다중혈관 관상동맥 환자에서 y-문합을 이용하여 양쪽 내흉동맥만을 사용한 우회술의 조기 성적

Preface to the Princeton Landmarks in Biology Edition vii Preface xi Symbols Used xiii 1. The Importance of Islands 3 2. Area and Number of Speicies 8 3. Further Explanations of the Area-Diversity Pattern 19 4. The Strategy of Colonization 68 5. Invasibility and the Variable Niche 94 6. Stepping Stones and Biotic Exchange 123 7. Evolutionary Changes Following Colonization 145 8. Prospect 181 Glossary 185 References 193 Index 201

The Theory of Island Biogeography

So far in this course we have dealt entirely with the evolution of characters that are controlled by simple Mendelian inheritance at a single locus. There are notes on the course website about gametic disequilibrium and how allele frequencies change at two loci simultaneously, but we didn’t discuss them. In every example we’ve considered we’ve imagined that we could understand something about evolution by examining the evolution of a single gene. That’s the domain of classical population genetics. For the next few weeks we’re going to be exploring a field that’s actually older than classical population genetics, although the approach we’ll be taking to it involves the use of population genetic machinery. If you know a little about the history of evolutionary biology, you may know that after the rediscovery of Mendel’s work in 1900 there was a heated debate between the “biometricians” (e.g., Galton and Pearson) and the “Mendelians” (e.g., de Vries, Correns, Bateson, and Morgan). Biometricians asserted that the really important variation in evolution didn’t follow Mendelian rules. Height, weight, skin color, and similar traits seemed to

Human biochemical genetics

When a population experiences a reduction of its effective size, it generally develops a heterozygosity excess at selectively neutral loci, i.e., the heterozygosity computed from a sample of genes is larger than the heterozygosity expected from the number of alleles found in the sample if the population were at mutation drift equilibrium. The heterozygosity excess persists only a certain number of generations until a new equilibrium is established. Two statistical tests for detecting a heterozygosity excess are described. They require measurements of the number of alleles and heterozygosity at each of several loci from a population sample. The first test determines if the proportion of loci with heterozygosity excess is significantly larger than expected at equilibrium. The second test establishes if the average of standardized differences between observed and expected heterozygosities is significantly different from zero. Type I and II errors have been evaluated by computer simulations, varying sample size, number of loci, bottleneck size, time elapsed since the beginning of the bottleneck and level of variability of loci. These analyses show that the most useful markers for bottleneck detection are those evolving under the infinite allele model (IAM) and they provide guidelines for selecting sample sizes of individuals and loci. The usefulness of these tests for conservation biology is discussed.

https://www.genetics.org/content/genetics/144/4/2001.full.pdf

Description and Power Analysis of Two Tests for Detecting Recent Population Bottlenecks from Allele Frequency Data

Genetics and analysis of quantitative traits

Natural populations consist of phenotypically diverse individuals that exhibit variation in their demographic parameters and intra- and inter-specific interactions. Recent experimental work indicates that such variation can have significant ecological effects. However, ecological models typically disregard this variation and focus instead on trait means and total population density. Under what situations is this simplification appropriate? Why might intraspecific variation alter ecological dynamics? In this review we synthesize recent theory and identify six general mechanisms by which trait variation changes the outcome of ecological interactions. These mechanisms include several direct effects of trait variation per se and indirect effects arising from the role of genetic variation in trait evolution.

/pdf/why-intraspecific-trait-variation-matters-in-community-1t7fee0dgv.pdf

Why intraspecific trait variation matters in community ecology

Although extensive work has been done on the relationship between population size and the risk of extinction due to demographic and environmental stochasticity, the role of genetic deterioration in the extinction process is poorly understood. We develop a general theoretical approach for evaluating the risk of small populations to extinction via the accumulation of mildly deleterious mutations, and we support this with extensive computer simulations. Unlike previous attempts to model the genetic consequences of small population size, our approach is genetically explicit and fully accounts for the mutations inherited by a founder population as well as those introduced by subsequent mutation. Application of empirical estimates of the properties of spontaneous deleterious mutations leads to the conclusion that populations with effective sizes smaller than 100 (and actual sizes smaller than 1,000) are highly vulnerable to extinction via a mutational meltdown on timescales of approximately 100 generations. We ...

