Population genetics is a genetic sub-field that deals with genetic differences within and between populations, and is part of evolutionary biology. Studies in this branch of biology examine phenomena such as adaptation, speciation, and population structure.
Population genetics is an important element in the emergence of modern evolutionary synthesis. Its main founders are Sewall Wright, J. B. S. Haldane and Ronald Fisher, who also laid the groundwork for related quantitative genetic disciplines. Traditionally a highly mathematical discipline, the genetics of modern populations include theoretical, laboratory, and employment. The population genetic model is used both for statistical inference of DNA sequence data and for proof/disproof of concept.
What distinguishes today's population genetics of a new approach to the evolution of phenotypic and modeling, such as evolutionary game theory and adaptive dynamics, is the emphasis on genetic phenomenon as dominance, epistasis, and the extent to which genetic recombination break the link imbalance. This makes it suitable for comparison with population genomic data.
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Histori
Population genetics begins as a reconciliation of Mendel's inheritance and biostatistics model. Natural selection will only cause evolution if there is enough genetic variation in a population. Prior to Mendel's genetic discovery, one common hypothesis was the mixing of inheritance. But with mixed inheritance, genetic variation will disappear quickly, making evolution through natural or sexual selection unreasonable. The Hardy-Weinberg principle provides a solution to how variations are preserved in populations with Mendel's legacy. According to this principle, the frequency of alleles (variations in genes) will remain constant in the absence of selection, mutation, migration and genetic shift.
The next key step is the work of British biologist and statistician Ronald Fisher. In a series of papers beginning in 1918 and culminating in his 1930 book, The Genetical Theory of Natural Selection, Fisher suggests that the continuous variations measured by biometrics can be generated by the combined action of many discrete genes, and natural selection can alter the frequency of alleles in a population, resulting in evolution. In a series of papers beginning in 1924, another British geneticist, J.B.S. Haldane, worked on the mathematical change of allele frequencies on a single gene locus under various conditions. Haldane also applies statistical analysis to real examples of natural selection, such as the evolution of peppered moth and industrial melanism, and suggests that the selection coefficient may outweigh what Fisher assumed, leading to a faster evolution of adaptation as a camouflage strategy after pollution increases.
American biologist Sewall Wright, who has a background in animal breeding experiments, focuses on the combination of interacting genes, and the inbreeding effect on a relatively isolated small population that shows a genetic shift. In 1932 Wright introduced the concept of adaptive landscapes and argued that genetic and inbreeding shifts can encourage isolated small subpopulations away from the adaptive peaks, allowing natural selection to propel it toward different adaptive peaks.
The work of Fisher, Haldane and Wright established the population genetic discipline. This natural selection is integrated with Mendel's genetics, which is a critical first step in developing a unified theory of how evolution works. John Maynard Smith is a student of Haldane, while W.D. Hamilton was deeply influenced by Fisher's writings. American George R. Price worked with Hamilton and Maynard Smith. American Richard Lewontin and Japan's Motoo Kimura are heavily influenced by Wright.
Modern synthesis
Mathematical population genetics was originally developed as the beginning of modern synthesis. Authors like Beatty have asserted that population genetics defines the essence of modern synthesis. During the first few decades of the 20th century, most field realists continue to believe that Lamarckism and orthogenesis provide the best explanation for the complexities they observe in the living world. During modern synthesis, these ideas are cleansed, and only evolutionary causes can be expressed in the mathematical framework of the population genetics maintained. Consensus is reached about which evolutionary factors can influence evolution, but not about the relative importance of various factors.
Theodosius Dobzhansky, a postdoctoral worker in T. H. Morgan's lab, has been influenced by work on genetic diversity by Russian geneticists such as Sergei Chetverikov. He helped bridge the gap between the foundations of microevolution developed by population geneticists and the macroevolution patterns observed by field biologists, with his 1937 book Genetics and Species Origins. Dobzhansky examines the genetic diversity of wild populations and suggests that, contrary to the population's genetic assumptions, this population has a large number of genetic diversity, with significant differences between sub-populations. The book also takes the highly mathematical work of population geneticists and puts it into a more accessible form. Many biologists are more influenced by population genetics through Dobzhansky than able to read works that are very mathematical in the original language.
In the United Kingdom E.B. Ford, a pioneer of ecological genetics, continued throughout the 1930s and 1940s to empirically 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, in collaboration with Fisher, contributed to a shift of emphasis during modern synthesis toward natural selection as a dominant force.
Neutral theory and dynamics of origin fixation
The view of modern and genuine synthesis of population genetics assumes that mutations provide a great deal of raw material, and only focus on changing the frequency of alleles in the population. The main processes affecting allele frequencies are natural selection, genetic drift, gene flow and recurrent mutations. Fisher and Wright have some fundamental disagreements about the role of selection and relative shift.
