Low genetic diversity in the wild cheetah population : Populations of wild cheetahs have very low genetic variation. Because wild cheetahs are threatened, their species has a very low genetic diversity. Variation allows some individuals within a population to adapt to the changing environment. Because natural selection acts directly only on phenotypes, more genetic variation within a population usually enables more phenotypic variation.
Other new alleles may be immediately detrimental such as a malformed oxygen-carrying protein and organisms carrying these new mutations will die out. Neutral alleles are neither selected for nor against and usually remain in the population. Genetic variation is advantageous because it enables some individuals and, therefore, a population, to survive despite a changing environment.
Some species display geographic variation as well as variation within a population. Geographic variation, or the distinctions in the genetic makeup of different populations, often occurs when populations are geographically separated by environmental barriers or when they are under selection pressures from a different environment. One example of geographic variation are clines: graded changes in a character down a geographic axis. Gene duplication, mutation, or other processes can produce new genes and alleles and increase genetic variation.
New genetic variation can be created within generations in a population, so a population with rapid reproduction rates will probably have high genetic variation. However, existing genes can be arranged in new ways from chromosomal crossing over and recombination in sexual reproduction.
Overall, the main sources of genetic variation are the formation of new alleles, the altering of gene number or position, rapid reproduction, and sexual reproduction.
Apply the law of segregation to determine the chances of a particular genotype arising from a genetic cross. Observing that true-breeding pea plants with contrasting traits gave rise to F 1 generations that all expressed the dominant trait and F 2 generations that expressed the dominant and recessive traits in a ratio, Mendel proposed the law of segregation.
The law of segregation states that each individual that is a diploid has a pair of alleles copy for a particular trait. Each parent passes an allele at random to their offspring resulting in a diploid organism. The allele that contains the dominant trait determines the phenotype of the offspring. In essence, the law states that copies of genes separate or segregate so that each gamete receives only one allele.
For the F 2 generation of a monohybrid cross, the following three possible combinations of genotypes could result: homozygous dominant, heterozygous, or homozygous recessive. The equal segregation of alleles is the reason we can apply the Punnett square to accurately predict the offspring of parents with known genotypes.
The behavior of homologous chromosomes during meiosis can account for the segregation of the alleles at each genetic locus to different gametes. As chromosomes separate into different gametes during meiosis, the two different alleles for a particular gene also segregate so that each gamete acquires one of the two alleles.
Independent assortment allows the calculation of genotypic and phenotypic ratios based on the probability of individual gene combinations.
Use the probability or forked line method to calculate the chance of any particular genotype arising from a genetic cross. The independent assortment of genes can be illustrated by the dihybrid cross: a cross between two true-breeding parents that express different traits for two characteristics.
Consider the characteristics of seed color and seed texture for two pea plants: one that has green, wrinkled seeds yyrr and another that has yellow, round seeds YYRR. Clearly the population had evolved to a higher adaptive condition.
Because population changes require changes in gene frequencies, it is important to understand how these frequencies can change. The three primary methods of change are mutation, migration and selection. Each will be considered individually. Mutation Mutations are classified as beneficial, harmful or neutral. Harmful mutations will be lost if they reduce the fitness of the individual.
If fitness is improved by a mutation, then frequencies of that allele will increase from generation to generation. The mutation could be a change in one allele to resemble one currently in the population, for example from a dominant to a recessive allele.
Alternatively, the mutation could generate an entirely new allele. Most of these mutations though will be detrimental and lost. But if the environment changes, then the new mutant allele may be favored and eventually become the dominant alelle in that population.
If the mutation is beneficial to the species as a whole, migration from the population in which it initially arose must occur for it to spread to other populations of the species. The most basic type of mutation is the change in a single nucleotide in the gene. Mutations are generally deleterious and are selected against. But the genome of a species can undergo another type of change, gene duplication, which actually favors mutational events.
