Wikia

Psychology Wiki

Population genetics

Talk0
34,117pages on
this wiki

Assessment | Biopsychology | Comparative | Cognitive | Developmental | Language | Individual differences | Personality | Philosophy | Social |
Methods | Statistics | Clinical | Educational | Industrial | Professional items | World psychology |

Biological: Behavioural genetics · Evolutionary psychology · Neuroanatomy · Neurochemistry · Neuroendocrinology · Neuroscience · Psychoneuroimmunology · Physiological Psychology · Psychopharmacology (Index, Outline)


Population genetics is the study of the allele frequency distribution and change under the influence of the four evolutionary processes: natural selection, genetic drift, mutation and gene flow. It also takes account of population subdivision and population structure in space. As such, it attempts to explain such phenomena as adaptation and speciation. Population genetics was a vital ingredient in the modern evolutionary synthesis, its primary founders were Sewall Wright, J. B. S. Haldane and R. A. Fisher, who also laid the foundations for the related discipline of quantitative genetics.

FundamentalsEdit

Population genetics concerns the genetic constitution of populations and how this constitution changes with time.

A population is a localized group of individuals belonging to the same species. For example, all of the moths of the same species living in an isolated forest represent a population. A single gene in this population may have several alternate forms, which account for variations between the phenotypes of the organisms. An example might be a gene for coloration in moths that has two alleles: black and white. A gene pool is the complete set of alleles for a gene in a single population; the allele frequency measures the fraction of the gene pool composed of a single allele (for example, what fraction of moth coloration genes are the black allele). Evolution occurs when there are changes in the frequencies of alleles within a population of interbreeding organisms; for example, the allele for black color in a population of moths becoming more common.

To understand the mechanisms that cause a population to evolve, it is useful to consider what conditions are required for a population not to evolve. The Hardy-Weinberg principle states that the frequencies of alleles (variations in a gene) in a sufficiently large population will remain constant if the only forces acting on that population are the random reshuffling of alleles during the formation of the sperm or egg, and the random combination of the alleles in these sex cells during fertilization.[1] Such a population is said to be in Hardy-Weinberg equilibrium; it is not evolving.[2]

File:Hardy-Weinberg.svg
Hardy–Weinberg principle for two alleles: the horizontal axis shows the two allele frequencies p and q and the vertical axis shows the genotype frequencies. Each graph shows one of the three possible genotypes.

Hardy–Weinberg principleEdit

Main article: Hardy–Weinberg principle

The Hardy–Weinberg principle states that both allele and genotype frequencies in a population remain constant—that is, they are in equilibrium—from generation to generation unless specific disturbing influences are introduced. Outside the lab, one or more of these "disturbing influences" are always in effect. That is, Hardy Weinberg equilibrium is impossible in nature. Genetic equilibrium is an ideal state that provides a baseline to measure genetic change against.

Allele frequencies in a population remain static across generations, provided the following conditions are at hand: random mating, no mutation (the alleles don't change), no migration or emigration (no exchange of alleles between populations), infinitely large population size, and no selective pressure for or against any traits.

In the simplest case of a single locus with two alleles: the dominant allele is denoted A and the recessive a and their frequencies are denoted by p and q; freq(A) = p; freq(a) = q; p + q = 1. If the population is in equilibrium, then we will have freq(AA) = p2 for the AA homozygotes in the population, freq(aa) = q2 for the aa homozygotes, and freq(Aa) = 2pq for the heterozygotes.

Based on these equations, we can determine useful but difficult-to-measure facts about a population. For example, a patient's child is a carrier of a recessive mutation that causes cystic fibrosis in homozygous recessive children. The parent wants to know the probability of her grandchildren inheriting the disease. In order to answer this question, the genetic counselor must know the chance that the child will reproduce with a carrier of the recessive mutation. This fact may not be known, but disease frequency is known. We know that the disease is caused by the homozygous recessive genotype; we can use the Hardy–Weinberg principle to work backward from disease occurrence to the frequency of heterozygous recessive individuals.

Scope and theoretical considerationsEdit

The mathematics of population genetics were originally developed as part of the modern evolutionary synthesis. According to Beatty (1986), for example, it defines the core of the modern synthesis.

