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Journal ArticleDOI

Ising quantum chain is equivalent to a model of biological evolution

Ellen Baake, +2 more
- 20 Jan 1997 - 
- Vol. 78, Iss: 3, pp 559-562
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TLDR
A problem of biochemical physics that may be mapped exactly onto a quantum chain is presented that can be solved without approximation and describes mutation and selection as going on in parallel.
Abstract
One-dimensional systems, and quantum chains in particular, have long been important tools to understand, at least approximately, various physical situations, and there is even a recipe “how to reduce practically any problem to one dimension” [1]. As a complement, we present a problem of biochemical physics that may be mapped exactly onto a quantum chain. Selected examples can then be solved without approximation. In the theory of (molecular) biological evolution, various sequence space models are well established, the best known being Kauffman’s adaptive walk [2] and Eigen’s quasispecies model [3]. Whereas the former describes a hill-climbing process of a genetically homogeneous population in tunably rugged fitness landscapes, the latter includes the genetic structure of the population due to the balance between mutation and selection. For equal fitness landscapes, the quasispecies model is thus more difficult to treat than the corresponding adaptive walk. Some progress was made in [4] through the identification of the quasispecies model with a specific, anisotropic 2D Ising model: The mutation-selection matrix is equivalent to the row transfer matrix, with the mutation probability as a temperaturelike parameter, and error thresholds corresponding to phase transitions. This equivalence was exploited to treat simple fitness landscapes as well as spin-glass Hamiltonians with methods from statistical mechanics [5–7]. Of these results, most are approximate or numerical, and the few exact ones in [5] are of limited value as the order parameter was not calculated correctly. The quasispecies model assumes mutations to originate as replication errors on the occasion of reproduction events. An alternative was introduced in [8] and describes mutation and selection as going on in parallel; we would like to abbreviate it as para-muse (parallel mutation selection) model. In subsequent investigations [9,10], this model turned out to be both more powerful and structurally simpler than the quasispecies model. Which is the more appropriate one from the biological point of view amounts to the question

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Citations
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Journal ArticleDOI

An introduction to critical points for biophysicists; observations of compositional heterogeneity in lipid membranes.

TL;DR: This work reports that lipid membranes can contain composition fluctuations that behave in a manner consistent with the two-dimensional Ising universality class, and reviews other models describing submicron lateral inhomogeneity in membranes, including microemulsions, nanodomains, and mean field critical fluctuations.
Journal ArticleDOI

On the application of statistical physics to evolutionary biology.

TL;DR: An entropy, S(Omega), is defined, which measures the volume of allele frequency space that is consistent with the observed trait distribution, and justifies a maximum entropy approximation to the dynamics of quantitative traits.
Journal ArticleDOI

Mutation-selection balance: ancestry, load, and maximum principle.

TL;DR: The results are applied to threshold phenomena caused by the interplay of selection and mutation (known as error thresholds) and lead to a clarification of concepts, as well as criteria for the existence of error thresholds.
Journal ArticleDOI

On the Selection and Evolution of Regulatory DNA Motifs

TL;DR: In this article, the authors constructed an explicit model for the evolution of regulatory sequences, making use of the known biophysics of the binding of regulatory proteins to DNA sequences, under the assumption that fitness of a sequence depends only on its binding affinity to the regulatory protein.
Journal ArticleDOI

Mutational pathway determines whether drug gradients accelerate evolution of drug-resistant cells.

TL;DR: It is shown that a nonuniform drug distribution has the potential to accelerate the emergence of resistance when the mutational pathway involves a long sequence of mutants with increasing resistance, but if the pathway is short or crosses a fitness valley, the evolution of resistance may actually be slowed down by drug gradients.
References
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Book

The Origins of Order: Self-Organization and Selection in Evolution

TL;DR: The structure of rugged fitness landscapes and the structure of adaptive landscapes underlying protein evolution, and the architecture of genetic regulatory circuits and its evolution.
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