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Register a new userDiscordance between genomic divergence and phenotypic variation in a rapidly evolving avian genus (Motacilla)
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Generally, genotypes and phenotypes are expected to be spatially congruent, however, in widespread species complexes with few barriers to dispersal, multiple contact zones, and limited reproductive isolation, discordance between phenotypes and phylogeographic groups is more probable. Wagtails (Aves: Motacilla) are a genus of birds with striking plumage pattern variation across Eurasia. Up to 13 subspecies are recognized within a single species, yet previous studies using mitochondrial DNA have supported phylogeographic groups that are inconsistent with subspecies plumage characteristics. In this study, we investigate the link between phenotypes and genotype by comparing populations thought to be at different stages along the speciation continuum. We take a phylogeographic approach by estimating population structure, testing for isolation by distance, conducting demographic modeling, and estimating the first time-calibrated species tree for the genus. Our study provides strong evidence for species-level patterns of differentiation in wagtails, however population-level differentiation is less pronounced. We find evidence that three of four widespread Eurasian species exhibit an east-west divide that contradicts both subspecies taxonomy and phenotypic variation. Both the geographic location of this divide and time estimates from demographic models are overlapping in two sympatric species, indicating that coincident Pleistocene events shaped their histories.
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We examine the distribution of heterozygous sites in nine European and nine Yoruban individuals whose genomic sequences were made publicly available by Complete Genomics. We show that it is possible to obtain detailed information about inbreeding when a relatively small set of whole-genome sequences is available. Rather than focus on testing for deviations from Hardy-Weinberg genotype frequencies at each site, we analyze the entire distribution of heterozygotes conditioned on the number of copies of the derived (non-chimpanzee) allele. Using Levenes exact test, we reject Hardy-Weinberg in both populations. We generalized Levenes distribution to obtain the exact distribution of the number of heterozygous individuals given that every individual has the same inbreeding coefficient, F. We estimated F to be 0.0026 in Europeans and 0.0005 in Yorubans, but we could also reject the hypothesis that F was the same in each individual. We used a composite likelihood method to estimate F in each individual and within each chromosome. Variation in F across chromosomes within individuals was too large to be consistent with sampling effects alone. Furthermore, estimates of F for each chromosome in different populations were not correlated. Our results show how detailed comparisons of population genomic data can be made to theoretical predictions. The application of methods to the Complete Genomics data set shows that the extent of apparent inbreeding varies across chromosomes and across individuals, and estimates of inbreeding coefficients are subject to unexpected levels of variation which might be partly accounted for by selection.
When analysing in vitro data, growth kinetics of influenza strains are often compared by computing their growth rates, which are sometimes used as proxies for fitness. However, analogous to mechanistic epidemic models, the growth rate can be defined as a function of two parameters: the basic reproduction number (the average number of cells each infected cell infects) and the mean generation time (the average length of a replication cycle). Using a mechanistic model, previously published data from experiments in human lung cells, and newly generated data, we compared estimates of all three parameters for six influenza A strains. Using previously published data, we found that the two human-adapted strains (pre-2009 seasonal H1N1, and pandemic H1N1) had a lower basic reproduction number, shorter mean generation time and slower growth rate than the two avian-adapted strains (H5N1 and H7N9). These same differences were then observed in data from new experiments where two strains were engineered to have different internal proteins (pandemic H1N1 and H5N1), but the same surface proteins (PR8), confirming our initial findings and implying that differences between strains were driven by internal genes. Also, the model predicted that the human-adapted strains underwent more replication cycles than the avian-adapted strains by the time of peak viral load, potentially accumulating mutations more quickly. These results suggest that the in vitro reproduction number, generation time and growth rate differ between human-adapted and avian-adapted influenza strains, and thus could be used to assess host adaptation of internal proteins to inform pandemic risk assessment.
The unwelcome evolution of malignancy during cancer progression emerges through a selection process in a complex heterogeneous population structure. In the present work, we investigate evolutionary dynamics in a phenotypically heterogeneous population of stem cells (SCs) and their associated progenitors. The fate of a malignant mutation is determined not only by overall stem cell and differentiated cell growth rates but also differentiation and dedifferentiation rates. We investigate the effect of such a complex population structure on the evolution of malignant mutations. We derive exact analytic results for the fixation probability of a mutant arising in each of the subpopulations. The analytic results are in almost perfect agreement with the numerical simulations. Moreover, a condition for evolutionary advantage of a mutant cell versus the wild type population is given in the present study. We also show that microenvironment-induced plasticity in invading mutants leads to more aggressive mutants with higher fixation probability. Our model predicts that decreasing polarity between stem and differentiated cells turnover would raise the survivability of non-plastic mutants; while it would suppress the development of malignancy for plastic mutants. We discuss our model in the context of colorectal/intestinal cancer (at the epithelium). This novel mathematical framework can be applied more generally to a variety of problems concerning selection in heterogeneous populations, in other contexts such as population genetics, and ecology.
Movement tracks of wild animals frequently fit models of anomalous rather than simple diffusion, mostly reported as ergodic superdiffusive motion combining area-restricted search within a local patch and larger-scale commuting between patches, as highlighted by the Levy walk paradigm. Since Levy walks are scale invariant, superdiffusive motion is also expected within patches, yet investigation of such local movements has been precluded by the lack of accurate high-resolution data at this scale. Here, using rich high-resolution movement datasets ($>! 7 times 10^7$ localizations) from 70 individuals and continuous-time random walk modeling, we found subdiffusive behavior and ergodicity breaking in the localized movement of three species of avian predators. Small-scale, within-patch movement was qualitatively different, not inferrable and separated from large-scale inter-patch movement via a clear phase transition. Local search is characterized by long power-law-distributed waiting times with diverging mean, giving rise to ergodicity breaking in the form of considerable variability uniquely observed at this scale. This implies that wild animal movement is scale specific rather than scale free, with no typical waiting time at the local scale. Placing these findings in the context of the static-ambush to mobile-cruise foraging continuum, we verify predictions based on the hunting behavior of the study species and the constraints imposed by their prey.
Woolly mammoths (Mammuthus primigenius) populated Siberia, Beringia, and North America during the Pleistocene and early Holocene. Recent breakthroughs in ancient DNA sequencing have allowed for complete genome sequencing for two specimens of woolly mammoths (Palkopoulou et al. 2015). One mammoth specimen is from a mainland population ~45,000 years ago when mammoths were plentiful. The second, a 4300 yr old specimen, is derived from an isolated population on Wrangel island where mammoths subsisted with small effective population size more than 43-fold lower than previous populations. These extreme differences in effective population size offer a rare opportunity to test nearly neutral models of genome architecture evolution within a single species. Using these previously published mammoth sequences, we identify deletions, retrogenes, and non-functionalizing point mutations. In the Wrangel island mammoth, we identify a greater number of deletions, a larger proportion of deletions affecting gene sequences, a greater number of candidate retrogenes, and an increased number of premature stop codons. This accumulation of detrimental mutations is consistent with genomic meltdown in response to low effective population sizes in the dwindling mammoth population on Wrangel island. In addition, we observe high rates of loss of olfactory receptors and urinary proteins, either because these loci are non-essential or because they were favored by divergent selective pressures in island environments. Finally, at the locus of FOXQ1 we observe two independent loss-of-function mutations, which would confer a satin coat phenotype in this island woolly mammoth.
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