If a single gene that is important undergoes a duplication, mutation in the duplicated copy would not necessarily reduce the fitness of the individual because it still would have a functioning copy of the original gene. With this adaptive constraint removed, further changes can occur that generate a new gene that has a similar function in the organism, but may function at a specific time in development, or in a unique location in the individual. This type of evolution generates multigene families.
Many important genes such as hemoglobin and muscle genes in humans, and seed storage and photosynthetic genes in plants are organized as multigene families. Populations of pathogens undergoing selection will constantly evolve to increase their overall level of fitness. The type of selection that operates will determine the direction of change in allele frequency to achieve the optimum overall fitness for the population Figure Figure The effects of selection on allele frequency in a one-locus, two allele fitness model.
In case 1, the A allele has a fitness advantage over the a allele. In case 2, the a allele has a fitness advantage over the A allele.
According to Fisher's Fundamental Theorem of Natural Selection the mean fitness of a population always increases in a fluctuating environment. The change in fitness of a selected population will be proportional to the additive genetic variation for genes affecting fitness in the population.
Therefore, populations will move to the nearest local optimum of allele frequencies that maximize fitness, which is not necessarily the global optimum.
As the amount of genetic variation in populations increases, the rate of change in fitness of the population increases proportionally. As a result, populations with the greatest genetic diversity have the greatest potential for evolution. Natural selection is the driving force for boom and bust cycles and for the evolution of fungicide resistance in plant pathogens. Selection can occur on genes increasing and decreasing the frequencies of specific alleles or on genotypes increasing and decreasing the frequencies of specific clones.
Both types of selection are well documented in pathogen populations. As an example, selection on genes alleles occurs when mutants that lost an avirulence allele encounter a plant with a resistance gene.
This process has been documented dozens of times for cereal rusts and mildews. Selection on genotypes occurs for Fusarium oxysporum formae speciales and probably explains the displacement of the "old" clone of Phytophthora infestans by the "new" clones of P. A further example comes from the barley pathogen Rhynchosporium secalis. Figure 25 shows evidence of directional selection as the R. A final example comes from oat crown rust and stem rust, caused by Puccinia coronata and Puccinia graminis f.
Following the development of Victoria blight caused by Helminthosporium victoriae which caused a devastating disease only on oat cultivars carrying a crown rust resistance gene originating from the oat cultivar Victoria, oat farmers rapidly shifted to new varieties carrying rust resistance derived from the oat cultivar Bond.
The corresponding pathogen populations rapidly shifted from virulence against the Victoria resistance genes toward virulence against the Bond resistance genes Figure The haploid model of natural selection is based on one locus with two alleles, and is applicable to haploid fungal pathogens such as ascomycetes , bacteria and viruses. This model can be applied to selection for multilocus haplotypes as well as individual alleles at single loci.
This model can be used to estimate rates of change for avirulence alleles sexual reproduction or for measuring competition among multilocus haplotypes under asexual reproduction.
If w 1 and w 2 are the fitnesses associated with alleles haplotypes A 1 and A 2 respectively, then we can predict the change in frequency of the A 2 allele haplotype after one generation of selection as follows:. This formula represents the general selection formula that can be applied to any case of selection involving a haploid organism.
This model is used to predict how fast allele or haplotype frequencies will change when an avirulent pathotype encounters a host population with the corresponding resistance allele. Neither dominance nor overdominance is possible in this case. Selection quickly removes deleterious e. Though our prediction from selection models is that avirulence alleles should rapidly disappear after resistance genes are introduced into plant populations, many empirical studies indicate that populations of haploid pathogens are quite variable at avirulence loci.
Individual pathogen strains vary in other phenotypes as well as for avirulence genes. Three important questions to consider are:. Many plant pathologists such as Van der Plank considered these questions in the framework of the gene-for-gene interaction between plants and pathogens.
They believed that "stabilizing selection" that we now know is really directional selection against unnecessary virulence alleles was one of the mechanisms maintaining genetic variation of haploid pathogens. The basic idea of gene-for-gene interactions according to Van der Plank was that if the virulence allele loss of elicitor is not needed for the pathogen to infect the plant, and there is a fitness cost associated with losing the elicitor, then in the presence of the resistant host, selection will favor strains with the avirulence allele, and the level of virulence in the pathogen population will "stabilize.
