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| {{Evolutionary biology}}
| | The writer is known as Wilber Pegues. Ohio is where my house is but my spouse desires us to move. Distributing production is where her primary earnings comes from. Doing ballet is something she would never give up.<br><br>Feel free to surf to my web-site - [http://sasari.dothome.co.kr/board_BDwr92/23714 psychic phone] |
| '''Population genetics''' is the study of [[allele frequency]] distribution and change under the influence of the four main evolutionary processes: [[natural selection]], [[genetic drift]], [[mutation]] and [[gene flow]]. It also takes into account the factors of [[Genetic recombination|recombination]], population subdivision and [[population structure]]. It attempts to explain such phenomena as [[Adaptation (biology)|adaptation]] and [[speciation]].
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| Population genetics was a vital ingredient in the emergence of the [[modern evolutionary synthesis]]. Its primary founders were [[Sewall Wright]], [[J. B. S. Haldane]] and [[Ronald Fisher|R. A. Fisher]], who also laid the foundations for the related discipline of [[quantitative genetics]].
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| Traditionally a highly mathematical discipline, modern population genetics encompasses theoretical, lab and field work. Computational approaches, often using [[coalescent theory]], have played a central role since the 1980s.
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| ==Fundamentals==
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| {{Multiple image|direction=vertical|align=right|image1=Biston.betularia.7200.jpg|image2=Biston.betularia.f.carbonaria.7209.jpg|width=200|caption1=''Biston betularia f. typica'' is the white-bodied form of the [[peppered moth]].|caption2=''Biston betularia f. carbonaria'' is the black-bodied form of the peppered moth.}}Population genetics is the study of the frequency and interaction of alleles and genes in populations.<ref>{{cite book|last=Postlethwalt|first=John|title=Modern Biology|year=2009|publisher=Holt, Rinehart and Winston|pages=317}}</ref> A sexual population is a set of organisms in which any pair of members can [[Breeding in the wild|breed]] together. This implies that all members belong to the same species and live near each other.<ref>{{cite book
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| | last = Hartl
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| | first = Daniel
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| | title = Principles of Population Genetics
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| | publisher = [[Sinauer Associates]]
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| | series =
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| | year = 2007
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| | doi =
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| | isbn = 978-0-87893-308-2
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| | page = 95}}</ref>
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| For example, all of the moths of the same species living in an isolated forest are a population. A gene in this population may have several alternate forms, which account for variations between the [[phenotype]]s of the organisms. An example might be a gene for coloration in moths that has two [[allele]]s: black and white. A [[gene pool]] is the complete set of alleles for a gene in a single population; the [[allele frequency]] for an allele is the fraction of the genes in the pool that is composed of that 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; for example, the allele for black color in a population of moths becoming more common.
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| [[File:Hardy-Weinberg.svg|thumb|320px|Hardy–Weinberg genotype frequencies for two [[allele]]s: the horizontal axis shows the two [[allele frequency|allele frequencies]] ''p'' and ''q'' and the vertical axis shows the [[genotype frequencies]]. Each curve shows one of the three possible genotypes.]]
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| ==Hardy–Weinberg principle==
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| {{Main|Hardy–Weinberg principle}}
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| [[Natural selection]] will only cause evolution if there is enough [[genetic variation]] in a population. Before the discovery of [[Mendelian genetics]], one common hypothesis was [[blending inheritance]]. But with blending inheritance, genetic variance would be rapidly lost, making evolution by natural selection implausible. The ''[[Hardy–Weinberg principle]]'' provides the solution to how variation is maintained in a population with [[Mendelian inheritance]]. According to this principle, the frequencies of alleles (variations in a gene) will remain constant in the absence of selection, mutation, migration and genetic drift.<ref name="Ewens W.J. 2004">{{cite book |author=Ewens W.J. |year=2004 |title=Mathematical Population Genetics (2nd Edition) |publisher=Springer-Verlag, New York |isbn=0-387-20191-2}}</ref> The Hardy–Weinberg "equilibrium" refers to this stability of allele frequencies over time.
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| A second component of the Hardy–Weinberg principle concerns the effects of a single generation of random mating. In this case, the genotype frequencies can be predicted from the allele frequencies. For example, in the simplest case of a single locus with two [[allele]]s: 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 genotype frequencies are in Hardy–Weinberg proportions resulting from random mating, then we will have freq('''AA''') = ''p''<sup>2</sup> for the '''AA''' [[homozygote]]s in the population, freq('''aa''') = ''q''<sup>2</sup> for the '''aa''' homozygotes, and freq('''Aa''') = 2''pq'' for the [[heterozygote]]s.
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| {{genetic genealogy}}
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| ==The four processes==
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| ===Natural selection===
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| {{Main|Natural selection}}
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| ''Natural selection'' is the fact that some [[trait (biology)|traits]] make it more likely for an [[organism]] to survive and [[reproduction|reproduce]]. Population genetics describes natural selection by defining [[fitness (biology)|fitness]] as a [[propensity probability|propensity or probability]] of survival and reproduction in a particular environment. The fitness is normally given by the symbol '''w'''=1-'''s''' where '''s''' is the [[selection coefficient]]. Natural selection acts on [[phenotype]]s, or the observable characteristics of organisms, but the [[heritability|genetically heritable]] basis of any phenotype which gives a reproductive advantage will become more common in a population (see [[allele frequency]]). In this way, natural selection converts differences in fitness into changes in allele frequency in a [[population]] over successive generations.
