Is it possible to eliminate a recessive allele

What will happen if two people who are carriers for the alleles have children? Each of your parents would have to be a heterozygote Tt. With each child they produced, there would be a one in four chance that this child would inherit two recessive alleles and have the tt genotype. Half of the children of parents who are heterozygotes will also be heterozygotes Tt.

The takeaway message: this harmful allele persists in gene pools because it can hide out in heterozygotes. There are, of course, harmful dominant alleles. Because dominant alleles always have an immediate effect upon the phenotype, they tend to be strongly selected against. People with achondroplasia not only survive to adulthood: they can also reproduce. If N e is large enough to discount the effects of genetic drift, then we expect directional selection to fix the favored allele within a given focal deme.

However, the continual introduction, via gene flow, of alleles that are advantageous in other demes but deleterious in the focal deme, can counteract the effects of selection. In this scenario, the deleterious allele will remain at an intermediate equilibrium frequency that reflects the balance between gene flow and natural selection.

The common conception of evolution focuses on change due to natural selection. Natural selection is certainly an important mechanism of allele-frequency change, and it is the only mechanism that generates adaptation of organisms to their environments.

Other mechanisms, however, can also change allele frequencies, often in ways that oppose the influence of selection. A nuanced understanding of evolution demands that we consider such mechanisms as genetic drift and gene flow, and that we recognize the error in assuming that selection will always drive populations toward the most well adapted state.

Carroll, S. Conservation Biology: Evolution in Action. Darwin, C. London, England: John Murray, Gillespie, J. Population Genetics: A Concise Guide , 2nd ed. Haldane, J. A mathematical theory of natural and artificial selection, Part I. Transactions of the Cambridge Philosophical Society 23 , 19—41 Hedrick, P.

Genetics of Populations, 3rd ed. The Hardy-Weinberg Principle. Evolution Introduction. Life History Evolution. Mutations Are the Raw Materials of Evolution. Speciation: The Origin of New Species. Avian Egg Coloration and Visual Ecology. The Ecology of Avian Brood Parasitism. The Maintenance of Species Diversity. Neutral Theory of Species Diversity. Population Genomics.

Semelparity and Iteroparity. Geographic Mosaics of Coevolution. Comparative Genomics. Cybertaxonomy and Ecology. Ecological Opportunity: Trigger of Adaptive Radiation. Evidence for Meat-Eating by Early Humans. As soon as the first genetic markers became available breed associations started to test animals for these markers and started to eliminate heterozygote animals from breeding. It requires testing all the animals and that is often too costly.

Sometimes, e. The approved remaining rams with the desired alleles were highly related to each other and would give rise to a huge increase in inbreeding in later generations. Thus, as in case of scrapie, the allele frequencies for genetic defects might be rather high.

Then the best way is to test all the animals considered for breeding with the genetic marker. 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.

Pustules indicating a resistance reaction infection types 1 and 2 could be differentiated from pustules indicating a susceptible reaction infection types 3 and 4. On every differential variety, Leonard found an increase in the frequency of resistant-type pustules with increasing numbers of pathogen generations, consistent with directional selection against pathotypes with unnecessary virulence alleles.

He calculated that selection coefficients for unneeded virulence alleles ranged from 0. Prud'homme and Sackston used two pathotypes Race 1 and Race 3 of the sunflower rust pathogen Puccinia helianthi inoculated at equal frequencies onto a susceptible sunflower line CM and cycled through eight asexual generations. The resulting populations were inoculated onto the susceptible line and two sunflower lines CM29 and CM90RR carrying known resistance genes.

In this case, it was not possible to distinguish between selection against unnecessary virulence and selection for a particular genotype. Bronson and Ellingboe used two isolates of the wheat powdery mildew pathogen Blumeria graminis to inoculate an isogenic wheat line containing a known resistance gene. The virulence alleles present in the two pathogen strains were assayed on a set of isogenic wheat lines with known resistance genes.