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Linking dynamical and population genetic models of persistent viral infection.

This article develops a theoretical framework to link dynamical and population genetic models of persistent viral infection. This linkage is useful because, while the dynamical and population genetic theories have developed independently, the biological processes they describe are completely interrelated. Parameters of the dynamical models are important determinants of evolutionary processes such as natural selection and genetic drift. We develop analytical methods, based on coupled differential equations and Markov chain theory, to predict the accumulation of genetic diversity within the viral population as a function of dynamical parameters. These methods are first applied to the standard model of viral dynamics and then generalized to consider the infection of multiple host cell types by the viral population. Each cell type is characterized by specific parameter values. Inclusion of multiple cell types increases the likelihood of persistent infection and can increase the amount of genetic diversity within the viral population. However, the overall rate of gene sequence evolution may actually be reduced.

Biological Evolution↗

Population genetics of the Y chromosome of Drosophila melanogaster: rDNA variation and phenotypic correlates.

One means of examining the evolutionary significance of molecular variation on the Y chromosome is to identify phenotypes specifically affected by Y-linked genes, and to quantify the phenotypic variation and its correlation to the molecular variation. The functional importance of the Y-linked array of rRNA genes is demonstrated by the ability of Y chromosome to rescue X-linked bobbed lethal alleles, whose lethality is seen in homozygous females. Because low numbers of X-linked rDNA gene copies result in increased developmental time and shortened bristles, and because there is considerable natural variation in Y-linked copy number, a careful examination of Y-linked variation in these two traits may uncover a mode of selection acting on the multigene family. In this study, 36 Y-chromosome replacement lines were tested to detect subtle variation in bristle phenotypes and developmental rates. Correlations among these traits, rDNA gene copy number, and intergenic sequence length were quantified. The absence of significant correlations between phenotypic characters and rDNA copy number of intergenic sequence length suggests that the extant molecular variation in Y-linked rDNA can have at most very small selective effects.

Animals↗

Population genetic structure of Anopheles arabiensis mosquitoes in Ethiopia and Eritrea.

This study examined the population genetic structure of the major malaria vector, Anopheles arabiensis mosquitoes, in Ethiopia and Eritrea. Ethiopia and Eritrea have great geographical diversity, with high mountains, rugged plateaus, deep gorges, and rolling plains. The plateau is bisected diagonally by the Great Rift Valley into the Northwestern Highlands and the Southeastern Highlands. Five A. arabiensis populations from the Northwestern Highlands region and two populations from high-altitude sites in the Great Rift Valley were genotyped using six microsatellite markers to estimate the genetic diversity and population genetic structure of A. arabiensis. We found that A. arabiensis populations from the Northwestern Highlands and the Great Rift Valley region showed a similar level of genetic diversity. The genetic differentiation (F(ST)) of the five mosquito populations within the Northwestern Highlands region was 0.038 (P <.001), while the two populations within the Great Rift Valley showed little genetic differentiation (F(ST) = 0.007, P <.01). The degree of genetic differentiation between the Northwestern Highlands region and the Great Rift Valley region was small but statistically significant (F(ST) = 0.017, P <.001). The population genetic structure of A. arabiensis in the study area did not follow the isolation-by-distance model (r(2) = 0.014, P >.05). The low F(ST) estimates for A. arabiensis populations in Ethiopia and Eritrea are consistent with the general population genetic structure of this species in East Africa based on other molecular markers.

Animals↗

Population genetic structure of a colonising, triploid weed, Hieracium lepidulum.

Understanding the breeding system and population genetic structure of invasive weed species is important for biocontrol, and contributes to our understanding of the evolutionary processes associated with invasions. Hieracium lepidulum is an invasive weed in New Zealand, colonising a diverse range of habitats including native Nothofagus forest, pine plantations, scrubland and tussock grassland. It is competing with native subalpine and alpine grassland and herbfield vegetation. H. lepidulum is a triploid, diplosporous apomict, so theoretically all seed is clonal, and there is limited potential for the creation of variation through recombination. We used intersimple sequence repeats (ISSRs) to determine the population genetic structure of New Zealand populations of H. lepidulum. ISSR analysis of five populations from two regions in the South Island demonstrated high intrapopulation genotypic diversity, and high interpopulation genetic structuring; PhiST = 0.54 over all five populations. No private alleles were found in any of the five populations, and allelic differentiation was correlated to geographic distance. Cladistic compatibility analysis indicated that both recombination and mutation were important in the creation of genotypic diversity. Our data will contribute to any biocontrol program developed for H. lepidulum. It will also be a baseline data set for future comparisons of genetic structure during the course of H. lepidulum invasions.

Alleles↗

Notes on the population genetics of fragile X syndrome.

Our analysis of fragile X-inactivation in normal and mentally retarded heterozygotes led us to conclude that a fraction of female carriers of the imprinted (fully mutated) allele is phenotypically normal as a consequence of X-inactivation. Taking this into account, we derived equilibrium equations for the fragile X [fra(X)] genotype frequencies. We also showed that small variations in the value of s (selection coefficient of affected heterozygotes) and r (imprinting rate during oogenesis) affect genotype ratios significantly.

Dosage Compensation, Genetic↗