Speaker: Albert Goldbeter (Faculty of Sciences, Université Libre de Bruxelles (ULB), Brussels, Belgium. http://www.ulb.ac.be/sciences/utc)
Time: 10:00 am, May 4th (Wednesday)
Place: Room 1801, East Guanghua Tower
Sustained oscillations arise in genetic and metabolic networks as a result of various modes of cellular regulation. In view of the large number of variables involved and of the complexity of feedback processes that generate oscillations, mathematical models are needed to investigate the nonlinear dynamics of biological rhythms. The presentation will focus on two major cellular rhythms: circadian clocks, which occur spontaneously in most organisms with a period close to 24h, and the cell cycle. Based on experimental observations, mathematical models for circadian clocks predict the occurrence of sustained oscillations corresponding to the evolution toward a limit cycle. Chaos can also occur in these models, either in autonomous conditions or as a result of periodic forcing by light-dark cycles. A model for circadian rhythms in mammals permits to investigate the dynamical bases of physiological disorders of the sleep-wake cycle in humans. In regard to the cell cycle, models of increasing complexity have been proposed, first for the embryonic cell cycle, and, subsequently, for the yeast and mammalian cell cycles. The model for the mammalian cell cycle shows that it behaves as a self-sustained oscillator.
Goldbeter, A. 2002. Computational approaches to cellular rhythms. Nature 420, 238-245.
Leloup J.C.. & Goldbeter, A. 2003. Toward a detailed computational model for the mammalian circadian clock. Proc. Natl Acad. Sci. USA 100, 7051-7056.
Leloup, J.-C. & Goldbeter, A. 2008. Modeling the circadian clock : From molecular mechanism to physiological disorders. BioEssays 30, 590-600.
Gérard C, Goldbeter A. 2009. Temporal self-organization of the cyclin/Cdk network driving the mammalian cell cycle. Proc. Natl. Acad. Sci. USA 106, 21643-21648.
Gérard C, Goldbeter A. 2011. A skeleton model for the network of cyclin-dependent kinases driving the mammalian cell cycle. Interface Focus 1, 24-35.