How Mendel's genes are copied
Timothy John Mitchison
How does a large cell find its center?
Proliferation control and tumorigenesis in stem cell lineages of the nervous system: Lessons from Drosophila and mouse genetics
Causes and consequences of aneuploidy
Anthony A. Hyman
Cytoplasmic organization through phase transitions
How DNA recombination maintains genome integrity
Exploring the role of replicative stress in cancer and ageing
Preventing chromosomes from going rogue
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Dr. John Diffley took his doctorate at the New York University (USA) in 1985 and followed his postdoctoral fellowship in Cold Spring Harbor Laboratory (USA). In 1990 he established a lab at the Imperial Cancer Research Fund, UK (in 2002 the Imperial Cancer Research Fund became Cancer Research UK). Since 2006 he is the director of Clare Hall Laboratories and the deputy director of the Cancer Research UK London Research Institute. He was elected member of European Molecular Biology Organisation (EMBO) in 1998, awarded Paul Marks Prize for Cancer Research in 2003, elected Fellow of the Royal Society in 2005 and elected Fellow of the American Association for the Advancement of Science (AAAS) in 2007.
Dr. John Diffley is one of the world's leading experts in studying how cells grow and make copies of themselves. When new cells are needed - as we grow, or to replace dead and damaged cells - a cell splits into two 'daughter' cells. This is known as cell division. It is normally tightly controlled, but if it is faulty then cells grow out of control, which can lead to cancer. In order to produce two identical 'daughters', the original cell's DNA must be accurately copied and shared equally between the new cells. Dr Diffley is studying the molecular 'machinery' that copies DNA and ensures that each daughter cell receives a complete set of genetic instructions. For example, Dr. Diffley and his team are investigating why DNA is copied only once in healthy cells but many times in some cancer cells. And they are also studying how the process of DNA copying (called replication) is affected when DNA is damaged - a common occurrence in cancer. By uncovering the molecular 'nuts and bolts' of DNA replication, Dr Diffley's discoveries will form the foundations for new ways to diagnose and treat cancer in the future.
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Professor Timothy John "Tim" Mitchison, Ph.D., FRS is a British systems biologist. He is Hasib Sabbagh Professor of Systems Biology at Harvard University in the United States.
After completing his undergraduate degree at Merton College, Oxford he moved to the University of California, San Francisco in the United States in 1979, where he worked for the Ph.D. At this time he discovered the Dynamic Instability of Microtubules. Later he worked at the National Institute for Medical Research in London. In the late 1980s he returned to San Francisco to become an assistant professor at UCSF. In the late 1990s he moved to Harvard to become co-director of the Institute for Chemistry and Cell Biology at Harvard Medical School. Recently he became deputy chair of the newly formed Department of Systems Biology. He was elected Fellow of the Royal Society in 1997. Tim is the current (2010) president of the American Society for Cell Biology.
Tim´s lab is interested in the structure, dynamics, and function of the cytoskeleton. They use imaging-based assays in living cells and in vitro extracts, in conjunction with molecular biology and biochemical fractionation approaches, as well as theory and modeling. Most of the lab works on cell division in some way. One major focus is on the mechanism of mitotic spindle assembly in Xenopus egg extracts. He uses a variety of imaging methods, including single molecule imaging, to probe protein localization and dynamics, biochemistry and pharmacology to perturb assembly, and theory/modeling to rationalize the results. The lab is increasingly interested in an applied problem, cancer chemotherapy directed at the mitotic spindle. He is performing imaging and biochemistry experiments in different cancer cell lines to understand how current chemotherapy works, and how we might improve it. A key question is to understand differences between cell types in drug response. Part of the lab works on how the actin cytoskeleton is organized, during cytokinesis and also in the comet tails of Listeria, a pathogenic bacterium. Current foci include understanding monopolar cytokinesis, and the mechanism by which actin filaments turn over rapidly in the cytoplasm.
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Professor Dr. Jürgen Knoblich studied biochemistry at the University of Tübingen , Molecular Biology at University College London and in 1989 moved to the Max-Planck-Institute for Developmental Biology in Tübingen, where in 1994 he earned his doctorate. From 1994 to 1997 he was a postdoctoral fellow at the University of California, San Francisco. After his return to Europe he became group leader at the Research Institute of Molecular Pathology in Vienna, where he rose to Senior Scientist. Since 2005 he has worked at the Institute for Molecular Biotechnology (IMBA) in Vienna, where he is deputy scientific director. Knoblich is a member of several scientific societies, the Editorial Board of Current Biology and the European Journal of Cell Biology. He is a member of the advisory board of the cancer stem cell network of the Deutsche Krebshilfe eV. He has authored 67 original publications (PubMed June 7, 2009).