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| Before the advent of population genetics, many biologists doubted that small differences in fitness were sufficient to make a large difference to evolution.<ref name="Provine78">{{cite journal | author=William B. Provine | title=The role of mathematical population geneticists in the evolutionary synthesis of the 1930s and 1940s | journal=Studies of the History of Biology | year=1978 | volume=1 | pages=167–192}}</ref> Population geneticists addressed this concern in part by comparing selection to [[genetic drift]]. Selection can overcome genetic drift when '''s''' is greater than 1 divided by the [[effective population size]]. When this criterion is met, the probability that a new advantageous mutant becomes [[fixation (population genetics)|fixed]] is approximately equal to '''2s'''.<ref>{{cite journal | author=JBS Haldane | title=A Mathematical Theory of Natural and Artificial Selection, Part V: Selection and Mutation | journal=Mathematical Proceedings of the Cambridge Philosophical Society | year=1927 | volume=23 | pages=838–844 | bibcode=1927PCPS...23..838H | doi=10.1017/S0305004100015644 | issue=7}}</ref><ref>{{cite doi|10.1098/rstb.2009.0282}}</ref> The time until fixation of such an allele depends little on genetic drift, and is approximately proportional to log(sN)/s.<ref>{{cite journal | author=Hermisson J, Pennings PS | title=Soft sweeps: molecular population genetics of adaptation from standing genetic variation | journal=Genetics | year=2005| volume=169 | pages=2335–2352 | doi=10.1534/genetics.104.036947 | pmid=15716498 | issue=4 | pmc=1449620}}</ref>
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| ===Genetic drift===
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| {{Main|Genetic drift}}
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| ''Genetic drift'' is a change in [[Allele frequency|allele frequencies]] caused by [[Sampling (statistics)|random sampling]].<ref name="Masel 2011">{{Cite journal
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| | volume = 21
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| | pages = R837–R838
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| | author = Masel J
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| | title = Genetic drift
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| | journal = Current Biology
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| | year = 2011
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| | doi = 10.1016/j.cub.2011.08.007
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| | url = http://www.sciencedirect.com/science/article/pii/S0960982211008827
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| | issue=20
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| | pmid=22032182
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| }}</ref> That is, the alleles in the offspring are a random sample of those in the parents.<ref>{{cite book
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| | last = Futuyma
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| | first = Douglas
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| | authorlink =
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| | title = Evolutionary Biology
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| | publisher = [[Sinauer Associates]]
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| | series =
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| | year = 1998
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| | doi =
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| | isbn = 0-87893-189-9
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| | page = Glossary}}</ref> Genetic drift 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,<ref name = avers>{{Cite document | last = Avers | first = Charlotte | year = 1989 | title = Process and Pattern in Evolution | publisher = Oxford University Press | ref = harv | postscript = <!--None-->}}</ref> the changes due to genetic drift are not driven by environmental or adaptive pressures, and may be beneficial, neutral, or detrimental to reproductive success.
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| The effect of genetic drift is larger for alleles present in few copies than when an allele is present in many copies. Scientists wage vigorous debates 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 neutral mutations and genetic drift.<ref name="Futuyma 1998 320">{{cite book
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| | last = Futuyma
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| | first = Douglas
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| | authorlink =
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| | title = Evolutionary Biology
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| | publisher = [[Sinauer Associates]]
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| | series =
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| | year = 1998
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| | doi =
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| | isbn = 0-87893-189-9
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| | page = 320}}</ref> The role of genetic drift by means of sampling error in evolution has been criticized by [[John H Gillespie]]<ref>{{cite journal |author=Gillespie JH |title=Genetic Drift in an Infinite Population: The Pseudohitchhiking Model |journal=Genetics |volume=155 |issue=2 |pages=909–919 |year=2000 |pmid=10835409 |pmc=1461093}}</ref> and [[Will Provine]], who argue that selection on linked sites is a more important stochastic force.
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| The population genetics of genetic drift are described using either [[branching process]]es or a [[diffusion equation]] describing changes in allele frequency.<ref>{{Cite journal
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| | volume = 188
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| | pages = 783–785
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| | author = Wahl L.M.
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| | title = Fixation when N and s Vary: Classic Approaches Give Elegant New Results
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| | journal = Genetics
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| | year = 2011
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| | doi = 10.1534/genetics.111.131748
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| | url = http://www.genetics.org/content/188/4/783.full
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| | issue=4
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| | pmid=21828279
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| | pmc=3176088
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| }}</ref> These approaches are usually applied to the Wright-Fisher and Moran models of population genetics. Assuming genetic drift is the only evolutionary force acting on an allele, after t generations in many replicated populations, starting with allele frequencies of p and q, the variance in allele frequency across those populations is
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| :<math>
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| V_t \approx pq\left(1-\exp\left\{-\frac{t}{2N_e} \right\}\right).
