Excellence from the University as well as from the Academy of Finland. Her research interest is the mechanisms of epithelial mesenchymal interactions regulating organ development. She is best known for work on tooth development and the model she presented on how sequential and reciprocal signalling regulates the morphogenesis of teeth. Her group has developed mouse models and a variety of novel organ culture methods for examining the functions of signal molecules, and the research has expanded to include the development of bone and several organs developing as ectodermal appendages.

Title & Synopsis
Fine tuning of signalling in tooth development & regeneration

The growth, morphogenesis and cell differentiation in teeth are regulated by interactions between epithelial and mesenchymal tissues. These interactions also regulate stem cell development in the epithelial stem cell niche discovered by our group in the continuously growing mouse incisors. The cell and tissue interactions are mediated by signalling molecules belonging to few conserved families including BMP, Activin, FGF, Wnt, Hh, Eda.  Our studies have pinpointed the importance of fine-tuning these signal pathways in the regulation of the numbers, shapes and sizes of mouse teeth as well as the formation of the dental hard tissues and regeneration of the incisors.


Kathryn Anderson

Sloan-Kettering Institute,
New York, US
Kathryn Anderson trained in Drosophila developmental genetics with Dr. Judith Lengyel at UCLA and Dr. Christiane Nüsslein-Volhard in Tübingen, DE. As a faculty member at UC Berkeley, her lab characterized the Drosophila Toll pathway. She did a sabbatical in Rosa Beddington's lab at NIMR in London, UK, where she began to learn about mouse embryogenesis. After the sabbatical, her lab began a forward genetic screen to identify new genes important in mouse embryonic development. In 1996 she moved to Sloan-Kettering Institute in New York, where she is now Chair of the Developmental Biology Program. Her lab now studies the genetic control of patterning in the mouse embryo, particularly the role of cilia in Hedgehog signalling and the role of the actin cytoskeleton in establishment of the mammalian body plan.
Title & Synopsis
Cilia & Hedgehog signalling in the mouse embryo

The specification of cell types in the ventral half of the mouse neural tube depends on graded activity of the Sonic hedgehog (Shh) signalling pathway. Our genetic studies on neural patterning led to the discovery that primary cilia are required for mammalian cells to transmit signals from the membrane protein Smoothened (Smo) to the Gli transcription factors. To understand why the primary cilium is an appropriate venue for Shh signal transduction, we are investigating the relationships among cilia genes and between cilia genes and the components of the Shh pathway that act between Smo and Gli proteins. Protein kinase A (PKA) is a conserved negative regulator that acts at that step of the pathway. We find that embryos that lack all PKA catalytic activity show a very strong activation of the pathway, and that PKA activity depends on the presence of cilia. Costal2 is a negative regulator of the Shh pathway, and we find that the mouse homologue of Costal2, Kif7, has complex roles as both a negative and positive regulator of Shh signaling.  Kif7 activity also depends on cilia, and the Kif7 protein appears to act as a motor within cilia. Finally, certain combinations of mutations in proteins that affect transport within the cilium partially restore normal Hedgehog signalling, suggesting that the balance of anterograde and retrograde trafficking within the cilium can control the level of signal output.


Christof Niehrs

Heidelberg, DE

Christof Niehrs studied biochemistry at the Freie Universität Berlin, DE. He did his PhD degree at the European Molecular Biology Laboratory (EMBL) in Heidelberg, DE in 1990 working on protein tyrosine sulfation. He then joined Dr. E. M. De Robertis' laboratory at the University of California in Los Angeles as a postdoctoral fellow from working on cell-fate determination by homeobox genes in Xenopus laevis. In 1994 he was appointed Head of the Division of Molecular Embryology at the German Cancer Research Center (DKFZ) in Heidelberg, DE where he became the Chair of Molecular Embryology in 2000. He and has received several scientific awards and distinctions. His field of research is developmental biology and his work has contributed to solve fundamental problems in early embryogenesis and growth factor signalling. In particular, he has contributed solving the molecular mechanism of the Spemann organizer function. Other major topics include Wnt signalling and DNA demethylation.
Title & Synopsis
Regulation of Wnt/Lrp6 signalling

The Wnt/β-catenin signaling pathway plays important roles in embryonic development and disease. Wnts transduce signals via transmembrane receptors of the Frizzled (Fzd) family and the low density lipoprotein receptor-related protein 5/6 (Lrp5/6). A key mechanism in their signal transduction is that Wnts induce Lrp6 signalosomes, which become phosphorylated at multiple conserved sites. Lrp6 phosphorylation is crucial to beta-catenin stabilization and pathway activation by promoting Axin and Gsk3 recruitment. I will discuss the regulation of this co-receptor and the significance for Xenopus early development.


Sarah E Millar

University of Pennsylvania,
Philadelphia, US

Sarah E Millar received her PhD from the University of London, UK in 1987, and carried out post-doctoral research at the National Institutes of Health and Stanford University, US. She was appointed Assistant Professor of Dermatology and Cell and Developmental Biology at the University of Pennsylvania, US in 1999, and Associate Professor and Director of Research for the Department of Dermatology in 2005. In 2009, she was appointed Chair of the Developmental, Stem Cell and Regenerative Biology Program of the Cell and Developmental Biology graduate group at Penn. She is a permanent member of the NIH ACTS study section and is an Editorial Board member for the journals Developmental Cell and Experimental Dermatology. Her research is funded by multiple NIH grants, and focuses on understanding molecular mechanisms controlling development, patterning, stem cell function and regeneration in ectodermal appendage organs including hair follicles, mammary glands, taste papillae and teeth.
Title & Synopsis
Wnt signalling in the specification, regeneration and neogenesis of ectodermal appendages

Ectodermal appendages, such as hair follicles, mammary glands, teeth and taste papillae, develop through interactions of embryonic surface ectoderm and underlying mesenchymal cells. In each case organ development is first evident morphologically as a local thickening of the surface ectoderm (a "placode"), that then either buds into the mesenchyme or evaginates around a mesenchymal core. Wnt/b-catenin signaling is activated locally at sites of placode formation. We find that in vivo inhibition of Wnt/b-catenin signaling or deletion of ectodermal b-catenin prevents placode development for a wide range of ectodermal organs including hair follicles, mammary glands and taste papillae. Conversely, forced activation of Wnt/b-catenin signalling in embryonic ectoderm by mutation of b-catenin to a constitutively active form promotes formation of ectopic placodes. These data identify Wnt/b-catenin pathway activation as a key event instructing surface ectodermal cells to begin to differentiate into appendage organs rather than epidermis. Our data further indicate that patterning of Wnt activity within the ectoderm involves Wnt-mediated activation of the EDA/EDAR/NF-kB pathway and expression of secreted Wnt inhibitors. Use of an inducible system for reversibly inhibiting Wnt activity in vivo reveals postnatal requirements in elongation and branching of mammary ducts, and for maintenance of the anagen growth phase in postnatal hair follicles. Conversely, forced activation of this pathway in adult ectodermal cells can promote the de novo formation of organs such as hair follicles and dental structures. These data suggest that manipulation of b-catenin signaling in adult ectodermal cells could contribute to strategies for organ regeneration in cases of congenital absence or loss through disease.




Robert Bosch Stiftung