The availability of molecular data on all genetic differences leads to a neutral molecular evolution theory. In this view, many mutations are destructive and never observed, and most of the rest are neutral, ie not in selection. With the fate of each neutral mutation left to chance (genetic aberration), the direction of evolutionary change is driven by mutation, so that it can not be captured by the alter (all alone) frequency change models alone.
The view of the genetic origin of the population generalizes this approach outside of a very neutral mutation, and looks at the rate at which certain changes occur as a product of the rate of mutation and the probability of fixation.
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Four processes
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Natural selection, which includes sexual selection, is the fact that some properties make it possible for organisms to survive and reproduce. The genetic population describes natural selection by defining fitness as a tendency or the possibility of survival and reproduction in certain environments. Fitness is usually given by the symbol w = 1- s where s is the selection coefficient. Natural selection acts on a phenotype, so the population genetic model considers a relatively simple relationship to predict the phenotype and hence the fitness of the allele at one or a small number of loci. In this way, natural selection alters the differences in individual fitness with different phenotypes into alel frequency changes in populations over successive generations.
Prior to the emergence of population genetics, many biologists doubt that small differences in fitness are enough to make a big difference to evolution. Population geneticists address these concerns in part by comparing selection with genetic drift. Selection can overcome the genetic shift when s is greater than 1 divided by the size of the effective population. When these criteria are met, it is likely that the new beneficial mutant becomes fixed approximately equal to 2s . The time to fixation of such an allele depends heavily on genetic drift, and is roughly proportional to log (sN)/s.
Domination
Dominance means that the phenotypic and/or fitness effects of an allele on the locus depend on which allele is in the second copy for that locus. Consider three genotypes in one locus, with the following fitness values
s is the selection coefficient and h is the coefficient of dominance. The value of h yields the following information:
Epistasis
Epistasis means that the phenotypic and/or allelic fitness effects of one locus depend on which allele is in another locus. Selection does not act on a single locus, but on a phenotype that appears through the development of a complete genotype. However, many of the genetic models of the population of sexual species are the "single locus" model, in which individual fitness is calculated as a product of the contribution of each locale - effectively assuming no epistasis.
In fact, the genotype to the fitness landscape is more complex. Population genetics should model these complexities in detail, or capture them with some simpler average rules. Empirically, beneficial mutations tend to have smaller fitness benefits when added to a high-fitness genetic background: this is known as reduced epistatic return. When a damaging mutation also has a smaller fitness effect on a high fitness background, this is known as "synergistic epistasis". However, damaging mutation effects tend to be on average very close to multiplication, or may even show opposite patterns, known as "epistatic antagonists".
Synergistic epistasis is central to several theories about the mutilation of mutation loads and the evolution of sexual reproduction.
Mutations
Mutations are the main source of genetic variation in the form of a new allele. In addition, mutations may influence the course of evolution when there is a mutation bias, ie different probabilities for different mutations occur. For example, recurrent mutations that tend to be in the opposite direction of selection may lead to a selection-mutation balance. At the molecular level, if mutations from G to A occur more often than mutations from A to G, then genotypes with A will tend to evolve. Different insertion vs. removal of mutation bias in different taxa can lead to the evolution of different genomic sizes. Developmental biases or mutations have also been observed in morphological evolution. For example, according to the theory of evolution of the first phenotype, mutations may eventually lead to genetic assimilation of properties previously caused by the environment.
The effect of mutation bias is superimposed on other processes. If the selection will support one of two mutations, but there is no additional advantage to having both, the most frequent mutations are the most likely to remain in the population.
Mutations can have no effect, alter gene products, or prevent genes from functioning. Rapid study Drosophila melanogaster suggests that if mutations alter proteins produced by genes, this may be dangerous, with about 70 percent of these mutations having a destructive effect, and the rest either neutral or highly profitable. Most loss of function mutations is selected against. But when selection is weak, a mutation bias against loss of function can affect evolution. For example, pigments are no longer useful when animals live in dark caves, and tend to disappear. Such loss of function can occur because of mutation bias, and/or because the function has a cost, and once the benefits of the function disappear, natural selection leads to a loss. The loss of sporulation ability in bacteria during laboratory evolution appears to have been caused by mutation bias, rather than natural selection on the cost of maintaining sporulation ability. When there is no selection for loss of function, the rate at which disadvantages evolve depends more on the rate of mutation than on the size of the effective population, indicating that it is driven more by mutation bias than by genetic aberrations.