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| </math><ref>{{cite book
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| | author = Nicholas H. Barton, Derek E. G. Briggs, Jonathan A. Eisen, David B. Goldstein, Nipam H. Patel
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| | title = Evolution
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| | publisher = Cold Spring Harbor Laboratory Press
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| | year = 2007
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| | isbn = 0-87969-684-2
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| | page = 417}}</ref>
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| ===Mutation===
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| {{Main|Mutation}}
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| Mutation is the ultimate source of [[genetic variation]] in the form of new alleles. Mutation can result in several different types of change in DNA sequences; these can either have no effect, alter the [[gene product|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.<ref>{{cite journal |author=Sawyer SA, Parsch J, Zhang Z, Hartl DL |title=Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=104 |issue=16 |pages=6504–10 |year=2007 |pmid=17409186 |doi=10.1073/pnas.0701572104 |pmc=1871816 |ref=harv|bibcode = 2007PNAS..104.6504S }}</ref>
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| Mutations can involve large sections of DNA becoming [[gene duplication|duplicated]], usually through [[genetic recombination]].<ref>{{Cite journal| doi = 10.1038/nrg2593| pmid = 19597530| volume = 10| issue = 8| pages = 551–564| last = Hastings| first = P J| title = Mechanisms of change in gene copy number| journal = Nature Reviews. Genetics| year = 2009| last2 = Lupski| first2 = JR| last3 = Rosenberg| first3 = SM| last4 = Ira| first4 = G| pmc = 2864001| ref = harv}}</ref> 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.<ref>{{cite book|last=Carroll SB, Grenier J, Weatherbee SD |title=From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design. Second Edition |publisher=Blackwell Publishing |year=2005 |location=Oxford |isbn=1-4051-1950-0|author=Sean B. Carroll; Jennifer K. Grenier; Scott D. Weatherbee.}}</ref> Most genes belong to larger [[gene family|families of genes]] of [[homology (biology)|shared ancestry]].<ref>{{cite journal |author=Harrison P, Gerstein M |title=Studying genomes through the aeons: protein families, pseudogenes and proteome evolution |journal=J Mol Biol |volume=318 |issue=5 |pages=1155–74 |year=2002 |pmid=12083509 |doi=10.1016/S0022-2836(02)00109-2 |ref=harv}}</ref> 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.<ref>{{cite journal |author=Orengo CA, Thornton JM |title=Protein families and their evolution-a structural perspective |journal=Annu. Rev. Biochem. |volume=74 |issue= |pages=867–900 |year=2005 |pmid=15954844 |doi=10.1146/annurev.biochem.74.082803.133029 |ref=harv}}</ref><ref>{{cite journal |author=Long M, Betrán E, Thornton K, Wang W |title=The origin of new genes: glimpses from the young and old |journal=Nat. Rev. Genet. |volume=4 |issue=11 |pages=865–75 |date=November 2003 |pmid=14634634 |doi=10.1038/nrg1204 |ref=harv}}</ref> Here, [[protein domain|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.<ref>{{cite journal |author=Wang M, Caetano-Anollés G |title=The evolutionary mechanics of domain organization in proteomes and the rise of modularity in the protein world |journal=Structure |volume=17 |issue=1 |pages=66–78 |year=2009 |doi=10.1016/j.str.2008.11.008 |pmid=19141283 |ref=harv}}</ref> For example, the human eye uses four genes to make structures that sense light: three for [[Cone cell|color vision]] and one for [[Rod cell|night vision]]; all four arose from a single ancestral gene.<ref>{{cite journal |author=Bowmaker JK |title=Evolution of colour vision in vertebrates |journal=Eye (London, England) |volume=12 |issue=Pt 3b |pages=541–7 |year=1998 |pmid=9775215 |ref=harv |doi=10.1038/eye.1998.143}}</ref> Another advantage of duplicating a gene (or even an [[Polyploidy|entire genome]]) is that this increases [[Redundancy (engineering)|redundancy]]; this allows one gene in the pair to acquire a new function while the other copy performs the original function.<ref>{{cite journal |author=Gregory TR, Hebert PD |title=The modulation of DNA content: proximate causes and ultimate consequences |url=http://genome.cshlp.org/content/9/4/317.full |journal=Genome Res. |volume=9 |issue=4 |pages=317–24 |year=1999 |pmid=10207154 |doi=10.1101/gr.9.4.317 |doi_brokendate=2009-11-14 |ref=harv}}</ref><ref>{{cite journal |author=Hurles M |title=Gene duplication: the genomic trade in spare parts |journal=PLoS Biol. |volume=2 |issue=7 |pages=E206 |date=July 2004 |pmid=15252449 |pmc=449868 |doi=10.1371/journal.pbio.0020206 |ref=harv}}</ref> Other types of mutation occasionally create new genes from previously noncoding DNA.<ref>{{cite journal | title=The evolution and functional diversification of animal microRNA genes| author=Liu N, Okamura K, Tyler DM| journal=Cell Res.| year=2008| volume=18| pages=985–96| doi=10.1038/cr.2008.278 |url=http://www.nature.com/cr/journal/v18/n10/full/cr2008278a.html |pmid=18711447 | issue=10 | pmc=2712117 | ref=harv}}</ref><ref>{{cite journal |author=Siepel A |title=Darwinian alchemy: Human genes from noncoding DNA |journal=Genome Res. |volume=19 |issue=10 |pages=1693–5 |date=October 2009 |pmid=19797681 |doi=10.1101/gr.098376.109 |url=http://genome.cshlp.org/content/19/10/1693.full |pmc=2765273 |ref=harv}}</ref>