Plant pathologists have tried to explain variation at the avirulence loci of pathogens for decades. The classic selection model in plant pathosystems is best exemplified by the models of K. Leonard and his colleagues Leonard and Czochor, Leonard, They explained why unnecessary virulence genes persist in natural and agricultural ecosystems.
They also explained how variation for virulence persists in the presence of resistant hosts. Leonard used the diploid host and haploid pathogen general selection models and the assumptions of a gene-for-gene interaction to calculate pathogen and host fitness as follows:. Host fitness is dependent on the virulence of the pathogen as well as pathogen fitness on each host as follows:. Leonard and his colleagues used these models to determine the equilibrium allele frequencies and conditions needed to achieve an equilibrium state i.
They determined the values of k and c that were necessary to achieve a stable equilibrium and found that there had to be a fitness cost associated with resistance and also with unnecessary virulence in order to achieve an equilibrium. They also used this selection model to show the effects of changing allele frequencies and parameter values on the ultimate fate of gene frequencies.
They concluded that:. Though it is very difficult to measure fitness and estimate selection coefficients, plant pathologists have made many attempts because of the profound implications of these measurements for the utilization of resistance genes. If the fitness cost of a mutation from avirulence to virulence is very low, then pathogen populations will retain the virulence mutation at a significant frequency even after the resistance gene is removed from the agroecosystem. In these cases, it is likely that the resistance gene will never again be effective.
But if the fitness cost of the virulence mutation is high, then resistance genes are likely to remain durable e. Leach et al. Most studies of pathogen fitness cannot be generalized because of the difficulties of conducting these experiments. Fitness should be determined at the level of populations rather than for individuals because a pathogen population is often composed of many different genotypes.
But plant pathologists almost always work with just a few individuals to evaluate fitness to simplify the experimental methods. To measure fitness, sample sizes must be large when s the selection coefficient is small, but sample sizes are usually small individuals in field or greenhouse experiments due to practical limitations on the number of samples that can be handled.
Fungi with mixed reproductive systems present special challenges when measuring fitness because selection can operate on alleles sexual populations , genotypes asexual populations or simultaneously on both alleles and genotypes mixed reproduction systems. While selection always occurs on the individual through its phenotype, it can be difficult to distinguish between selection for specific alleles e.
Different alleles can occur in a single genetic background as a result of mutation within clonal lineages. And the same allele can occur in different genetic backgrounds as a result of the same mutation in different clonal lineages. Many greenhouse experiments have been conducted to compare fitness of pathogen strains carrying different virulence alleles. The following representative examples were chosen to show how the experiments have been conducted and how the results have not led to a clear interpretation of the fitness cost associated with unneeded virulence alleles.
Kolmer used a diverse collection of Puccinia triticina syn. Puccinia recondita f. The diverse sexual progeny were cycled for 12 asexual generations through Roblin, Thatcher, and two isogenic Thatcher lines with different known resistance genes. Kolmer found no relationship between the number of unneeded virulence alleles and the fitness of the P.
The most susceptible host, Thatcher, maintained the pathogen population with the greatest diversity of virulence alleles, indicating little or no selection against unnecessary virulence alleles. Kolmer suggested that differences in effective population size at the start of the experiment had a significant impact on the results, while selection in favor of necessary specific virulence alleles was more relevant than selection against unnecessary virulence alleles.
It is also possible that at least some of these observations were due to selection for particular clones and clonal lineages carrying unnecessary virulence alleles in each host population.
Leonard used a diverse collection of Puccinia graminis f. The diverse pathogen population at the beginning of the experiment was derived from over aecial infections. This rust population was passaged through oat cultivars Craig susceptible and Clintland A with resistance gene A for eight asexual generations and then tested for presence of virulence alleles corresponding to resistance alleles in a set of oat differentials.
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