According to Lewontin (1974) the theoretical task for population genetics is a process in two spaces: a "genotypic space" and a "phenotypic space". The challenge of a complete theory of population genetics is to provide a set of laws that predictably map a population of genotypes (G1) to a phenotype space (P1), where selection takes place, and another set of laws that map the resulting population (P2) back to genotype space (G2) where Mendelian genetics can predict the next generation of genotypes, thus completing the cycle. Even leaving aside for the moment the non-Mendelian aspects of molecular genetics, this is clearly a gargantuan task. Visualizing this transformation schematically:

G_1 \; \stackrel{T_1}{\rightarrow} \; P_1 \; \stackrel{T_2}{\rightarrow} \; P_2 \; \stackrel{T_3}{\rightarrow} \; G_2 \;
\stackrel{T_4}{\rightarrow} \; G_1' \; \rightarrow \cdots

(adapted from Lewontin 1974, p. 12). XD

T1 represents the genetic and epigenetic laws, the aspects of functional biology, or development, that transform a genotype into phenotype. We will refer to this as the "genotype-phenotype map". T2 is the transformation due to natural selection, T3 are epigenetic relations that predict genotypes based on the selected phenotypes and finally T4 the rules of Mendelian genetics.

In practice, there are two bodies of evolutionary theory that exist in parallel, traditional population genetics operating in the genotype space and the biometric theory used in plant and animal breeding, operating in phenotype space. The missing part is the mapping between the genotype and phenotype space. This leads to a "sleight of hand" (as Lewontin terms it) whereby variables in the equations of one domain, are considered parameters or constants, where, in a full-treatment they would be transformed themselves by the evolutionary process and are in reality functions of the state variables in the other domain. The "sleight of hand" is assuming that we know this mapping. Proceeding as if we do understand it is enough to analyze many cases of interest. For example, if the phenotype is almost one-to-one with genotype (sickle-cell disease) or the time-scale is sufficiently short, the "constants" can be treated as such; however, there are many situations where it is inaccurate.

The four processesEdit

Natural selectionEdit

Main article: Natural selection

Natural selection is the process by which heritable traits that make it more likely for an organism to survive and successfully reproduce become more common in a population over successive generations.

The natural genetic variation within a population of organisms means that some individuals will survive more successfully than others in their current environment. Factors which affect reproductive success are also important, an issue which Charles Darwin developed in his ideas on sexual selection.

Natural selection acts on the phenotype, or the observable characteristics of an organism, but the genetic (heritable) basis of any phenotype which gives a reproductive advantage will become more common in a population (see allele frequency). Over time, this process can result in adaptations that specialize organisms for particular ecological niches and may eventually result in the emergence of new species.

Natural selection is one of the cornerstones of modern biology. The term was introduced by Darwin in his groundbreaking 1859 book On the Origin of Species,[3] in which natural selection was described by analogy to artificial selection, a process by which animals and plants with traits considered desirable by human breeders are systematically favored for reproduction. The concept of natural selection was originally developed in the absence of a valid theory of heredity; at the time of Darwin's writing, nothing was known of modern genetics. The union of traditional Darwinian evolution with subsequent discoveries in classical and molecular genetics is termed the modern evolutionary synthesis. Natural selection remains the primary explanation for adaptive evolution.

Genetic driftEdit

Main article: Genetic drift

Genetic drift is the change in the relative frequency in which a gene variant (allele) occurs in a population due to random sampling and chance: The alleles in offspring are a random sample of those in the parents, and chance has a role in determining whether a given individual survives and reproduces. A population's allele frequency is the fraction of the gene copies that share a particular form.[4]

Genetic drift is an important evolutionary process which leads to changes in allele frequencies over time. It may cause gene variants to disappear completely, and thereby reduce genetic variability. In contrast to natural selection, which makes gene variants more common or less common depending on their reproductive success,[5] the changes due to genetic drift are not driven by environmental or adaptive pressures, and may be beneficial, neutral, or detrimental to reproductive success.

