Bulletin of the American Physical Society
APS March Meeting 2011
Volume 56, Number 1
Monday–Friday, March 21–25, 2011; Dallas, Texas
Session Q7: System Biology III: The Physics of Evolution |
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Sponsoring Units: DBP DCP Chair: Wouter Hoff, Oklahoma State University Room: Ballroom C3 |
Wednesday, March 23, 2011 11:15AM - 11:51AM |
Q7.00001: Does Tumor Development Follow a Programmed Path? Invited Speaker: The initiation and progression of a tumor is a complex process, resembling the growth of a embryo in terms of the stages of development and increasing differentiation and somatic evolution of constituent cells in the community of cells that constitute the tumor. Typically we view cancer cells as rogue individuals violating the rules of the games played within an organism, but I would suggest that what we see is a programmed and algorithmic process. I will then question If tumor progression is dominated by the random acquisition of successive survival traits, or by a systematic and sequential unpacking of ``weapons'' from a pre-adapted ``toolkit'' of genetic and epigenetic potentialities? Can we then address this hypothesis by data mining solid tumors layer by layer? [Preview Abstract] |
Wednesday, March 23, 2011 11:51AM - 12:27PM |
Q7.00002: Adaptation Driven by Spatial Heterogeneities Invited Speaker: Biological evolution and ecology are intimately linked, because the reproductive success or ``fitness'' of an organism depends crucially on its ecosystem. Yet, most models of evolution (or population genetics) consider homogeneous, fixed-size populations subjected to a constant selection pressure. To move one step beyond such ``mean field'' descriptions, we discuss stochastic models of evolution driven by spatial heterogeneity. We imagine a population whose range is limited by a spatially varying environmental parameter, such as a temperature or the concentration of an antibiotic drug. Individuals in the population replicate, die and migrate stochastically. Also, by mutation, they can adapt to the environmental stress and expand their range. This way, adaptation and niche expansion go hand in hand. This mode of evolution is qualitatively different from the usual notion of a population climbing a fitness gradient. We analytically calculate the rate of adaptation by solving a first passage time problem. Interestingly, the joint effects of reproduction, death, mutation and migration result in two distinct parameter regimes depending on the relative time scales of mutation and migration. We argue that the proposed scenario may be relevant for the rapid evolution of antibiotic resistance. [Preview Abstract] |
Wednesday, March 23, 2011 12:27PM - 1:03PM |
Q7.00003: Experimental Ignition of Evolution on Fitness Landscapes Invited Speaker: Microbiologist are starting to revise the single cell centered view of evolution to a multicellular view, considering it at entire population scale, and even whole ecosystem. Indeed, as Darwin recognized on the Galapagos Island, evolution of a community of bacteria is strongly influenced by the global spatial stress and depends of the neighboring communities. This collective dynamical process can be studied using micro-nanofabricated landscape to create stressed conditions. Our microfluidic device consists of interconnected chambers in 2D hexagonal geometries. The design of our ecology enables to combine gradients of antibiotic and nutrient, thus generating population gradient and motion of bacteria across them. We study here evolution of resistance to the antibiotic ciprofloxacin in highly-stressed conditions. Non-random mutations are induced in the collectivity to develop resistance to the antibiotic. Channels between microhabitats allow motion of bacteria between different islands, and once evolution is ignited in a local metapopulation, a very fast spread through the collectivity happens. In such environments, evolution is observed in typical time scales of few hours. Knowing the complexity of natural world, we believe that our approach provide a model to understand the rapid emergence of resistance to antibiotic and its spread in the entire population. [Preview Abstract] |
Wednesday, March 23, 2011 1:03PM - 1:39PM |
Q7.00004: Towards a Quantitative Endogenous Network Theory of Cancer Genesis and Progression: beyond ``cancer as diseases of genome'' Invited Speaker: There has been a tremendous progress in cancer research. However, it appears the current dominant cancer research framework of regarding cancer as diseases of genome leads impasse. Naturally questions have been asked that whether it is possible to develop alternative frameworks such that they can connect both to mutations and other genetic/genomic effects and to environmental factors. Furthermore, such framework can be made quantitative and with predictions experimentally testable. In this talk, I will present a positive answer to this calling. I will explain on our construction of endogenous network theory based on molecular-cellular agencies as dynamical variable. Such cancer theory explicitly demonstrates a profound connection to many fundamental concepts in physics, as such stochastic non-equilibrium processes, ``energy'' landscape, metastability, etc. It suggests that neneath cancer's daunting complexity may lie a simplicity that gives grounds for hope. The rationales behind such theory, its predictions, and its initial experimental verifications will be presented. \\[4pt] References:\\[0pt] [1] Cancer as Robust Intrinsic State of Endogenous Molecular-Cellular Network Shaped by Evolution. P. Ao, D. Galas, L. Hood, X.-M. Zhu, Medical Hypotheses \textbf{70} (2008) 678-684. http://dx.doi.org/10.1016/j.mehy.2007.03.043\\[0pt] [2] Towards Predictive Stochastic Dynamical Modeling of Cancer Genesis and Progression. P. Ao, D. Galas, L. Hood, L.Yin, X.M.Zhu. Interdiscip Sci Comput Life Sci (2010) 2: 140-144 DOI: 10.1007/s12539-010-0072-3\\[0pt] [3] Orders of Magnitude Change in Phenotype Rate Caused by Mutations. P. Ao, Cellular Oncology (2007) \textbf{29}: 67-69. http://arxiv.org/PS\_cache/arxiv/pdf/0704/0704.0429v1.pdf [Preview Abstract] |
Wednesday, March 23, 2011 1:39PM - 2:15PM |
Q7.00005: Understanding the distribution of fitness effects of mutations by a biophysical-organismal approach Invited Speaker: The distribution of fitness effects of mutations is central to many questions in evolutionary biology. However, it remains poorly understood, primarily due to the fact that a fundamental connection that exists between the fitness of organisms and molecular properties of proteins encoded by their genomes is largely overlooked by traditional research approaches. Past efforts to breach this gap followed the ``evolution first'' paradigm, whereby populations were subjected to selection under certain conditions, and mutations which emerged in adapted populations were analyzed using genomic approaches. The results obtained in the framework of this approach, while often useful, are not easily interpretable because mutations get fixed due to a convolution of multiple causes. We have undertaken a conceptually opposite strategy: Mutations with known biophysical and biochemical effects on E. coli's essential proteins (based on computational analysis and in vitro measurements) were introduced into the organism's chromosome and the resulted fitness effects were monitored. Studying the distribution of fitness effects of such fully controlled replacements revealed a very complex fitness landscape, where impact of the microscopic properties of the mutated proteins (folding, stability, and function) is modulated on a macroscopic, whole genome level. Furthermore, the magnitude of the cellular response to the introduced mutations seems to depend on the thermodynamic status of the mutant. [Preview Abstract] |
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