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| In addition to being a major source of variation, mutation may also function as a mechanism of evolution when there are different probabilities at the molecular level for different mutations to occur, a process known as mutation bias.<ref>{{cite journal |author=Lynch, M. |year=2007 |title=The frailty of adaptive hypotheses for the origins of organismal complexity |journal=PNAS |volume=104 | pages=8597–8604 |doi=10.1073/pnas.0702207104 |bibcode = 2007PNAS..104.8597L |pmid=17494740 |pmc=1876435 |issue=suppl. 1}}</ref> If two genotypes, for example one with the nucleotide G and another with the nucleotide A in the same position, have the same fitness, but mutation from G to A happens more often than mutation from A to G, then genotypes with A will tend to evolve.<ref>{{cite journal| title=Deterministic Mutation Rate Variation in the Human Genome |journal=Genome Research|author= Smith N.G.C., Webster M.T., Ellegren, H. | year=2002 |volume=12 |pages=1350–1356 |doi=10.1101/gr.220502 |url=http://genome.cshlp.org/content/12/9/1350.abstract |issue=9 |pmid=12213772 |pmc=186654}}</ref> Different insertion vs. deletion mutation biases in different taxa can lead to the evolution of different genome sizes.<ref>{{cite journal |author=Petrov DA, Sangster TA, Johnston JS, Hartl DL, Shaw KL |year=2000 |title=Evidence for DNA loss as a determinant of genome size |journal=Science |volume=287 | pages=1060–1062 |doi=10.1126/science.287.5455.1060 |issue=5455 |bibcode = 2000Sci...287.1060P |pmid=10669421}}</ref><ref>{{cite journal |author=Petrov DA |year=2002 |title=DNA loss and evolution of genome size in Drosophila |journal=Genetica |volume=115 | pages=81–91 |doi=10.1023/A:1016076215168 |issue=1 |pmid=12188050}}</ref> Developmental or mutational biases have also been observed in [[Morphology (biology)|morphological]] evolution.<ref>{{cite journal |author=Kiontke K, Barriere A , Kolotuev I, Podbilewicz B , Sommer R, Fitch DHA , Felix MA |year=2007 |title=Trends, stasis, and drift in the evolution of nematode vulva development |journal=Current Biology|volume=17 | pages=1925–1937 |doi=10.1016/j.cub.2007.10.061 |issue=22 |pmid=18024125}}</ref><ref>{{cite journal |author=Braendle C, Baer CF, Felix MA |year=2010 |title=Bias and Evolution of the Mutationally Accessible Phenotypic Space in a Developmental System |journal=PLoS Genetics |volume=6 |doi=10.1371/journal.pgen.1000877 |issue=3 |pmid=20300655 |pmc=2837400 |editor1-last=Barsh |editor1-first=Gregory S |pages=e1000877 |article number =e1000877}}</ref> For example, according to the [[Baldwin effect|phenotype-first theory of evolution]], mutations can eventually cause the [[genetic assimilation]] of traits that were previously [[phenotypic plasticity|induced by the environment]].<ref name="Palmer 2004">{{cite journal | last=Palmer |first=RA | title=Symmetry breaking and the evolution of development | journal=[[Science (journal)|Science]] | year=2004 | pages=828–833 | volume=306 | doi=10.1126/science.1103707 | pmid=15514148 | issue=5697 |bibcode = 2004Sci...306..828P }}</ref><ref name="West-Eberhard 2003">{{cite book |last=West-Eberhard |first=M-J. |year=2003 |title=Developmental plasticity and evolution |publisher=Oxford University Press |location=New York |isbn=978-0-19-512235-0 }}</ref>
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| Mutation bias effects are superimposed on other processes. If selection would favor either one out of two mutations, but there is no extra advantage to having both, then the mutation that occurs the most frequently is the one that is most likely to become fixed in a population.<ref>{{cite journal |author=Stoltzfus, A and Yampolsky, L.Y. |year=2009 |title=Climbing Mount Probable: Mutation as a Cause of Nonrandomness in Evolution |journal=J Hered |volume=100 | pages=637–647 |doi=10.1093/jhered/esp048 |pmid=19625453 |issue=5 }}</ref><ref>{{cite journal |author=Yampolsky, L.Y. and Stoltzfus, A |year=2001 |title=Bias in the introduction of variation as an orienting factor in evolution |journal=Evol Dev|volume=3 | pages=73–83 |doi=10.1046/j.1525-142x.2001.003002073.x |pmid=11341676 |issue=2}}</ref> Mutations leading to the loss of function of a gene are much more common than mutations that produce a new, fully functional gene. Most loss of function mutations are selected against. But when selection is weak, mutation bias towards loss of function can affect evolution.<ref>{{cite journal |author=Haldane, JBS |year=1933|title=The Part Played by Recurrent Mutation in Evolution |journal=American Naturalist|volume=67 | pages=5–19 |jstor=2457127 |doi=10.1086/280465 |issue=708}}</ref> For example, [[pigment]]s are no longer useful when animals live in the darkness of caves, and tend to be lost.<ref>{{Cite journal | doi = 10.1016/j.cub.2007.01.051 | pmid = 17306543 | volume = 17 | issue = 5 | pages = 452–454 | last = Protas | first = Meredith | title = Regressive evolution in the Mexican cave tetra, Astyanax mexicanus | journal = Current Biology | year = 2007 | last2 = Conrad | first2 = M | last3 = Gross | first3 = JB | last4 = Tabin | first4 = C |last5 = Borowsky | first5 = R | pmc = 2570642 | ref = harv }}</ref> This kind of loss of function can occur because of mutation bias, and/or because the function had a cost, and once the benefit of the function disappeared, natural selection leads to the loss. Loss of [[endospore|sporulation]] ability in a [[Bacillus subtilis|bacterium]] during laboratory evolution appears to have been caused by mutation bias, rather than natural selection against the cost of maintaining sporulation ability.<ref>{{cite journal |author=Maughan H, Masel J, Birky WC, Nicholson WL |title=The roles of mutation accumulation and selection in loss of sporulation in experimental populations of Bacillus subtilis |doi= 10.1534/genetics.107.075663 |journal=Genetics |volume=177 |pages=937–948 |year=2007 |pmid=17720926 |pmc=2034656 |issue=2}}</ref> When there is no selection for loss of function, the speed at which loss evolves depends more on the mutation rate than it does on the [[effective population size]],<ref>{{cite journal |author=Masel J, King OD, Maughan H |title=The loss of adaptive plasticity during long periods of environmental stasis |doi= 10.1086/510212 |journal=American Naturalist|volume=169 |issue=1 |pages=38–46 |year=2007 |pmid=17206583 |pmc=1766558}}</ref> indicating that it is driven more by mutation bias than by genetic drift.
