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A noise-based molecular evolutionary model for the modulation of evolvability| old_uid | 9320 |
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| title | A noise-based molecular evolutionary model for the modulation of evolvability |
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| start_date | 2010/11/26 |
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| schedule | 14h-15h30 |
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| online | no |
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| summary | Living organisms evolve to survive in environments fluctuating in terms of competitors, nutritional resources and physical or chemical stresses. This necessity to diversify is variable depending on environmental constraints, but always exists. What is the driving force for this diversification ? In the neo-Darwinian perspective, genetic variants appear stochastically and the environment selects the fittest ones. But is environmental pressure able to increase the rate of appearance of genetic variants ? In the last thirty-five years, these fundamental issues have often been questioned by looking for regulated stress-inducible molecular mechanisms that could have been selected for their ability to produce genetic diversity.
After vigorous discussion among biologists and philosophers of science about phenomenons of non-random mutation in challenging environments, Lamarckian hypotheses for the appearance of adaptive mutations have been rejected in favour of more conventional Darwinian explanations. Studies on bacteria have now revealed mechanisms of regulated increase in the rate of appearance of genetic variants entirely consistent with the modern Darwinian concept of adaptation by natural selection on randomly occurring variation. Nevertheless equivalents in eukaryotic systems have not been observed. As variations in this rate are also observed in these cells, an alternative model is needed for the appearance of genetic plasticity in fluctuating environments and the modulation of evolvability. The stochastic nature of gene expression allows a model in which the rate of appearance of genetic variants in the population can be rapidly tuned as a result of a simple Darwinian process acting on noise-driven heterogeneity in this rate from cell to cell. The high flexibility conferred through this model could resolve paradoxical situations especially concerning the mutator phenotype in cancer cells. |
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| responsibles | Kostyrka, Laplane |
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