Mutation accumulation and the extinction of small populations

Burger has writtenan outstandingbook. As well asdiscussingselection,recombination and mutation, he explains howrandom driftinteracts withthese evolutionaryforces. Thus, his book covers a largefraction of population genetics, the mainexception being the neutral theory ofmolecular evolution. Although the book is primarily theoretical, it focuses on thebiological issues and includes excellentconcise summaries of our presentempirical knowledge. The main concern of this book, andindeed of the field as a whole, is tounderstand the processes that maintainthe abundant genetic variation that weobserve for almost all traits and in almostall populations. Related questions followfrom this central issue. How will apopulation respond to natural and artificialselection on quantitative variation? Havesex and recombination evolved becausethey facilitate natural selection?Such questions have been at the centre of evolutionary genetics since its beginning, a century ago. It issurprising that our exquisitely detailedunderstanding of genetic mechanismsgives us no solution to these questions,and shows no immediate prospect of doing so. Molecular biology has revealedphylogenetic relationships among speciesand among genes; it has provided ways ofdetecting selection on DNAsequence andon proteins; and it has shown how (at leastin principle) phenotype is determined bygenotype. But finding the effects of largenumbers of individual genetic variationson phenotype and on fitness seems adistant prospect: plans to model wholecells appear wildly overambitious

https://www.cell.com/trends/genetics/pdf/S0168-9525(01)02315-0.pdf

The Mathematical Theory of Selection, Recombination, and Mutation

Because of the ubiquity of genetic variation for quantitative traits, virtually all populations have some capacity to respond evolutionarily to selective challenges. However, natural selection imposes demographic costs on a population, and if these costs are sufficiently large, the likelihood of extinction will be high. We consider how the mean time to extinction depends on selective pressures (rate and stochasticity of environmental change, and strength of selection), population parameters (carrying capacity, and reproductive capacity), and genetics (rate of polygenic mutation). We assume that in a randomly mating, finite population subject to density-dependent population growth, individual fitness is determined by a single quantitative-genetic character under Gaussian stabilizing selection with the optimum phenotype exhibiting directional change, 'or random fluctuations, or both. The quantitative trait is de- termined by a finite number of freely recombining, mutationally equivalent, additive loci. The dynamics of evolution and extinction are investigated, assuming that the population is initially under mutation-selection-drift balance. Under this model, in a directionally changing environment, the mean phenotype lags behind the optimum, but on the average evolves parallel to it. The magnitude of the lag determines the vulnerability to extinction. In finite populations, stochastic variation in the genetic variance can be quite pronounced, and bottlenecks in the genetic variance temporarily can impair the population's adaptive capacity enough to cause extinction when it would otherwise be unlikely in an effectively infinite population. We find that maximum sustainable rates of evolution or, equivalently, critical rates of environmental change, may be considerably less than 10% of a phenotypic standard deviation per generation.

Evolution and extinction in a changing environment: a quantitative-genetic analysis.

Loss of fitness due to the accumulation of deleterious mutations appears to be inevitable in small, obligately asexual populations, as these are incapable of reconstituting highly fit genotypes by recombination or back mutation. The cumulative buildup of such mutations is expected to lead to an eventual reduction in population size, and this facilitates the chance accumulation of future mutations. This synergistic interaction between population size reduction and mutation accumulation leads to an extinction process known as the mutational meltdown, and provides a powerful explanation for the rarity of obligate asexuality. We give an overview of the theory of the mutational meltdown, showing how the process depends on the demographic properties of a population, the properties of mutations, and the relationship between fitness and number of mutations incurred.

/pdf/the-mutational-meltdown-in-asexual-populations-1twrt5sg7w.pdf

Reinhard Bürger

Papers

Why intraspecific trait variation matters in community ecology

Mutation accumulation and the extinction of small populations

The Mathematical Theory of Selection, Recombination, and Mutation

Evolution and extinction in a changing environment: a quantitative-genetic analysis.

The mutational meltdown in asexual populations