Search for more papers by this author. First published: March vinttililmelu.ga //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.
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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.
Genetic restoration: a more comprehensive perspective than "genetic rescue. Philip Hedrick, L Waits. What ancient DNA tells us.
Hedrick, Philip W. Genetics of Populations. World Book Encyclopedia C Hurt, Philip Hedrick. Conservation genetics in aquatic species. Aquatic Sciences Mating behavior in the endangered Sonoran topminnow: speciation in action. Behav Comment on "Parasite Selection for Immunogenetic Optimality. Estimation of relative fitness from relative risk data and the predicted future of hemoglobin alleles S and C.
6 editions of this work
Biol Foxy MHC selection story. Recent developments in conservation genetics. Manag Hedrick, Philip W Author. Conservation biology: The impact of population biology and a current perspective. World Book Encyclopedia, Volume 9 H Neutral, detrimental, and adaptive genetic variation in conservation genetics. Conservation Genetics in the Age of Genomics A Giese, Philip Hedrick. Genetic variation and resistance to a bacterial infection in the endangered Gila topminnow.
Cons Initial stages of reproductive isolation in two species of the endangered Sonoran topminnow. D Garrigan, Philip Hedrick. Perspective: Detecting adaptive molecular evolution, lessons from the MHC.
A heterozygote advantage.
Hopi Indians, "cultural selection", and albinism. Anthrop Canine parvovirus, canine distemper, and MHC genetic variation in Mexican wolves. Wildlife Dis A conservation plan for native fishes of the lower Colorado River. BioScience The major histocompatibility complex MHC in declining populations: an example of adaptive variation. Reproduction Science and Integrated Conservation Resistance to three pathogens in the endangered winter-run Chinook salmon: effects of inbreeding and MHC genotypes.
Lethals in finite populations. Pathogen resistance and genetic variation at MHC loci. MHC variation in red wolves: evidence for ancestry from coyotes and balancing selection. R Fredrickson, Philip Hedrick. Body size in endangered Mexican wolves: effects of captivity, inbreeding, and cross-lineage matings. Review of: Conservation Genetics Application of molecular genetics to managing endangered species. Immunogenetics Is the decline of desert bighorn sheep from infectious disease the result of low MHC variation?.
P Miller, Philip Hedrick.
Purging of inbreeding depression and fitness decline in bottlenecked populations of Drosophila melanogaster. Conservation genetics: where are we now?.
Evol Invasion of transgenes in salmon or other genetically modified organisms into natural populations. Founder effect in an island population of desert bighorn sheep. Evaluation of d2, a microsatellite measure of inbreeding, in wolves with known inbreeding. Philip Hedrick, S Kumar.
Mutation and linkage disequilibrium in human mtDNA. Parasite resistance and genetic variation in the endangered Gila topminnow. Effects of captivity and inbreeding on body size in Mexican wolves. Endangered Species Update S Kalinowski, Philip Hedrick.
Estimation of gametic disequilibrium for loci with multiple alleles: basic approach and an application using data from bighorn sheep. Inbreeding depression in captive bighorn sheep.
Genetics of Populations
MHC variation and tissue transplantation in fish. Evolutionary conservation biology. Evolutionary Ecology: Synthesis and Perspectives Genetic variation and population structure in desert bighorn sheep: Implications for conservation. J Parker, Philip Hedrick. Gene flow and selection balance in haplodiploid social insects.
Ten generic seminar questions.
Genetics of populations
Amer The impact of supplementation in winter-run chinook salmon on effective population size. Major histocompatibility complex variation in the Arabian oryx.
Major histocompatibility complex MHC variation in the endangered Mexican wolf and related canids. Philip Hedrick, S Kalinowski. Inbreeding depression and conservation biology. Syst Establishing a captive broodstock for an endangered species: Bonytail chub Gila elegans as a case study.
Effective population size in returning winter run chinook salmon. Aquat Inbreeding depression in the Speke's gazelle captive breeding program.
Genetics of Populations
Linkage disequilibrium and human mtDNA recombination. Populations structure in desert bighorn sheep: Implications for conservation in Arizona. Genetics, Demography, and Viability of Fragmented Populations Application of population genetics and molecular techniques to conservation.
Selection and genetic polymorphism: Introductory remarks. Evolutionary Genetics: From Molecules to Morphology Culver, M. Estimation of the bottleneck size in Florida panthers. Cons 0. Hedrick, p. East Asian ancestry in Polynesians. Amer J Hum Genet 0. Neutral, detrimental, and adaptive variation in conservation genetics. Conservation Genetics in the Age of Genomics 0. Conservation Genetics of Arizona Talussnails. Presentations Phil Hedrick.
Adaptive introgression and genetic rescue. Society for Molecular Biology and Evolution Jul Phil Hedrick. Genetic rescue in Isle Royale Wolves. Symposium at Conservation Biology Meeting Jul Bighorn sheep genetics and small population size. Desert bighorn Council Apr Conservation genetics: recent developments. Inbreeding and conservation in Navajo-Churro sheep. Annual meeting of Navajo-Churro sheep association Sep Population Genetics of Malaria Resistance in Medicine.
Conservation genetics. Bison and cattle ancestry. Recent devalopments in conservation genetics. University lecture at Donana in Seville, Spain Feb Global change and infectious disease.
Measuring population structure. Evolution and Conservation Genetics. Evolution Meeting at Emmental Switzerland Jun Conservation Genetics. Lecture at Univ. Uppsala, Sweden May Zurich, Zwitzerland May Measures of genetic differentiation. MHC and effects on mate choice in endangered species. University lecture at Univ Costa Rica Mar Conservation Genetics and North American Bison.
Hedrick and R.
Genetic Rescue and Hybridization. Population genetics and theory. Physics seminar at ASU Apr San Diego Nov Interior in Nebraska City, Nebraska Sep UC Davis May Hedrick, Philip.
Effective population size in conservation. Symposium speaker at 33rd Natural Areas Conference Sep Measuring diversity among breeds and populations.
Washington May Population size. Invited seminar Sep Recent Developments in Evolutionary Genetics. Seminar in Wildlife and Biology Departments Sep Invited talk Jun Seminar in Biology Department Jun 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.
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.
In addition, both premating and postmating reproductive isolation between Gila and Yaqui topminnows have been experimentally determined, and the predicted and observed ancestry of these two species in experimental crosses has been examined over time.
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. Paul Hedrick, Philip. Motivation This is, most of all, not a book about R. Conservation Genetics Genetic population substructure in bison in Yellowstone National Park. March