Mutations can involve large parts of duplicated DNA, usually through genetic recombination. This leads to a variation in the number of copies in a population. Duplication is the main source of raw materials for developing new genes. Other types of mutations sometimes create new genes from previously unmodified DNA.
Genetic drift
Genetic drift is the frequency change of alleles caused by random sampling. That is, the allele in the offspring is a random sample of parents. Genetic drift can cause the gene variant to completely disappear, and thus reduce genetic variability. In contrast to natural selection, which makes gene variants more common or less common depending on their reproductive success, changes because genetic drift is not driven by environmental or adaptive stresses, and equally tend to make the allele more common because it is less common.
The effect of genetic drift is greater for alleles present in multiple copies than when alleles are present in multiple copies. Genetics of genetic drift populations are described using a branching process or a diffusion equation that describes the change in allele frequencies. This approach is usually applied to the genetic model of the Wright-Fisher and Moran populations. Assuming genetic aberrations are the only evolutionary forces acting on alleles, after generation t in many replicated populations, starting with the frequency of allele p and q, the variance in allele frequency in that population is
Ronald Fisher argues that genetic drift plays the smallest role in evolution, and this has remained the dominant view for decades. There is no genetic perspective of the population that ever gave genetic shifts as a central role by itself, but some have made important genetic drift in combination with other non-selective forces. Sewall Wright's shifting balance theory suggests that combinations of population structures and genetic drift are important. Molecular evolutionary theory Motoo Kimura claims that most of the genetic differences within and between populations are caused by a combination of neutral mutations and genetic drift.
The role of genetic drift by way of sampling error in evolution has been criticized by John H. Gillespie and Will Provine, who argue that selection on related sites is a more important stochastic force, doing jobs traditionally thought to originate from genetic drift by sampling error. The mathematical properties of the genetic concept differ from the drifting genetic. The direction of random changes in allele frequencies is cross-generational autocorrelation.
Gene flow
Because of the physical barriers to migration, along with the limited tendency for individuals to move or spread (vagilitas), and the tendency to remain or return to the birth place (philopatry), a rare natural population of all crossbreeding can be assumed in a theoretical random model (panmixy). There is usually a geographical range in which individuals are more closely related to each other than randomly selected from the general population. This is described as to what extent a population is genetically structured. Structuring genetics can be caused by migration due to historical climate change, extending the range of species or the availability of current habitats. Gene flow is blocked by mountains, oceans and deserts or even man-made structures such as the Great Wall of China, which has inhibited the flow of plant genes.
The flow genes are the exchange of genes between populations or species, breaking down structures. Examples of genetic flow within a species include migration and then the cultivation of organisms, or pollen exchanges. Gene transfer between species includes the formation of hybrid organisms and horizontal gene transfer. The population genetic model can be used to identify which populations show significant gene isolation from each other, and to reconstruct its history.
Subdue population to isolation causes inbreeding depression. Migration to a population may introduce new genetic variants, potentially contributing to evolutionary salvation. If most individuals or gametes migrate, it can also change the frequency of alleles, e.g. thereby causing a migration load.
In the presence of gene flow, another obstacle to hybridization between two populations deviating from aberrant species is required for the population to become a new species.
Horizontal gene transfer
Horizontal gene transfer is the transfer of genetic material from one organism to another non-hereditary organism; this is most common among prokaryotes. In the medical world, this contributes to the spread of antibiotic resistance, such as when one bacterium acquires the resistance gene it quickly transfers it to another species. Horizontal gene switching from bacteria to eukaryotes such as yeast Saccharomyces cerevisiae and adzuki beetle Callosobruchus chinensis may also have occurred. A large-scale transfer example is the eukaryotic bdelloid rotifer, which appears to have received many genes from bacteria, fungi, and plants. Viruses can also carry DNA between organisms, enabling the transfer of genes even across biological domains. Large-scale gene transfer also occurs between ancestral eukaryotic and prokaryotic cells, during the acquisition of chloroplasts and mitochondria.
Link
If all genes are in the linkage balance, the allele effect on one locus can be averaged across genes in other loci. In fact, one allele is often found in an imbalance of relationships with genes in other loci, especially with genes located nearby on the same chromosome. Recombination breaks up this relationship imbalance too slowly to avoid a genetic jump, in which alleles at one locus rise to high frequencies as they are related to the selected allele at the nearby locus. The association also slows the rate of adaptation, even in the sexual population. The disequilibrium linked effect in slowing the rate of adaptive evolution arises from a combination of Hill-Robertson effects (delays in bringing mutations favorable together) and background selection (delays in separating beneficial mutations from destructive hitchhikers).
Linkage is a problem for the population's genetic model that treats one gene locus at a time. However, it can be exploited as a method for detecting natural selection actions through selective sweeps.