The effect of genetic drift is larger in small populations, and smaller in large populations. Vigorous debates wage among scientists over the relative importance of genetic drift compared with natural selection. Ronald Fisher held the view that genetic drift plays at the most a minor role in evolution, and this remained the dominant view for several decades. In 1968 Motoo Kimura rekindled the debate with his neutral theory of molecular evolution which claims that most of the changes in the genetic material are caused by genetic drift.[6]

MutationEdit

Main article: Mutation

Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.[7][8][9] Errors are introduced particularly often in the process of DNA replication, in the polymerization of the second strand. These errors. They can also be induced by the organism itself, by cellular processes such as hypermutation.

Mutations can have an impact on the phenotype of an organism, especially if they occur within the protein coding sequence of a gene. Error rates are usually very low—1 error in every 10 million–100 million bases—due to the "proofreading" ability of DNA polymerases.[10][11] Without proofreading, error rates are a thousand-fold higher. Chemical damage to DNA occurs naturally as well, and cells use DNA repair mechanisms to repair mismatches and breaks in DNA. Nevertheless, the repair sometimes fails to return the DNA to its original sequence.

In organisms that use chromosomal crossover to exchange DNA and recombine genes, errors in alignment during meiosis can also cause mutations.[12] Errors in crossover are especially likely when similar sequences cause partner chromosomes to adopt a mistaken alignment; this makes some regions in genomes more prone to mutating in this way. These errors create large structural changes in DNA sequence—duplications, inversions or deletions of entire regions, or the accidental exchanging of whole parts between different chromosomes (called translocation).

Mutation can result in several different types of change in DNA sequences; these can either have no effect, alter the product of a gene, or prevent the gene from functioning. Studies in the fly Drosophila melanogaster suggest that if a mutation changes a protein produced by a gene, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[13] Due to the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as DNA repair to remove mutations.[7] Therefore, the optimal mutation rate for a species is a trade-off between costs of a high mutation rate, such as deleterious mutations, and the metabolic costs of maintaining systems to reduce the mutation rate, such as DNA repair enzymes.[14] Viruses that use RNA as their genetic material have rapid mutation rates,[15] which can be an advantage since these viruses will evolve constantly and rapidly, and thus evade the defensive responses of e.g. the human immune system.[16]

Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.[17] These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.[18] Most genes belong to larger families of genes of shared ancestry.[19] Novel genes are produced by several methods, commonly through the duplication and mutation of an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[20][21] Here, domains act as modules, each with a particular and independent function, that can be mixed together to produce genes encoding new proteins with novel properties.[22] For example, the human eye uses four genes to make structures that sense light: three for color vision and one for night vision; all four arose from a single ancestral gene.[23] Another advantage of duplicating a gene (or even an entire genome) is that this increases redundancy; this allows one gene in the pair to acquire a new function while the other copy performs the original function.[24][25] Other types of mutation occasionally create new genes from previously noncoding DNA.[26][27]

Gene flowEdit

Main article: Gene flow

Gene flow is the exchange of genes between populations, which are usually of the same species.[28] Examples of gene flow within a species include the migration and then breeding of organisms, or the exchange of pollen. Gene transfer between species includes the formation of hybrid organisms and horizontal gene transfer.

Migration into or out of a population can change allele frequencies, as well as introducing genetic variation into a population. Immigration may add new genetic material to the established gene pool of a population. Conversely, emigration may remove genetic material. As barriers to reproduction between two diverging populations are required for the populations to become new species, gene flow may slow this process by spreading genetic differences between the populations. Gene flow is hindered by mountain ranges, oceans and deserts or even man-made structures such as the Great Wall of China, which has hindered the flow of plant genes.[29]

Depending on how far two species have diverged since their most recent common ancestor, it may still be possible for them to produce offspring, as with horses and donkeys mating to produce mules.[30] Such hybrids are generally infertile, due to the two different sets of chromosomes being unable to pair up during meiosis. In this case, closely related species may regularly interbreed, but hybrids will be selected against and the species will remain distinct. However, viable hybrids are occasionally formed and these new species can either have properties intermediate between their parent species, or possess a totally new phenotype.[31] The importance of hybridization in creating new species of animals is unclear, although cases have been seen in many types of animals,[32] with the gray tree frog being a particularly well-studied example.[33]

Hybridization is, however, an important means of speciation in plants, since polyploidy (having more than two copies of each chromosome) is tolerated in plants more readily than in animals.[34][35] Polyploidy is important in hybrids as it allows reproduction, with the two different sets of chromosomes each being able to pair with an identical partner during meiosis.[36] Polyploids also have more genetic diversity, which allows them to avoid inbreeding depression in small populations.[37]

