@article{3787,
abstract = {DNA samples were extracted from ethanol and formalin-fixed decapod crustacean tissue using a new method based on Tetramethylsilane (TMS)-Chelex. It is shown that neither an indigestible matrix of cross-linked protein nor soluble PCR inhibitors impede PCR success when dealing with formalin-fixed material. Instead, amplification success from formalin-fixed tissue appears to depend on the presence of unmodified DNA in the extracted sample. A staining method that facilitates the targeting of samples with a high content of unmodified DNA is provided.},
author = {Palero, Ferran and Hall, Sally and Clark, Paul and Johnston, David and Mackenzie Dodds, Jackie and Thatje, Sven},
journal = {Scientia Marina},
number = {3},
pages = {465 -- 470},
publisher = {Consejo Superior de Investigaciones Científicas},
title = {{DNA extraction from formalin-fixed tissue: new light from the deep sea}},
doi = {10.3989/scimar.2010.74n3465},
volume = {74},
year = {2010},
}
@article{4136,
abstract = {Populations living in a spatially and temporally changing environment can adapt to the changing optimum and/or migrate toward favorable habitats. Here we extend previous analyses with a static optimum to allow the environment to vary in time as well as in space. The model follows both population dynamics and the trait mean under stabilizing selection, and the outcomes can be understood by comparing the loads due to genetic variance, dispersal, and temporal change. With fixed genetic variance, we obtain two regimes: (1) adaptation that is uniform along the environmental gradient and that responds to the moving optimum as expected for panmictic populations and when the spatial gradient is sufficiently steep, and (2) a population with limited range that adapts more slowly than the environmental optimum changes in both time and space; the population therefore becomes locally extinct and migrates toward suitable habitat. We also use a population‐genetic model with many loci to allow genetic variance to evolve, and we show that the only solution now has uniform adaptation.},
author = {Polechova, Jitka and Barton, Nicholas H and Marion, Glenn},
journal = {American Naturalist},
number = {5},
pages = {E186 -- E204},
publisher = {University of Chicago Press},
title = {{Species' range: Adaptation in space and time}},
doi = {10.1086/605958},
volume = {174},
year = {2009},
}
@article{4231,
abstract = {The evolution of quantitative characters depends on the frequencies of the alleles involved, yet these frequencies cannot usually be measured. Previous groups have proposed an approximation to the dynamics of quantitative traits, based on an analogy with statistical mechanics. We present a modified version of that approach, which makes the analogy more precise and applies quite generally to describe the evolution of allele frequencies. We calculate explicitly how the macroscopic quantities (i.e., quantities that depend on the quantitative trait) depend on evolutionary forces, in a way that is independent of the microscopic details. We first show that the stationary distribution of allele frequencies under drift, selection, and mutation maximizes a certain measure of entropy, subject to constraints on the expectation of observable quantities. We then approximate the dynamical changes in these expectations, assuming that the distribution of allele frequencies always maximizes entropy, conditional on the expected values. When applied to directional selection on an additive trait, this gives a very good approximation to the evolution of the trait mean and the genetic variance, when the number of mutations per generation is sufficiently high (4Nμ > 1). We show how the method can be modified for small mutation rates (4Nμ → 0). We outline how this method describes epistatic interactions as, for example, with stabilizing selection.},
author = {Barton, Nicholas H and De Vladar, Harold},
journal = {Genetics},
number = {3},
pages = {997 -- 1011},
publisher = {Genetics Society of America},
title = {{Statistical mechanics and the evolution of polygenic quantitative traits}},
doi = {10.1534/genetics.108.099309},
volume = {181},
year = {2009},
}
@article{4242,
abstract = {Felsenstein distinguished two ways by which selection can directly strengthen isolation. First, a modifier that strengthens prezygotic isolation can be favored everywhere. This fits with the traditional view of reinforcement as an adaptation to reduce deleterious hybridization by strengthening assortative mating. Second, selection can favor association between different incompatibilities, despite recombination. We generalize this “two allele” model to follow associations among any number of incompatibilities, which may include both assortment and hybrid inviability. Our key argument is that this process, of coupling between incompatibilities, may be quite different from the usual view of reinforcement: strong isolation can evolve through the coupling of any kind of incompatibility, whether prezygotic or postzygotic. Single locus incompatibilities become coupled because associations between them increase the variance in compatibility, which in turn increases mean fitness if there is positive epistasis. Multiple incompatibilities, each maintained by epistasis, can become coupled in the same way. In contrast, a single-locus incompatibility can become coupled with loci that reduce the viability of haploid hybrids because this reduces harmful recombination. We obtain simple approximations for the limits of tight linkage, and strong assortment, and show how assortment alleles can invade through associations with other components of reproductive isolation.},
author = {Barton, Nicholas H and De Cara, Maria},
journal = {Evolution; International Journal of Organic Evolution},
number = {5},
pages = {1171 -- 1190},
publisher = {Wiley},
title = {{The evolution of strong reproductive isolation}},
doi = {10.1111/j.1558-5646.2009.00622.x},
volume = {63},
year = {2009},
}
@inbook{3675,
abstract = {Sex and recombination have long been seen as adaptations that facilitate natural selection by generating favorable variations. If recombination is to aid selection, there must be negative linkage disequilibria—favorable alleles must be found together less often than expected by chance. These negative linkage disequilibria can be generated directly by selection, but this must involve negative epistasis of just the right strength, which is not expected, from either experiment or theory. Random drift provides a more general source of negative associations: Favorable mutations almost always arise on different genomes, and negative associations tend to persist, precisely because they shield variation from selection.
We can understand how recombination aids adaptation by determining the maximum possible rate of adaptation. With unlinked loci, this rate increases only logarithmically with the influx of favorable mutations. With a linear genome, a scaling argument shows that in a large population, the rate of adaptive substitution depends only on the expected rate in the absence of interference, divided by the total rate of recombination. A two-locus approximation predicts an upper bound on the rate of substitution, proportional to recombination rate.
If associations between linked loci do impede adaptation, there can be substantial selection for modifiers that increase recombination. Whether this can account for the maintenance of high rates of sex and recombination depends on the extent of selection. It is clear that the rate of species-wide substitutions is typically far too low to generate appreciable selection for recombination. However, local sweeps within a subdivided population may be effective.},
author = {Barton, Nicholas H},
booktitle = {Cold Spring Harbor Symposia on Quantitative Biology},
pages = {187 -- 195},
publisher = {Cold Spring Harbor Laboratory Press},
title = {{Why sex and recombination? }},
doi = {10.1101/sqb.2009.74.030},
volume = {74},
year = {2009},
}