In the extreme case of asexual populations, the relationship is complete, and the population genetic equation can be derived and solved in terms of genotype frequency travel waves along a simple fitness landscape. Most microbes, such as bacteria, are asexual. The genetics of their adaptation population have two contrasting regimes. When mutation rate products are favorable and small population size, asexual populations follow the "successful regime" of the dynamics of the original fixation, with adaptation rates dependent heavily on this product. When the product is much larger, the asexual population follows a "concurrent mutation" of the regime with a product-dependent adaptation level, characterized by clonal disturbance and the emergence of a favorable new mutation before the latter has been repaired.
Apps
Describes the level of genetic variation
Neutral theory predicts that the level of nucleotide diversity in a population will be proportional to the product of the population size and the rate of neutral mutation. The fact that the level of genetic diversity varies is much smaller than the population size known as the "variation paradox". While a high degree of genetic diversity is one of the original arguments in favor of neutral theory, the paradox of variation has been one of the strongest arguments against neutral theory.
It is clear that the extent of genetic diversity varies greatly within a species as a function of local recombination rates, due to both genetic jumps and background selection. Most of the current solutions to the variation paradox call some level of selection on related sites. For example, one analysis shows that larger populations have more selective sweep, eliminating more neutral genetic diversity. A negative correlation between the rate of mutation and population size can also contribute.
Life history affects genetic diversity beyond the history of the population, e.g. r-strategies have more genetic diversity.
Detects selection
The population genetic model is used to infer which genes are undergoing selection. One common approach is to look for areas with high relative disequilibrium and low genetic variances along the chromosomes, to detect recent selective sweeps.
The second common approach is the McDonald-Kreitman test. The McDonald-Kreitman test compares the number of variations in a species (polymorphism) with the difference between species (substitutions) on two types of sites, which are assumed to be neutral. Typically, identical sites are considered neutral. The genes that undergo a positive selection have different site advantages relative to polymorphic sites. This test can also be used to obtain an approximate area of ​​the genome of the proportion of substitutions established by positive selection,.. According to the theory of neutral molecular evolution, this figure should be close to zero. Hence the high numbers have been interpreted as falsifying the broad-genral neutral theory.
Demographic deviation
The simplest test for population structure in sexually transmloated species, is to see whether the genotype frequency follows the proportion of Hardy-Weinberg as an allele frequency function. For example, in the simple case of a single locus with two alleles denoted A and a at frequencies p and q , random mating predicts the freq ( AA ) Ã, = p 2 for homozygous AA , freq ( aa ) Ã, =
Coalescence theory attributes genetic diversity in the sample to the demographic history of the population from which it was taken. It is usually assumed to be neutrality, and so the sequence of the more neutral-evolution part of the genome is chosen for the analysis. It can be used to infer the relationship between species (phylogenetic) and population structure, demographic history (eg population congestion or population growth), and introgression within a species.
Another approach to demographic inference depends on the frequency spectrum of the allele.
Evolution of the genetic system
Assuming that there is a locus that controls the genetic system itself, the population's genetic model is made to illustrate the evolution of dominance and other forms of robustness, the evolution of sexual reproduction and the rate of recombination, the evolution of the mutation rate, the evolutionary evolutionary capacities. , the evolution of expensive signaling features, the evolution of aging, and the evolution of cooperation. For example, most mutations are damaging, so the optimal mutation rate for a species can be a trade-off between damage from very destructive mutation rates and metabolic costs of system maintenance to reduce mutation rates, such as DNA repair enzymes.
One important aspect of the model is that selection is only strong enough to eradicate damaging mutations and therefore defeat the mutation bias against degradation if the selection coefficient is greater than the inverse of the effective population size. This is known as a drift barrier and is associated with almost neutral molecular evolutionary theory. The drift barrier theory predicts that species with large effective population sizes will have very efficient and efficient genetic systems, while those with small population sizes will have a swollen and complex genome containing eg introns and transposable elements. However, rather paradoxically, species with large population sizes may be very tolerant of the consequences of certain types of errors so they develop higher error rates, eg. in transcription and translation, from a small population.
See also
References
External links
- Population Genetics Tutorial
- Molecular population genetics
- ALlele Frequency Database at Yale University
- EHSTRAFD.org - Earth Human STR Allele Frequencies Database
- Population genetic history
- How Selection Changes Genetic Composition Population, video lecture by Stephen C. Stearns (Yale University)
- National Geographic: Human Traffic Atlas (Haplogroup-based human migration map)
- Monash Virtual Laboratory - Simulation of habitat fragmentation and population genetics online at Virtual Laboratory Monash University.
Source of the article : Wikipedia
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