A number of selective forces might act to structure genetic variation. Genetic variation among isolates in factors such as transmission route or resistance to host immune genotypes would lead to cryptic stratification within populations; that is, the pathogen population could be divided into isolated subpopulations, each specializing in the colonization of different groups of hosts.
In this scenario, gene flow between subpopulations would be most greatly limited at sites closely genetically linked to genes responsible for host specialization. This process could, however, exert an influence over the entire genome through hitchhiking Maynard Smith and Haigh An extension of these ideas is that stratification is a dynamic process, emerging from the ongoing coevolution between the pathogen and the host immune system.
New variants that are more efficient at transmitting e. These ideas are related to the epidemic-clone model Maynard Smith et al. In the case of the meningococcus, this model is apparently inapplicable, as transmission is not disease associated Levin and Bull ; Maiden ; however, increased disease risk, although not adaptive to isolates, could be an unavoidable consequence of increased transmission efficiency.
The ST complex and the other hyperinvasive lineages, could, therefore, be recent in evolutionary origin and associated with increased transmission rates, perhaps through the possession of novel genotypes at antigen-encoding loci, such as the capsule operon. Such variants would tend to rapidly increase in frequency, generating a hitchhiking event at linked sites and, therefore, generating high-frequency STs.
As host immunity increased at the population level, so the selective advantage of the novel variant would decrease, preventing any single variant from dominating the entire population.
This dynamic would lead to repeated structuring of genetic variation and differentiation between disease-associated and carrier isolates at the ST level, as reported here. The repeated and independent origin of such variants would mean that disease-associated and carriage populations would share a common gene pool at the level of nucleotide polymorphisms; this is also consistent with our findings.
More extensive genome-wide analyses of variation would identify candidate genes for disease association through showing elevated levels of structuring. Estimates of the population-mutation rate, the population-recombination rate, and the average size of DNA fragments introduced by recombination enabled a comparison of the relative influence of recombination and mutation on patterns of diversity observed. The relative rate of recombination to mutation has been proposed to be of fundamental importance in determining the degree of clonal structure present in a given bacterial population Feil et al.
It is also informative to consider the relative role of recombination and mutation in generating diversity at the interlocus or genome level. Across loci, estimates of this ratio lie in the remarkably narrow range of 6.
In summary, in terms of generating novel genomes, recombination is roughly 10 times as important as mutation. The average tract length in recombination events was estimated to be 1. This is considerably less than the value of 7. The discrepancy is most likely a result of the difference between those events that occur and those that persist over evolutionary time.
Larger tracts will introduce more nucleotide differences into the existing genome and, if epistatic interactions are important, are more likely to lead to a decrease in fitness Zhu et al. Shorter recombination tracts are less likely to lead to fitness decreases but are also harder to detect by direct methods. It is also worth noting that the average size of coding sequences in the meningococcal genome, at bp Parkhill et al. Consequently, many recombination events will include complete coding sequences.
In other words, gene replacement events would be more common than the generation of new alleles with mosaic structure when compared with the rates observed in bacteria that exhibit recombination fragment sizes that are smaller than the average coding sequence, such as Helicobacter pylori Falush et al.
The emergence of pathogenic variants within populations of commensal organisms can be rationalized when the disease syndrome contributes to the spread of the pathogen May and Anderson ; however, it is more difficult to explain the emergence and persistence of pathogenic variants in populations of bacteria such as N. As suggested above, this apparent paradox is resolved if disease is a consequence of increased transmission efficacy in recently arisen or introduced variants.
The behavior of the ST clonal complex is particularly illustrative of this effect. Previous studies indicated that normally these meningococci exhibit very low point prevalence in carriage, even during disease outbreaks Caugant et al.
However, at the time of the sample, the Czech Republic was experiencing a major epidemic of serogroup C ST complex meningococci. This work was funded by the Wellcome Trust.