Horizontal gene transfer is the transfer of genetic material from one organism to another organism that is not its offspring; this is most common among bacteria.[38] In medicine, this contributes to the spread of antibiotic resistance, as when one bacteria acquires resistance genes it can rapidly transfer them to other species.[39] Horizontal transfer of genes from bacteria to eukaryotes such as the yeast Saccharomyces cerevisiae and the adzuki bean beetle Callosobruchus chinensis may also have occurred.[40][41] An example of larger-scale transfers are the eukaryotic bdelloid rotifers, which appear to have received a range of genes from bacteria, fungi, and plants.[42] Viruses can also carry DNA between organisms, allowing transfer of genes even across biological domains.[43] Large-scale gene transfer has also occurred between the ancestors of eukaryotic cells and prokaryotes, during the acquisition of chloroplasts and mitochondria.[44]


Gene flow is the transfer of alleles from one population to another.

Migration into or out of a population may be responsible for a marked change in allele frequencies. Immigration may also result in the addition of new genetic variants to the established gene pool of a particular species or population.

There are a number of factors that affect the rate of gene flow between different populations. One of the most significant factors is mobility, as greater mobility of an individual tends to give it greater migratory potential. Animals tend to be more mobile than plants, although pollen and seeds may be carried great distances by animals or wind.

Maintained gene flow between two populations can also lead to a combination of the two gene pools, reducing the genetic variation between the two groups. It is for this reason that gene flow strongly acts against speciation, by recombining the gene pools of the groups, and thus, repairing the developing differences in genetic variation that would have led to full speciation and creation of daughter species.

For example, if a species of grass grows on both sides of a highway, pollen is likely to be transported from one side to the other and vice versa. If this pollen is able to fertilise the plant where it ends up and produce viable offspring, then the alleles in the pollen have effectively been able to move from the population on one side of the highway to the other.

Genetic structureEdit

Because of physical barriers to migration, along with limited vagility, and natal philopatry, natural populations are rarely panmictic (Buston et al., 2007). There is usually a geographic range within which individuals are more closely related to one another than those randomly selected from the general population. This is described as the extent to which a population is genetically structured (Repaci et al., 2007).

Microbial population geneticsEdit

Microbial population genetics is a rapidly advancing field of investigation with relevance to many other theoretical and applied areas of scientific investigations. The population genetics of microorganisms lays the foundations for tracking the origin and evolution of antibiotic resistance and deadly infectious pathogens. Population genetics of microorganisms is also an essential factor for devising strategies for the conservation and better utilization of beneficial microbes (Xu, 2010).

HistoryEdit

Biston betularia f. typica is the white-bodied form of the peppered moth.
 
Biston betularia f. carbonaria is the black-bodied form of the peppered moth.

Population geneticsEdit

The Mendelian and biometrician models were eventually reconciled, when population genetics] was developed. A key step was the work of the British biologist and statistician R.A. Fisher. In a series of papers starting in 1918 and culminating in his 1930 book The Genetical Theory of Natural Selection, Fisher showed that the continuous variation measured by the biometricians could be produced by the combined action of many discrete genes, and that natural selection could change gene frequencies in a population, resulting in evolution. In a series of papers beginning in 1924, another British geneticist, J.B.S. Haldane, applied statistical analysis to real-world examples of natural selection, such as the evolution of industrial melanism in peppered moths, and showed that natural selection worked at an even faster rate than Fisher assumed.[45][46]

The American biologist Sewall Wright, who had a background in animal breeding experiments, focused on combinations of interacting genes, and the effects of inbreeding on small, relatively isolated populations that exhibited genetic drift. In 1932, Wright introduced the concept of an adaptive landscape and argued that genetic drift and inbreeding could drive a small, isolated sub-population away from an adaptive peak, allowing natural selection to drive it towards different adaptive peaks. Fisher and Wright had some fundamental disagreements and a controversy about the relative roles of selection and drift continued for much of the century between the Americans and the British. The Frenchman Gustave Malécot was also important early in the development of the discipline.