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| ====Evolution of mutation rate====
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| Due to the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as [[DNA repair]] to remove mutations.<ref name=Bertram>{{cite journal |author=Bertram J |title=The molecular biology of cancer |journal=Mol. Aspects Med. |volume=21 |issue=6 |pages=167–223 |year=2000 |pmid=11173079 |doi=10.1016/S0098-2997(00)00007-8 |ref=harv}}</ref> 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 [[metabolism|metabolic]] costs of maintaining systems to reduce the mutation rate, such as DNA repair enzymes.<ref name=Sniegowski>{{cite journal |author=Sniegowski P, Gerrish P, Johnson T, Shaver A |title=The evolution of mutation rates: separating causes from consequences |journal=BioEssays |volume=22 |issue=12 |pages=1057–66 |year=2000 |pmid=11084621 |doi=10.1002/1521-1878(200012)22:12<1057::AID-BIES3>3.0.CO;2-W |ref=harv}}</ref> Viruses that use RNA as their genetic material have rapid mutation rates,<ref>{{cite journal |author=Drake JW, Holland JJ |title=Mutation rates among RNA viruses |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=96 |issue=24 |pages=13910–3 |year=1999 |pmid=10570172 |pmc=24164 |url=http://www.pnas.org/content/96/24/13910.long |doi=10.1073/pnas.96.24.13910 |ref=harv|bibcode = 1999PNAS...9613910D }}</ref> 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]].<ref>{{cite journal |author=Holland J, Spindler K, Horodyski F, Grabau E, Nichol S, VandePol S |title=Rapid evolution of RNA genomes |journal=Science |volume=215 |issue=4540 |pages=1577–85 |year=1982 |pmid=7041255 |doi=10.1126/science.7041255 |ref=harv|bibcode = 1982Sci...215.1577H }}</ref>
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| === Gene flow and transfer ===
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| {{Main|Gene flow}}
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| [[Gene flow]] is the exchange of genes between populations, which are usually of the same species.<ref>{{cite journal |author=Morjan C, Rieseberg L |title=How species evolve collectively: implications of gene flow and selection for the spread of advantageous alleles |journal=Mol. Ecol. |volume=13 |issue=6 |pages=1341–56 |year=2004 |pmid=15140081 |doi=10.1111/j.1365-294X.2004.02164.x |pmc=2600545 |ref=harv}}</ref> 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 (biology)|hybrid]] organisms and [[horizontal gene transfer]].
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| 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. Population genetic models can be used to reconstruct the history of gene flow between populations.<ref>{{cite journal|last=Gravel, S.|title=Population Genetics Models of Local Ancestry|year=2012|bibcode=2012arXiv1202.4811G|volume=1202|pages=4811|arxiv=1202.4811|class=q-bio.PE|doi=10.1534/genetics.112.139808|first1=S.|journal=Genetics|issue=2}}</ref>
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| ==== Reproductive isolation ====
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| As [[reproductive isolation|barriers to reproduction]] between two diverging populations are required for the populations to [[speciation|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.<ref>{{cite journal |author=Su H, Qu L, He K, Zhang Z, Wang J, Chen Z, Gu H |title=The Great Wall of China: a physical barrier to gene flow? |journal=Heredity |volume=90 |issue=3 |pages=212–9 |year=2003 |pmid=12634804 |doi=10.1038/sj.hdy.6800237 |ref=harv}}</ref>
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| 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 [[horse]]s and [[donkey]]s mating to produce [[mule]]s.<ref>{{cite journal |author=Short RV |title=The contribution of the mule to scientific thought |journal=J. Reprod. Fertil. Suppl. |issue=23 |pages=359–64 |year=1975 |pmid=1107543 |ref=harv}}</ref> Such [[Hybrid (biology)|hybrid]]s are generally [[infertility|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.<ref>{{cite journal |author=Gross B, Rieseberg L |title=The ecological genetics of homoploid hybrid speciation |doi= 10.1093/jhered/esi026 |journal=J. Hered. |volume=96 |issue=3 |pages=241–52 |year=2005 |pmid=15618301 |pmc=2517139 |ref=harv}}</ref> The importance of hybridization in creating [[hybrid speciation|new species]] of animals is unclear, although cases have been seen in many types of animals,<ref>{{cite journal |author=Burke JM, Arnold ML |title=Genetics and the fitness of hybrids |journal=Annu. Rev. Genet. |volume=35 |issue= |pages=31–52 |year=2001 |pmid=11700276 |doi=10.1146/annurev.genet.35.102401.085719 |ref=harv }}</ref> with the [[gray tree frog]] being a particularly well-studied example.<ref>{{cite journal |author=Vrijenhoek RC |title=Polyploid hybrids: multiple origins of a treefrog species |journal=Curr. Biol. |volume=16 |issue=7 |year=2006 |pmid=16581499 |doi=10.1016/j.cub.2006.03.005 |ref=harv |pages=R245–7 }}</ref>
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| 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.<ref name=Wendel>{{cite journal |author=Wendel J |title=Genome evolution in polyploids |journal=Plant Mol. Biol. |volume=42 |issue=1 |pages=225–49 |year=2000 |pmid=10688139 |doi=10.1023/A:1006392424384 |ref=harv }}</ref><ref name=Semon>{{cite journal |author=Sémon M, Wolfe KH |title=Consequences of genome duplication |journal=Curr Opin Genet Dev |volume=17 |issue=6 |pages=505–12 |year=2007 |pmid=18006297 |doi=10.1016/j.gde.2007.09.007 |ref=harv }}</ref> 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.<ref>{{cite journal |author=Comai L |title=The advantages and disadvantages of being polyploid |journal=Nat. Rev. Genet. |volume=6 |issue=11 |pages=836–46 |year=2005 |pmid=16304599 |doi=10.1038/nrg1711 |ref=harv }}</ref> Polyploids also have more genetic diversity, which allows them to avoid [[inbreeding depression]] in small populations.<ref>{{cite journal |author=Soltis P, Soltis D |title=The role of genetic and genomic attributes in the success of polyploids |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=97 |issue=13 |pages=7051–7 |date=June 2000 |pmid=10860970 |pmc=34383 |doi=10.1073/pnas.97.13.7051 |ref=harv |bibcode = 2000PNAS...97.7051S }}</ref>
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| ====Genetic structure====
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| Because of physical barriers to migration, along with limited tendency for individuals to move or spread ([[wiktionary:vagility|vagility]]), and tendency to remain or come back to natal place ([[philopatry]]), natural populations rarely all interbreed as convenient in theoretical random models ([[panmixy]]) (Buston ''et al.'', 2007). There is usually a geographic range within which individuals are more closely [[coefficient of relatedness|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). Genetic structuring can be caused by migration due to historical [[climate change]], species [[range expansion]] or current availability of [[habitat]].