Part of the work performed in the Czech Republic was supported by grant No. Balding, D. Likelihood-based inference for genetic correlation coefficients. Biol 63 : — Broome, C. The carrier state: Neisseria meningitidis. A : 25 — Caugant, D. Population genetics and molecular epidemiology of Neisseria meningitidis. Apmis : — Kristiansen, L. Bovre, and R. Clonal diversity of Neisseria meningitidis from a population of asymptomatic carriers.
Excoffier, L. Smouse, and J. Analysis of molecular variance inferred from metric distances among DNA haplotypes: application to human mitochondrial DNA restriction data. Genetics : — Falush, D. Kraft, N. Taylor, P. Correa, J. Fox, M. Achtman, and S. Recombination and mutation during long-term gastric colonization by Helicobacter pylori : estimates of clock rates, recombination size, and minimal age.
USA 98 : — Feavers, I. Gray, R. Urwin, J. Russell, J. Bygraves, E. Kaczmarski, and M. Multilocus sequence typing and antigen gene sequencing in the investigation of a meningococcal disease outbreak. Feil, E. Holmes, D. Bessen et al. Recombination within natural populations of pathogenic bacteria: short-term empirical estimates and long-term phylogenetic consequences.
Maiden, M. Achtman, and B. The relative contributions of recombination and mutation to the divergence of clones of Neisseria meningitidis. Maynard Smith, M. Enright, and B. Estimating recombinational parameters in Streptococcus pneumoniae from multilocus sequence typing data. Fu, Y. New statistical tests of neutrality for DNA samples from a population.
Holmes, E. Urwin, and M. The influence of recombination on the population structure and evolution of the human pathogen Neisseria meningitidis. Jolley, K. Chan, and M. BMC Bioinformatics 5 : Kalmusova, E. Feil, S. Gupta, M. Musilek, P. Kriz, and M.
Carried meningococci in the Czech Republic: a diverse recombining population. Kellerman, S. McCombs, M. Ray et al. Genotype-specific carriage of Neisseria meningitidis in Georgia counties with hyper- and hyposporadic rates of meningococcal disease. Krizova, P. Changing epidemiology of meningococcal invasive disease in the Czech Republic caused by new clone Neisseria meningitidis C:2a:P1.
Central Eur. Public Health 3 : — Levin, B. The evolution and maintenance of virulence in microparasites. Short-sighted evolution and the virulence of pathogenic microorganisms. Trends Microbiol. Linz, B. Schenker, P.
Zhu, and M. 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. Learning Objectives Assess the ways in which genetic variance affects the evolution of populations.
Key Points Genetic variation is an important force in evolution as it allows natural selection to increase or decrease frequency of alleles already in the population. Genetic variation is advantageous to a population because it enables some individuals to adapt to the environment while maintaining the survival of the population. Key Terms genetic diversity : the level of biodiversity, refers to the total number of genetic characteristics in the genetic makeup of a species crossing over : the exchange of genetic material between homologous chromosomes that results in recombinant chromosomes phenotypic variation : variation due to underlying heritable genetic variation ; a fundamental prerequisite for evolution by natural selection genetic variation : variation in alleles of genes that occurs both within and among populations.
Genetic Variation Genetic variation is a measure of the genetic differences that exist within a population. Genetic variation is caused by: mutation random mating between organisms random fertilization crossing over or recombination between chromatids of homologous chromosomes during meiosis The last three of these factors reshuffle alleles within a population, giving offspring combinations which differ from their parents and from others.
This phenotypic variation is due at least partly to genetic variation within the coquina population. Evolution and Adaptation to the Environment Variation allows some individuals within a population to adapt to the changing environment.
In the example below, one end of each chromosome of this homologous pair is exchanged along with the genes that they contain. The next generation inherits chromosomes with partially new sequences of alleles.
The consequence of this recombination is the production of sperm and ova that can potentially add even greater diversity to a population's gene pool. However, it does not result in new alleles. Subsequently, recombination by itself does not cause evolution to occur. Rather, it is a contributing mechanism that works with natural selection by creating combinations of genes that nature selects for or against.
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