The work of Fisher, Haldane and Wright founded the discipline of population genetics. This integrated natural selection with Mendelian genetics, which was the critical first step in developing a unified theory of how evolution worked.[45][46]

John Maynard Smith was Haldane's pupil, whilst W.D. Hamilton was heavily influenced by the writings of Fisher. The American George R. Price worked with both Hamilton and Maynard Smith. American Richard Lewontin and Japanese Motoo Kimura were heavily influenced by Wright.

Modern evolutionary synthesisEdit

In the first few decades of the 20th century, most field naturalists continued to believe that Lamarckian and orthogenic mechanisms of evolution provided the best explanation for the complexity they observed in the living world. However, as the field of genetics continued to develop, those views became less tenable.[47] Theodosius Dobzhansky, a postdoctoral worker in T. H. Morgan's lab, had been influenced by the work on genetic diversity by Russian geneticists such as Sergei Chetverikov. He helped to bridge the divide between the foundations of microevolution developed by the population geneticists and the patterns of macroevolution observed by field biologists, with his 1937 book Genetics and the Origin of Species. Dobzhansky examined the genetic diversity of wild populations and showed that, contrary to the assumptions of the population geneticists, these populations had large amounts of genetic diversity, with marked differences between sub-populations. The book also took the highly mathematical work of the population geneticists and put it into a more accessible form. In Great Britain E.B. Ford, the pioneer of ecological genetics, continued throughout the 1930s and 1940s to demonstrate the power of selection due to ecological factors including the ability to maintain genetic diversity through genetic polymorphisms such as human blood types. Ford's work would contribute to a shift in emphasis during the course of the modern synthesis towards natural selection over genetic drift.[45][46][48][49]

See alsoEdit

.

