Search for more papers by this author. First published: March //aaa About. Related; Information. ePDF PDF. Trove: Find and get Australian resources. Books, images, historic newspapers, maps, archives and more. byPhilip W. Hedrick. Publication date Topics Population genetics, Genetics, Population Borrow this book to access EPUB and PDF files.

Genetics Of Populations Hedrick Pdf

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Population Genetics and Ecology. Philip Hedrick. OUTLINE. 1. Introduction. 2. Genetic drift and effective population size. 3. Neutral theory. 4. Gene flow and. Request PDF on ResearchGate | Genetics of Populations (2nd edn) | Some drift (Crow and Kimura, ; Frankham, ; Hedrick, ). Fill Genetics Of Populations Hedrick Pdf, download blank or editable online. Sign , fax and printable from PC, iPad, tablet or mobile with PDFfiller ✓ Instantly.

Minckley and Deacon detailed the effects of many of these factors on the native fishes of the arid western United States in the same period see also Minckley and Marsh Because of the limited geographic distribution for many aquatic species in arid lands, they are particularly susceptible to habitat degradation and fragmentation, introduced non-natives species, and other factors potentially causing population declines and extinction.

Genetics Of Populations

Conservation biology was developed to understand the processes influencing extinction. Genetics has been an important focus of conservation biology because it helps determine the evolutionary context of endangered species and enables the development of better management strategies.

Genetic variation interpreted in a population genetics context can be used to reconstruct the evolutionary history, examine the contemporary status, and predict the future of endangered species. Overall, the framework of evolutionary genetics theory furnishes an elegant approach to interpret the measured amounts of genetic variation and predict the future effects of evolutionary factors and management strategies.

Model organisms have sometimes been used to examine the bases of conservation management approaches. In particular, some experiments using the fruitfly Drosophila have compared different management options; however, these experiments appear to be of rather limited use in vertebrate conservation genetics.

Although such fruitfly laboratory experiments may serve a useful heuristic purpose to illustrate evolutionary genetics principles or management options, it seems unlikely that laboratory experiments on insects with a history of a very large population size will provide new insight into conservation of endangered species, most of which are vertebrates with small population size, have a history of declining numbers, might have important social and mating structures, and so on.

Furthermore, if laboratory experiments on a model organism give counterintuitive findings, those results are probably only relevant to the model organism that is being used and not for endangered species in general. Some have suggested that endangered species themselves are unsuitable for experimentation because of both practical and ethical considerations.

However, experimentation has been possible on several endangered species, for example the Gila and Yaqui topminnows discussed below, Pacific salmon Arkush et al.

This tracking allows an understanding of details about movement, mating, life history, etc. Below, we will present a review of the extensive research on two species of the endangered Sonoran topminnow, the Gila and the Yaqui topminnow, most of which was conducted by us and our colleagues.

Our research includes both empirical observation and laboratory experimentation, which we were able to do because we had permission to collect small numbers of fish, bring them into the laboratory, increase their numbers, and provide refugia for them. We were then allowed to carry out experiments on excess fish following approved protocols.

Although we do not consider these fish as a model organism, they do have some attributes of one, that is, good survival and reproduction under appropriate laboratory conditions, short generation length, small size, etc.

However, we feel that extreme care should be taken when generalizing our results from topminnows to other endangered species. As an organizational theme for our evaluation of evolutionary and conservation genetics in Gila and Yaqui topminnows, three major types of genetic variation — neutral, detrimental, and adaptive — can be used Hedrick We first review theory about what to expect from mutation and selection in a population of finite size and generate predictions based on simulations using a plausible demographic scenario of recent human evolution.

For a highly mutable type of mutation, transitions at CpG sites, we find that the predictions are close to the observed frequencies of recessive lethal disease mutations.

For less mutable types, however, predictions substantially under-estimate the observed frequency. We discuss possible explanations for the discrepancy and point to a complication that, to our knowledge, is not widely appreciated: that there exists ascertainment bias in disease mutation discovery. Specifically, we suggest that alleles that have been identified to date are likely the ones that by chance have reached higher frequencies and are thus more likely to have been mapped.

