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Register a new userChloroplast microsatellites reveal colonization and metapopulation dynamics in the Canary Island pine
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Chloroplast microsatellites are becoming increasingly popular markers for population genetic studies in plants, but there has been little focus on their potential for demographic inference. In this work the utility of chloroplast microsatellites for the study of population expansions was explored. First, we investigated the power of mismatch distribution analysis and the F(S) test with coalescent simulations of different demographic scenarios. We then applied these methods to empirical data obtained for the Canary Island pine (Pinus canariensis). The results of the simulations showed that chloroplast microsatellites are sensitive to sudden population growth. The power of the F(S) test and accuracy of demographic parameter estimates, such as the time of expansion, were reduced proportionally to the level of homoplasy within the data. The analysis of Canary Island pine chloroplast microsatellite data indicated population expansions for almost all sample localities. Demographic expansions at the island level can be explained by the colonization of the archipelago by the pine, while population expansions of different ages in different localities within an island could be the result of local extinctions and recolonization dynamics. Comparable mitochondrial DNA sequence data from a parasite of P. canariensis, the weevil Brachyderes rugatus, supports this scenario, suggesting a key role for volcanism in the evolution of pine forest communities in the Canary Islands.
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We formulate a compartmental model for the propagation of a respiratory disease in a patchy environment. The patches are connected through the mobility of individuals, and we assume that disease transmission and recovery are possible during travel. Moreover, the migration terms are assumed to depend on the distance between patches and the perceived severity of the disease. The positivity and boundedness of the model solutions are discussed. We analytically show the existence and global asymptotic stability of the disease-free equilibrium. Without human movement, the global stability of the endemic equilibrium point is also established using Lyapunov functions. We study three different network topologies numerically and find that underlying network structure is crucial for disease transmission. Further numerical simulations reveal that infection during travel has the potential to change the stability of disease-free equilibrium from stable to unstable. The coupling strength and transmission coefficients are also very crucial in disease propagation. Different exit screening scenarios indicate that the patch with the highest prevalence may have adverse effects but other patches will be benefited from exit screening. Furthermore, while studying the multi-strain dynamics, it is observed that two co-circulating strains will not persist simultaneously in the community but only one of the strains may persist in the long run. Transmission coefficients corresponding to the second strain are very crucial and show threshold like behavior with respect to the equilibrium density of the second strain.
We study the extinction risk of a fragmented population residing on a network of patches coupled by migration, where the local patch dynamics include the Allee effect. We show that mixing between patches dramatically influences the populations viability. Slow migration is shown to always increase the populations global extinction risk compared to the isolated case. At fast migration, we demonstrate that synchrony between patches minimizes the populations extinction risk. Moreover, we discover a critical migration rate that maximizes the extinction risk of the population, and identify an early-warning signal when approaching this state. Our theoretical results are confirmed via the highly-efficient weighted ensemble method. Notably, our analysis can also be applied to studying switching in gene regulatory networks with multiple transcriptional states.
We study the dynamics of colonization of a territory by a stochastic population at low immigration pressure. We assume a sufficiently strong Allee effect that introduces, in deterministic theory, a large critical population size for colonization. At low immigration rates, the average pre-colonization population size is small thus invalidating the WKB approximation to the master equation. We circumvent this difficulty by deriving an exact zero-flux solution of the master equation and matching it with an approximate non-zero-flux solution of the pertinent Fokker-Planck equation in a small region around the critical population size. This procedure provides an accurate evaluation of the quasi-stationary probability distribution of population sizes in the pre-colonization state, and of the mean time to colonization, for a wide range of immigration rates. At sufficiently high immigration rates our results agree with WKB results obtained previously. At low immigration rates the results can be very different.
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.
The metapopulation framework is adopted in a wide array of disciplines to describe systems of well separated yet connected subpopulations. The subgroups or patches are often represented as nodes in a network whose links represent the migration routes among them. The connections have been so far mostly considered as static, but in general evolve in time. Here we address this case by investigating simple contagion processes on time-varying metapopulation networks. We focus on the SIR process and determine analytically the mobility threshold for the onset of an epidemic spreading in the framework of activity-driven network models. We find profound differences from the case of static networks. The threshold is entirely described by the dynamical parameters defining the average number of instantaneously migrating individuals and does not depend on the properties of the static network representation. Remarkably, the diffusion and contagion processes are slower in time-varying graphs than in their aggregated static counterparts, the mobility threshold being even two orders of magnitude larger in the first case. The presented results confirm the importance of considering the time-varying nature of complex networks.
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