He takes specific interest in the scientific question of cell division. A special case of cell division is the asymmetric one, which bears extraordinary significance for stem cell biology. Together with his international team of 18 scientists, Jürgen Knoblich was able to clarify all details of the biologic processes, which take part in this procedure. The asymmetric cell division is an elementary process, which enables the body to create a multitude of specialised cells from a reservoir of stem cells, without depleting its stock of stem cells. The detailed understanding of this mechanism and all involved molecules is essential, since an excessive production of stem cells is hold responsible for certain tumour diseases, e.g. for leukaemia. The exact processes of the asymmetric cell division have been mysterious for a long time. Step by step, the team around Jürgen Knoblich has solved the riddle in the recent years. The fruit fly Drosophila melanogaster served as a biologic model for the researchers. The scientists were now able to explain how stem cells equip their daughter cells with different features. Jürgen Knoblich’s contribution to stem cell biology could some day lead on to a therapeutic regulation of the asymmetric cell division. The ratio of newly produced stem cells and specialised cells would then be controllable, which could be followed by new prospects for tumour biology as well as for stem cell therapy.
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Professor Dr. Angelika Amon (1967) is an Austrian American molecular and cell biologist and professor at the Massachusetts Institute of Technology (MIT) in Cambridge, Massachusetts, United States. She received her B.S. from the University of Vienna and continued her doctoral work there at the Research Institute of Molecular Pathology, receiving the Ph.D. in 1993. She completed a two-year post-doctoral fellowship at the Whitehead Institute in Cambridge, Massachusetts and was subsequently named a Whitehead Fellow for three years. She joined the MIT Center for Cancer Research and MIT's Department of Biology in 1999 and was promoted to full professor in 2007. Amon won a Presidential Early Career Award for Scientists and Engineers in 1998, was named an associate investigator at the Howard Hughes Medical Institute in 2000, and was the 2003 recipient of the National Science Foundation's Alan T. Waterman Award. Amon also shared the 2007 Paul Marks Prize for Cancer Research and won the 2008 National Academy of Sciences Award in Molecular Biology.
Amon's research has investigated how cells control and organize the segregation of their chromosomes during cell division. More specifically, her research examines the regulation of exit from mitosis, the regulation of the meiotic cell cycle, and effects of aneuploidy on normal physiology and tumorigenesis. As a student, Amon demonstrated that CDC28 protein kinase is not required for the metaphase to anaphase transition and CLB2 proteolysis continues until reactivation of CDC28 toward the end of G1. The Amon lab primarily investigates yeast (Saccharomyces cerevisiae) as a model for understanding the controls that govern cell-cycle progression. As a Whitehead Fellow, her team discovered that CDC20 plays a crucial role in cell division. Her Whitehead team identified an interaction between phosphatase and CDC14 which initiates the exit of cells from mitosis to the G1 phase. Amon's team demonstrated that CDC20 is the target protein in the spindle checkpoint during mitosis. Amon's more recent work has investigated the regulation of chromosome segregation and how chromosomes are accurately transmitted to gametes in meiosis by examining gene regulatory networks. She identified two regulatory networks (FEAR and MEN) that promote the release of CDC14 which have the potential to identify the mechanisms that control the final stages of the mitotic cell cycle. Her research group recently created haploid yeast cells containing extra copies of chromosomes and discovered that these aneuploid strains elicit phenotypes independent of the identity of the additional chromosome such as defects in cell cycle progression, increased energy demands, and interference with protein biosynthesis. Amon has also examined trisomy in the mouse as a model of mammalian cell growth and physiology and demonstrated that mammalian aneuploidy results in a stress response analogous to yeast aneuploidy. Amon's aneuploidy research has potential applications to cancer research.