ReferencesEdit

  1. O'Neil, Dennis (2008). Hardy-Weinberg Equilibrium Model. The synthetic theory of evolution: An introduction to modern evolutionary concepts and theories. Behavioral Sciences Department, Palomar College. URL accessed on 2008-01-06.
  2. Bright, Kerry (2006). Causes of evolution. Teach Evolution and Make It Relevant. National Science Foundation. URL accessed on 2007-12-30.
  3. Darwin C (1859) On the Origin of Species by Means of Natural Selection, or the Preservation of Favoured Races in the Struggle for Life John Murray, London; modern reprint Charles Darwin, Julian Huxley (2003). The Origin of Species, Signet Classics. Published online at The complete work of Charles Darwin online: On the origin of species by means of natural selection, or the preservation of favoured races in the struggle for life.
  4. Futuyma, Douglas (1998). Evolutionary Biology, Sinauer Associates.
  5. Avers, Charlotte (1989), Process and Pattern in Evolution, Oxford University Press 
  6. Futuyma, Douglas (1998). Evolutionary Biology, Sinauer Associates.
  7. 7.0 7.1 Bertram J (2000). The molecular biology of cancer. Mol. Aspects Med. 21 (6): 167–223.
  8. Aminetzach YT, Macpherson JM, Petrov DA (2005). Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila. Science 309 (5735): 764–7.
  9. Burrus V, Waldor M (2004). Shaping bacterial genomes with integrative and conjugative elements. Res. Microbiol. 155 (5): 376–86.
  10. (2000) "Spontaneous mutations" An Introduction to Genetic Analysis, 7th, New York: W. H. Freeman.
  11. (2004). Lesion (in)tolerance reveals insights into DNA replication fidelity.. The EMBO journal 23 (7): 1494–505.
  12. (2000) "Chromosome Mutation I: Changes in Chromosome Structure: Introduction" An Introduction to Genetic Analysis, 7th, New York: W. H. Freeman.
  13. Sawyer SA, Parsch J, Zhang Z, Hartl DL (2007). Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila. Proc. Natl. Acad. Sci. U.S.A. 104 (16): 6504–10.
  14. Sniegowski P, Gerrish P, Johnson T, Shaver A (2000). The evolution of mutation rates: separating causes from consequences. Bioessays 22 (12): 1057–66.
  15. Drake JW, Holland JJ (1999). Mutation rates among RNA viruses. Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13910–3.
  16. Holland J, Spindler K, Horodyski F, Grabau E, Nichol S, VandePol S (1982). Rapid evolution of RNA genomes. Science 215 (4540): 1577–85.
  17. Hastings, P J (2009). Mechanisms of change in gene copy number. Nature Reviews. Genetics 10 (8): 551–564.
  18. Carroll SB, Grenier J, Weatherbee SD (2005). From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design. Second Edition, Oxford: Blackwell Publishing.
  19. Harrison P, Gerstein M (2002). Studying genomes through the aeons: protein families, pseudogenes and proteome evolution. J Mol Biol 318 (5): 1155–74.
  20. Orengo CA, Thornton JM (2005). Protein families and their evolution-a structural perspective. Annu. Rev. Biochem. 74: 867–900.
  21. Long M, Betrán E, Thornton K, Wang W (November 2003). The origin of new genes: glimpses from the young and old. Nat. Rev. Genet. 4 (11): 865–75.
  22. Wang M, Caetano-Anollés G (2009). The evolutionary mechanics of domain organization in proteomes and the rise of modularity in the protein world. Structure 17 (1): 66–78.
  23. Bowmaker JK (1998). Evolution of colour vision in vertebrates. Eye (London, England) 12 (Pt 3b): 541–7.
  24. Gregory TR, Hebert PD (1999). The modulation of DNA content: proximate causes and ultimate consequences. Genome Res. 9 (4): 317–24.
  25. Hurles M (July 2004). Gene duplication: the genomic trade in spare parts. PLoS Biol. 2 (7): E206.
  26. Liu N, Okamura K, Tyler DM (2008). The evolution and functional diversification of animal microRNA genes. Cell Res. 18 (10): 985–96.
  27. Siepel A (October 2009). Darwinian alchemy: Human genes from noncoding DNA. Genome Res. 19 (10): 1693–5.
  28. Morjan C, Rieseberg L (2004). How species evolve collectively: implications of gene flow and selection for the spread of advantageous alleles. Mol. Ecol. 13 (6): 1341–56.
  29. Su H, Qu L, He K, Zhang Z, Wang J, Chen Z, Gu H (2003). The Great Wall of China: a physical barrier to gene flow?. Heredity 90 (3): 212–9.
  30. Short RV (1975). The contribution of the mule to scientific thought. J. Reprod. Fertil. Suppl. (23): 359–64.
  31. Gross B, Rieseberg L (2005). The ecological genetics of homoploid hybrid speciation. J. Hered. 96 (3): 241–52.
  32. Burke JM, Arnold ML (2001). Genetics and the fitness of hybrids. Annu. Rev. Genet. 35: 31–52.
  33. Vrijenhoek RC (2006). Polyploid hybrids: multiple origins of a treefrog species. Curr. Biol. 16 (7).
  34. Wendel J (2000). Genome evolution in polyploids. Plant Mol. Biol. 42 (1): 225–49.
  35. Sémon M, Wolfe KH (2007). Consequences of genome duplication. Curr Opin Genet Dev 17 (6): 505–12.
