C H Taubes

Harvard University, Cambridge, MA, United States

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Publications (2)4.05 Total impact

  • D L Hartl, C H Taubes
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    ABSTRACT: Most theoretical models in population genetics fail to deal in a realistic manner with the process of mutation. They are consequently not informative about the central evolutionary problem of the origin, progression, and limit of adaptation. Here we present an explicit distribution of phenotypes expected in an ensemble of populations under a mutation-selection-drift model that allows mutations with a distribution of adaptive values to occur randomly in time. The model of mutation is a geometrical model in which the effect of a new mutation is determined by a random angle in n dimensional space and in which the adaptive value (fitness) of an organism decreases as the square of the deviation of its phenotype from an optimum. Each new mutation is subjected to random genetic drift and fixed or lost according to its selective value and the effective population number. Time is measured in number of fixation events, so that, at any point in time, each population is regarded as genetically homogeneous. In this mutation-selection-drift model, among an ensemble of populations, the equilibrium average phenotype coincides with the optimum because the distribution of positive and negative deviations from the optimum is symmetrical. However, at equilibrium the mean of the absolute value of the deviation from the optimum equals square root of n-/8Ns), where n is the dimensionality of the trait space, N is the effective population size, and s is the selection coefficient against a mutation whose phenotype deviates by one unit from the optimum. Furthermore, at equilibrium, the average fitness across the ensemble of populations equals 1 - (n + 1)/8N. When n is sufficiently large, there is a strong mutation pressure toward the fixation of slightly deleterious mutations. This feature relates our model to the nearly neutral theory of molecular evolution.
    Genetica 02/1998; 102-103(1-6):525-33. · 1.75 Impact Factor
  • D L Hartl, C H Taubes
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    ABSTRACT: One implication of Kacser's analysis of complex metabolic systems is that mutations with small effects exist as a consequence of the typically small flux control coefficient relating enzyme activity to the rate of a metabolic process. Although a slightly detrimental mutation is somewhat less likely to become fixed by chance than a slightly favorable mutation, mutations that are slightly detrimental might be expected to be more numerous than favorable mutations owing to the previous incorporation of favorable mutations by a long history of natural selection. The result is that, as Ohta has pointed out, a significant fraction of mutations that are fixed in evolution are slightly detrimental. In the long run, the fixation of detrimental mutations in a gene increases the opportunity for the occurrence of a compensatory favorable mutation, either in the same gene or in an interacting gene. On a suitably long timescale, therefore, every gene incorporates favorable mutations that compensate for detrimental mutations previously fixed. This form of evolution is driven primarily by natural selection, but it results in no change or permanent improvement in enzymatic function.
    Journal of Theoretical Biology 11/1996; 182(3):303-9. · 2.30 Impact Factor

Publication Stats

127 Citations
4.05 Total Impact Points

Top co-authors


  • 1996–1998
    • Harvard University
      • Department of Organismic and Evolutionary Biology
      Cambridge, MA, United States