More generally, our study highlights the factors that influence the frequencies of Mendelian disease alleles. Introduction New disease mutations arise in heterozygotes and either drift to higher frequencies or are rapidly purged from the population, depending on the strength of selection and the demographic history of the population [ 1 — 6 ].

Elucidating the relative contributions of mutation, natural selection and genetic drift will help to understand why disease alleles persist in humans.

Genetics of Populations (2nd edn)

Answers to these questions are also of practical importance, in informing how genetic variation data can be used to identify additional disease mutations [ 7 ]. In this regard, rare, Mendelian diseases, which are caused by single highly penetrant and deleterious alleles, are perhaps most amenable to investigation.

A simple model for the persistence of mutations that lead to Mendelian diseases is that their frequencies reflect an equilibrium between their introduction by mutation and elimination by purifying selection, i. In finite populations, random drift leads to stochastic changes in the frequency of any mutation, so demographic history, in addition to mutation and natural selection, plays an important role in shaping the frequency distribution of deleterious mutations [ 3 ].

Another factor that may be important in determining the frequencies of highly penetrant disease mutations is genetic interactions.

The mutation-selection balance model has been extended to scenarios with more than one disease allele, as is often seen for Mendelian diseases [ 8 , 9 ]. When compound heterozygotes have the same fitness as homozygotes for the disease allele i. In other cases, a disease mutation may be rescued by another mutation in the same gene [ 10 — 12 ] or by a modifier locus elsewhere in the genome that modulates the severity of the disease symptoms or the penetrance of the disease allele e.

For a subset of disease alleles that are recessive, an alternative model for their persistence in the population is that there is an advantage to carrying one copy but a disadvantage to carrying two or none, such that the alleles persist due to overdominance, a form of balancing selection.

Well known examples include sickle cell anemia, thalassemia and G6PD deficiency in populations living where malaria exerts strong selection pressures [ 16 ].

The importance of overdominance in maintaining the high frequency of disease mutations is unknown beyond these specific cases. Here, we tested hypotheses about the persistence of mutations that cause lethal, recessive, Mendelian disorders. This case provides a good starting point, because a large number of Mendelian disorders have been mapped e. Moreover, while the fitness effects of most diseases are hard to estimate, for recessive lethal diseases, the selection coefficient is clearly 1 for homozygote carriers in the absence of modern medical care which, when available, became so only in the last couple of generations, a timescale that is much too short to substantially affect disease allele frequencies.


Thus, sample sizes in human genetics are now sufficiently large that we should be able to observe completely recessive, lethal disease alleles segregating in heterozygote carriers. To this end, we compiled genetic information for a set of mutations reported to cause fatal, recessive Mendelian diseases and estimated the frequencies of the disease-causing alleles from large exome datasets.

We then compared these data to the expected frequencies of deleterious alleles based on models of mutation-selection balance in order to evaluate the effects of mutation rates and other factors in influencing these frequencies.

Based on clinical genetics datasets and the medical literature see Methods for details , we were able to confirm that Single Nucleotide Variants SNVs in 32 of the 44 genes had been reported with compelling evidence of association to the severe form of the corresponding disease and an early-onset, as well as no indication of effects in heterozygote carriers S2 Table. By this approach, we obtained a set of mutations for which, at least in principle, there is no heterozygote effect, i.Virgin birth, genetic variation, and inbreeding.

Paige Dyer marked it as to-read Aug 19, Society for Molecular Biology and Evolution Jul Loeschcke, C. Estimation of gametic disequilibrium for loci with multiple alleles: basic approach and an application using data from bighorn sheep.

Dec 30, Sarah rated it liked it Shelves: Trends Genet. Genetics has been an important focus of conservation biology because it helps determine the evolutionary context of endangered species and enables the development of better management strategies. The major topics covered include; measures of diversity, selection theory, inbreeding, genetic drift, effective population size, gene flow, population structure and metapopulations, mutation, molecular population genetics including phylogenetic tree building , multiple gene models and linkage disequilibrium, and quantitative genetics including modern QTL techniques.

Genetics, Demography, and Viability of Fragmented Populations

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