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| ====Horizontal Gene Transfer====
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| {{Main|Horizontal gene transfer}}
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| ''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]].<ref>{{cite journal |author=Boucher Y, Douady CJ, Papke RT, Walsh DA, Boudreau ME, Nesbo CL, Case RJ, Doolittle WF |title=Lateral gene transfer and the origins of prokaryotic groups |doi=10.1146/annurev.genet.37.050503.084247 |journal=Annu Rev Genet |volume=37 |pages=283–328 |year=2003 |pmid=14616063 |ref=harv}}</ref> 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.<ref>{{cite journal |author=Walsh T |title=Combinatorial genetic evolution of multiresistance |journal=Curr. Opin. Microbiol. |volume=9 |issue=5 |pages=476–82 |year=2006 |pmid=16942901 |doi=10.1016/j.mib.2006.08.009 |ref=harv }}</ref> 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.<ref>{{cite journal |author=Kondo N, Nikoh N, Ijichi N, Shimada M, Fukatsu T |title=Genome fragment of Wolbachia endosymbiont transferred to X chromosome of host insect |journal=Proc. Natl. Acad. Sci. U.S.A. |volume=99 |issue=22 |pages=14280–5 |year=2002 |pmid=12386340 |doi=10.1073/pnas.222228199 |pmc=137875 |ref=harv |bibcode = 2002PNAS...9914280K }}</ref><ref>{{cite journal |author=Sprague G |title=Genetic exchange between kingdoms |journal=Curr. Opin. Genet. Dev. |volume=1 |issue=4 |pages=530–3 |year=1991 |pmid=1822285 |doi=10.1016/S0959-437X(05)80203-5 |ref=harv}}</ref> An example of larger-scale transfers are the eukaryotic [[Bdelloidea|bdelloid rotifers]], which appear to have received a range of genes from bacteria, fungi, and plants.<ref>{{cite journal |author=Gladyshev EA, Meselson M, Arkhipova IR |title=Massive horizontal gene transfer in bdelloid rotifers |journal=Science |volume=320 |issue=5880 |pages=1210–3 |date=May 2008 |pmid=18511688 |doi=10.1126/science.1156407 |ref=harv|bibcode = 2008Sci...320.1210G }}</ref> [[Virus]]es can also carry DNA between organisms, allowing transfer of genes even across [[domain (biology)|biological domains]].<ref>{{cite journal |author=Baldo A, McClure M |title=Evolution and horizontal transfer of dUTPase-encoding genes in viruses and their hosts |journal=J. Virol. |volume=73 |issue=9 |pages=7710–21 |date=1 September 1999|pmid=10438861 |pmc=104298 |ref=harv }}</ref> Large-scale gene transfer has also occurred between the ancestors of [[eukaryote|eukaryotic cells]] and prokaryotes, during the acquisition of [[chloroplast]]s and [[Mitochondrion|mitochondria]].<ref name = "rgruqh">{{cite journal |author=Poole A, Penny D |title=Evaluating hypotheses for the origin of eukaryotes |journal=BioEssays |volume=29 |issue=1 |pages=74–84 |year=2007 |pmid=17187354 |doi=10.1002/bies.20516 |ref=harv }}</ref>
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| ==Complications==
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| Basic models of population genetics consider only one gene locus at a time. In practice, [[epistasis|epistatic]] and [[Genetic linkage|linkage]] relationships between loci may also be important.
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| ===Epistasis===
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| Because of [[epistasis]], the phenotypic effect of an allele at one locus may depend on which alleles are present at many other loci. Selection does not act on a single locus, but on a phenotype that arises through development from a complete genotype.
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| According to [[Richard Lewontin|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 [[genotype]]s (''G''<sub>1</sub>) to a [[phenotype]] space (''P''<sub>1</sub>), where [[natural selection|selection]] takes place, and another set of laws that map the resulting population (''P''<sub>2</sub>) back to genotype space (''G''<sub>2</sub>) where [[Mendelism|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:
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| :<math>G_1 \; \stackrel{T_1}{\rightarrow} \; P_1 \; \stackrel{T_2}{\rightarrow} \; P_2 \; \stackrel{T_3}{\rightarrow} \; G_2 \;
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| \stackrel{T_4}{\rightarrow} \; G_1' \; \rightarrow \cdots</math>
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| (adapted from Lewontin 1974, p. 12). XD
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| ''T''<sub>1</sub> represents the genetic and [[epigenetic]] laws, the aspects of functional biology, or [[developmental biology|development]], that transform a genotype into phenotype. We will refer to this as the "[[genotype-phenotype map]]". ''T''<sub>2</sub> is the transformation due to natural selection, ''T''<sub>3</sub> are epigenetic relations that predict genotypes based on the selected phenotypes and finally ''T''<sub>4</sub> the rules of Mendelian genetics.
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| In practice, there are two bodies of evolutionary theory that exist in parallel, traditional population genetics operating in the genotype space and the [[biometry|biometric]] theory used in [[plant breeding|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.
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| ===Linkage===
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| If all genes are in [[linkage equilibrium]], the effect of an allele at one locus can be averaged across the [[gene pool]] at other loci. In reality, one allele is frequently found in [[linkage disequilibrium]] with genes at other loci, especially with genes located nearby on the same chromosome. [[Recombination (biology)|Recombination]] breaks up this linkage disequilibrium too slowly to avoid [[genetic hitchhiking]], where an allele at one locus rises to high frequency because it is [[genetic linkage|linked]] to an allele under selection at a nearby locus. This is a problem for population genetic models that treat one gene locus at a time. It can, however, be exploited as a method for detecting the action of [[natural selection]] via [[selective sweep]]s.