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Professor Dr. Anthony Hyman, FRS studied zoology at Imperial College in London, took his doctorate at Cambridge, and completed his post-doctoral studies at the University of California in San Francisco. He subsequently became a Group Leader at the European Molecular Biology Laboratory (EMBL) in Heidelberg, and was called to the newly established Max Planck Institute of Molecular Cell Biology and Genetics (MPI – CBG) in Dresden in 1999, where he continues to research today. Hyman is a Director of the MPI-CBG.
Located at the interface between cell biology and developmental biology, his research has focussed primarily on the role of so-called microtubules in cell division. Functioning as dynamic "molecular machines", these cytoskeletal components organise the distribution of a cell's components to its daughter cells. Prof. Hyman has developed a range of innovative physical and genomic methods of studying the microtubular cytoskeleton, including laser microsurgery techniques. Using video microscopy and high-throughput processes Hyman has successfully identified hundreds of genes which cause cell division defects. His findings have greatly improved our understanding of cell division as one of the most fundamental and complex biological processes, and his research has also led to important breakthroughs in both cell and systems biology. Widely regarded as one of the world's leading cell biologists, prof. Anthony A. Hyman has been awarded the Leibniz Prize.
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Professor Dr. Roland Kanaar studied chemistry at Leiden University and obtained his Ph.D. degree in 1988 for research on the action of an enhancer in site-specific DNA recombination and the elucidation of how nucleoprotein complexes assembled at distant sites along a DNA chain communicate with each other to provide selectivity during recombination. His post-doctoral work at the University of California, Berkeley aimed at understanding mechanisms of homologous recombination (with Nick Cozzarelli) and at understanding how proteins and RNA interact to achieve accurate but flexible recognition of splice sites (with Don Rio).
His current research addresses the mechanisms and biological relevance of genome surveillance processes with particular emphasis on homologous DNA recombination and DNA double-strand break repair. Genome surveillance is essential to prevent chromosomal abnormalities, which in their turn may lead to hereditary diseases, cancer or cell decay. In 2000 he was appointed Professor of Molecular Radiation Genetics. Prof. Kanaar is a scientific co-founder of the biotechnology company DNage, which is focused on the development of products for medical and health problems associated with ageing. In 2002 he was elected as a member of the European Molecular Biology Organization.
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Dr. Óscar Fernández-Capetillo obtained his Ph.D. in 2001 from the Universidad del País Vasco working on the role of E2F transcription factors on the development of the immune. He then joined the laboratory of A. Nussenzweig at the National Cancer Institute, USA, where he started to work on the cellular response to DNA damage (DDR), focusing particularly on the role of the histone variant H2AX and other chromatin-related aspects.
After three years at the NCI he joined the CNIO to lead the Genomic Instability Group where his work has continued to focus on chromatin but now mainly concentrates on developing cellular and animal tools for studying the role of the ATR/Chk1 signalling cascade in the protection against cancer and ageing.
Dr. Fernández-Capetillo‘s work has been recognised through several national and international awards/honours including the Eppendorf Award for Young Investigators (2009), elected EMBO Young Investigator (2008), an ERC Starting Grant (2007), the membership to the EPIGENOME Network of Excellence (2006), and the Swiss Bridge Award (2005).
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Professor Dr. Doug Koshland earned his B.A. degree in chemistry from Haverford College and his Ph.D. degree in microbiology with David Botstein at the Massachusetts Institute of Technology, where he studied the secretion of λ-lactamase in Salmonella typhimurium. Postdoctoral work was done at the University of Washington, Seattle, where he studied yeast chromosome segregation in vivo, and at the University of California, San Francisco, where he studied vertebrate kinetochore function in vitro.
Professor Dr. Koshland’s laboratory uses genetic, cell biological and biochemical approaches in budding yeast to understand genome integrity, genome evolution and most recently desiccation tolerance. The maintenance of genome integrity during cell division impacts cell viability, speciation, birth defects and human disease. Similarly desiccation tolerance, the ability of cells to survive extreme changes in available water, influences cell survival, crop productivity and wound recovery. However, the molecular bases for desiccation tolerance and genome integrity remain major unsolved problems of cell biology. By studying these two processes in the simple unicellular budding yeast using genetic, biochemical and cell biological approaches, they hope to uncover mechanisms that enlighten our understanding of genome and water homeostasis in all eukaryotes.
Doug Koshland was named Professor of Molecular and Cell Biology at the University of California, Berkeley. Prof. Koshland was recently elected to the American Academy of Arts and Sciences and the American Association for the Advancement of Science.