  36. Comai L (2005). The advantages and disadvantages of being polyploid. Nat. Rev. Genet. 6 (11): 836–46.
  37. Soltis P, Soltis D (June 2000). The role of genetic and genomic attributes in the success of polyploids. Proc. Natl. Acad. Sci. U.S.A. 97 (13): 7051–7.
  38. Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau ME, Nesbo CL, Case RJ, Doolittle WF (2003). Lateral gene transfer and the origins of prokaryotic groups. Annu Rev Genet 37: 283–328.
  39. Walsh T (2006). Combinatorial genetic evolution of multiresistance. Curr. Opin. Microbiol. 9 (5): 476–82.
  40. Kondo N, Nikoh N, Ijichi N, Shimada M, Fukatsu T (2002). Genome fragment of Wolbachia endosymbiont transferred to X chromosome of host insect. Proc. Natl. Acad. Sci. U.S.A. 99 (22): 14280–5.
  41. Sprague G (1991). Genetic exchange between kingdoms. Curr. Opin. Genet. Dev. 1 (4): 530–3.
  42. Gladyshev EA, Meselson M, Arkhipova IR (May 2008). Massive horizontal gene transfer in bdelloid rotifers. Science 320 (5880): 1210–3.
  43. Baldo A, McClure M (1 September 1999). Evolution and horizontal transfer of dUTPase-encoding genes in viruses and their hosts. J. Virol. 73 (9): 7710–21.
  44. Poole A, Penny D (2007). Evaluating hypotheses for the origin of eukaryotes. Bioessays 29 (1): 74–84.
  45. 45.0 45.1 45.2 Bowler 2003, pp. 325–339
  46. 46.0 46.1 46.2 Larson 2004, pp. 221–243
  47. Mayr & Provine 1998, pp. 295–298, 416
  48. Mayr, E§year=1988. Towards a new philosophy of biology: observations of an evolutionist, 402, Harvard University Press.
  49. Mayr & Provine 1998, pp. 338–341
  • J. Beatty. "The synthesis and the synthetic theory" in Integrating Scientific Disciplines, edited by W. Bechtel and Nijhoff. Dordrecht, 1986.
  • Buston, PM, et al. (2007). Are clownfish groups composed of close relatives? An analysis of microsatellite DNA vraiation in Amphiprion percula. Molecular Ecology 12: 733–742.
  • Luigi Luca Cavalli-Sforza. Genes, Peoples, and Languages. North Point Press, 2000.
  • Luigi Luca Cavalli-Sforza et al. The History and Geography of Human Genes. Princeton University Press, 1994.
  • James F. Crow and Motoo Kimura. Introduction to Population Genetics Theory. Harper & Row, 1972.
  • Warren J Ewens. Mathematical Population Genetics. Springer-Verlag New York, Inc., 2004. ISBN 0-387-20191-2
  • John H. Gillespie Population Genetics: A Concise Guide, Johns Hopkins Press, 1998. ISBN 0-8018-5755-4.
  • Richard Halliburton. Introduction to Population Genetics. Prentice Hall, 2004
  • Daniel Hartl. Primer of Population Genetics, 3rd edition. Sinauer, 2000. ISBN 0-87893-304-2
  • Daniel Hartl and Andrew Clark. Principles of Population Genetics, 3rd edition. Sinauer, 1997. ISBN 0-87893-306-9.
  • Richard C. Lewontin. The Genetic Basis of Evolutionary Change. Columbia University Press, 1974.
  • William B. Provine. The Origins of Theoretical Population Genetics. University of Chicago Press. 1971. ISBN 0-226-68464-4.
  • Repaci, V, Stow AJ, Briscoe DA (2007). Fine-scale genetic structure, co-founding and multiple mating in the Australian allodapine bee (Ramphocinclus brachyurus. Journal of Zoology 270: 687–691.
  • Spencer Wells. The Journey of Man. Random House, 2002.
  • Spencer Wells. Deep Ancestry: Inside the Genographic Project. National Geographic Society, 2006.
  • Cheung, KH, Osier MV, Kidd JR, Pakstis AJ, Miller PL, Kidd KK (2000). ALFRED: an allele frequency database for diverse populations and DNA polymorphisms. Nucleic Acids Research 28 (1): 361–3.
  • Xu, J. Microbial Population Genetics. Caister Academic Press, 2010. ISBN 978-1-904455-59-2

External linksEdit

Topics in population genetics(edit)
Key concepts: Hardy-Weinberg law | linkage disequilibrium | Fisher's fundamental theorem | neutral theory
Selection: natural | sexual | artificial | ecological
Genetic drift: small population size | population bottleneck | founder effect | coalescence
Founders: Ronald Fisher | J.B.S. Haldane | Sewall Wright
Related topics: evolution | microevolution | evolutionary game theory | fitness landscape
List of evolutionary biology topics


Basic topics in evolutionary biology(edit)
Processes of evolution: evidence - macroevolution - microevolution - speciation
Mechanisms: selection - genetic drift - gene flow - mutation - phenotypic plasticity
Modes: anagenesis - catagenesis - cladogenesis
History: History of evolutionary thought - Charles Darwin - The Origin of Species - modern evolutionary synthesis
Subfields: population genetics - ecological genetics - human evolution - molecular evolution - phylogenetics - systematics - evo-devo
List of evolutionary biology topics | Timeline of evolution | Timeline of human evolution
This page uses Creative Commons Licensed content from Wikipedia (view authors).

Around Wikia's network

Random Wiki