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| In the extreme case of primarily [[asexual reproduction|asexual populations]], linkage is complete, and different population genetic equations can be derived and solved, which behave quite differently to the sexual case.<ref name = "Desai">{{cite journal |author=Michael M. Desai, Daniel S. Fisher |title=Beneficial Mutation Selection Balance and the Effect of Linkage on Positive Selection |journal=Genetics|volume=176 |issue=3 |pages=1759–1798 |year=2007 |doi=10.1534/genetics.106.067678 | url=http://www.genetics.org/cgi/content/abstract/176/3/1759 |pmid=17483432 |pmc=1931526 }}</ref> Most [[microorganisms|microbes]], such as [[bacteria]], are asexual. The population genetics of [[microorganism]]s lays the foundations for tracking the origin and evolution of [[antibiotic resistance]] and deadly infectious [[pathogen]]s. Population genetics of microorganisms is also an essential factor for devising strategies for the conservation and better utilization of beneficial microbes (Xu, 2010).
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| ==History==
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| {{See also|Modern evolutionary synthesis}}
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| ''Population genetics'' began as a reconciliation of the [[Mendelian inheritance|Mendelian]] and [[Biostatistics|biometrician]] models. A key step was the work of the British biologist and statistician [[Ronald Fisher|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 [[Allele frequency|allele frequencies]] in a population, resulting in evolution. In a series of papers beginning in 1924, another British geneticist, [[J. B. S. Haldane|J.B.S. Haldane]] worked out the mathematics of allele frequency change at a single gene locus under a broad range of conditions. Haldane also applied statistical analysis to real-world examples of natural selection, such as the [[Peppered moth evolution|evolution of industrial melanism in peppered moths]], and showed that [[selection coefficient]]s could be larger than Fisher assumed, leading to more rapid adaptive evolution.<ref name="Bowler325-339">{{Harvnb |Bowler|2003| pp=325–339}}</ref><ref name="Larson221-243">{{Harvnb |Larson|2004| pp=221–243}}</ref>
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| 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 [[Fitness landscape|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.
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| 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.<ref name="Bowler325-339"/><ref name="Larson221-243"/> [[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.
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| ===Modern evolutionary synthesis===
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| The mathematics of population genetics were originally developed as the beginning of the [[modern evolutionary synthesis]]. According to Beatty (1986), population genetics defines the core of the modern synthesis. 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.<ref>{{Harvnb |Mayr|Provine|1998| pp=295–298, 416}}</ref> During the modern evolutionary synthesis, these ideas were purged, and only evolutionary causes that could be expressed in the mathematical framework of population genetics were retained.<ref name="Provine88">{{cite book |last=Provine | first=W. B. |year=1988| title=Evolutionary progress |chapter= Progress in evolution and meaning in life | pages=49–79 |publisher=University of Chicago Press}}</ref> Consensus was reached as to which evolutionary factors might influence evolution, but not as to the relative importance of the various factors.<ref name="Provine88" />
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| [[Theodosius Dobzhansky]], a postdoctoral worker in T. H. Morgan's lab, had been influenced by the work on genetic diversity by [[Russia]]n 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. Many more biologists were influenced by population genetics via Dobzhansky than were able to read the highly mathematical works in the original.<ref name="Provine78">{{cite journal|last=Provine | first=William B. |year=1978| title=The role of mathematical population geneticists in the evolutionary synthesis of the 1930s and 1940s |journal=Studies of the History of Biology|volume=2 | pages=167–192}}</ref>
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| ===Selection vs. genetic drift===
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| 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.
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| 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 [[polymorphism (biology)|genetic polymorphisms]] such as human [[blood type]]s. Ford's work, in collaboration with Fisher, contributed to a shift in emphasis during the course of the modern synthesis towards [[natural selection]] over [[genetic drift]].<ref name="Bowler325-339"/><ref name="Larson221-243"/><ref>{{cite book|author=Mayr, E§|year=1988|title=Towards a new philosophy of biology: observations of an evolutionist|publisher=[[Harvard University Press]]|pages=402}}</ref><ref>{{Harvnb |Mayr|Provine|1998| pp=338–341}}</ref>
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| Recent studies of eukaryotic [[transposable element]]s, and of their impact on [[speciation]], point again to a major role of nonadaptive processes such as [[mutation]] and [[genetic drift]].<ref>{{cite journal | author = Jurka, Jerzy, Weidong Bao, Kenji K. Kojima|date=September 2011 | title = Families of transposable elements, population structure and the origin of species |journal = [[Biology Direct]] | volume = 6 | pages = 44 | url = http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3183009/?tool=pubmed %7C | pmid = 21929767 | pmc=3183009 | doi=10.1186/1745-6150-6-44}}</ref> Mutation and genetic drift are also viewed as major factors in the evolution of genome complexity <ref>{{cite journal | author = Lynch, Michael, John S. Conery | year = 2003 | title = The origins of genome complexity |journal = [[Science (journal)|Science]] | volume = 302 | pages = 1401–1404 | pmid = 14631042 | doi=10.1126/science.1089370 | issue=5649|bibcode = 2003Sci...302.1401L }}</ref>
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| ==See also==
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| {{Columns-list|2|
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| * [[Coalescent theory]]
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| * [[Dual inheritance theory]]
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| * [[Ecological genetics]]
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| * [[Evolutionarily Significant Unit]]
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| * [[Ewens's sampling formula]]
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| * [[Fitness landscape]]
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| * [[Founder effect]]
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| * [[Genetic algebra]]
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| * [[Genetic diversity]]
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| * [[Genetic drift]]
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| * [[Genetic erosion]]
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| * [[Genetic hitchhiking]]
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| * [[Genetic monitoring]]
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| * [[Genetic pollution]]
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| * [[Gene pool]]
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| * [[Genotype-phenotype distinction]]
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| * [[Habitat fragmentation]]
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| * [[Haldane's dilemma]]
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| * [[Hill–Robertson effect]]
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| * [[Human genetic clustering]]
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| * [[Identity by descent]]
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| * [[Linkage disequilibrium]]
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| * [[Microevolution]]
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| * [[Molecular evolution]]
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| * [[Muller's ratchet]]
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| * [[Mutational meltdown]]
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| * [[Neutral theory of molecular evolution]]
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| * [[Population bottleneck]]
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| * [[Quantitative genetics]]
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| * [[Reproductive compensation]]
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| * [[Selection]]
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| * [[Selective sweep]]
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| * [[Snpstr]]
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| * [[Small population size]]
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| * [[Viral quasispecies]]
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| }}
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| == Notes and references ==
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| {{Reflist|2}}
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| ==Bibliography==
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| * J. Beatty. "The synthesis and the synthetic theory" in Integrating Scientific Disciplines, edited by W. Bechtel and Nijhoff. Dordrecht, 1986.
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| *{{cite book|last=Bowler|first=Peter J.|title=Evolution : the history of an idea|year=2003|publisher=University of California Press|location=Berkeley|isbn=978-0-520-23693-6|edition=3rd |ref=harv}}
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| * {{cite journal | last = Buston | first = PM | coauthors = ''et al.'' | year = 2007 | title = Are clownfish groups composed of close relatives? An analysis of microsatellite DNA vraiation in ''Amphiprion percula'' | journal = Molecular Ecology | volume = 12 | pages = 733–742 | pmid = 12675828 | issue = 3 | ref = harv | doi=10.1046/j.1365-294X.2003.01762.x}}
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| * [[Luigi Luca Cavalli-Sforza]]. Genes, Peoples, and Languages. North Point Press, 2000.
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| * [[Luigi Luca Cavalli-Sforza]] et al. The History and Geography of Human Genes. Princeton University Press, 1994.
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| * [[James F. Crow]] and [[Motoo Kimura]]. Introduction to Population Genetics Theory. Harper & Row, 1972.
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| * [[Warren Ewens|Warren J Ewens]]. Mathematical Population Genetics. Springer-Verlag New York, Inc., 2004. ISBN 0-387-20191-2
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| * [[John H. Gillespie]] Population Genetics: A Concise Guide, Johns Hopkins Press, 1998. ISBN 0-8018-5755-4.
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| * Richard Halliburton. Introduction to Population Genetics. Prentice Hall, 2004
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| * Daniel Hartl. Primer of Population Genetics, 3rd edition. Sinauer, 2000. ISBN 0-87893-304-2
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| * Daniel Hartl and Andrew Clark. Principles of Population Genetics, 3rd edition. Sinauer, 1997. ISBN 0-87893-306-9.
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| * {{cite book|last=Larson|first=Edward J.|title=Evolution : the remarkable history of a scientific theory|year=2004|publisher=Modern Library|location=New York|isbn=978-0-679-64288-6|edition=Modern Library |ref=harv}}
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| * [[Richard Lewontin|Richard C. Lewontin]]. The Genetic Basis of Evolutionary Change. [[Columbia University Press]], 1974.
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| * [[William B. Provine]]. The Origins of Theoretical Population Genetics. [[University of Chicago Press]]. 1971. ISBN 0-226-68464-4.
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| * {{cite journal | last = Repaci | first = V | coauthors = Stow AJ, Briscoe DA | year = 2007 | title = Fine-scale genetic structure, co-founding and multiple mating in the Australian allodapine bee (''Ramphocinclus brachyurus'' | journal = Journal of Zoology | volume = 270 | pages = 687–691 | doi = 10.1111/j.1469-7998.2006.00191.x | ref = harv | issue = 4 }}
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| * [[Spencer Wells]]. The Journey of Man. Random House, 2002.
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| * [[Spencer Wells]]. Deep Ancestry: Inside the Genographic Project. National Geographic Society, 2006.
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| * {{cite journal |last=Cheung|first=KH |coauthors=Osier MV, Kidd JR, Pakstis AJ, Miller PL, Kidd KK |title=ALFRED: an allele frequency database for diverse populations and DNA polymorphisms |journal=Nucleic Acids Research |volume=28 |issue=1 |year=2000 |pages=361–3 |doi=10.1093/nar/28.1.361 |pmid=10592274 |pmc=102486 |ref=harv }}
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| * Xu, J. Microbial Population Genetics. [[Caister Academic Press]], 2010. ISBN 978-1-904455-59-2
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| ==External links==
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| *[http://www.extension.org/pages/68167/population-development-and-genetics Population Genetics Tutorials]
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| * [http://alfred.med.yale.edu/alfred/ The ALlele FREquency Database] at [[Yale University]]
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| * [http://www.ehstrafd.org EHSTRAFD.org - Earth Human STR Allele Frequencies Database]
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| * [http://www.esp.org/books/sturt/history/contents/sturt-history-ch-17.pdf History of population genetics]
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| * [http://www.cosmolearning.com/video-lectures/how-selection-changes-the-genetic-composition-of-population-6688/ How Selection Changes the Genetic Composition of Population], video of lecture by [[Stephen C. Stearns]] ([[Yale University]])
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| * [[National Geographic Society|National Geographic]]: [https://www5.nationalgeographic.com/genographic/atlas.html Atlas of the Human Journey] ([[Haplogroup]]-based human migration maps)
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| * [http://vlab.infotech.monash.edu.au/simulations/cellular-automata/population-genetics/ Monash Virtual Laboratory] - Simulations of habitat fragmentation and population genetics online at Monash University's Virtual Laboratory.
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| {{Population genetics}}
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| {{Genetics}}
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| {{Evolution}}
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| {{Portal bar|Evolutionary biology}}
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| {{DEFAULTSORT:Population Genetics}}
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| [[Category:Genetics]]
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| [[Category:Population genetics|*]]
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| [[Category:Evolutionary biology]]
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| [[Category:Statistical genetics]]
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