35,597 research outputs found
Simple model for the Darwinian transition in early evolution
It has been hypothesized that in the era just before the last universal
common ancestor emerged, life on earth was fundamentally collective. Ancient
life forms shared their genetic material freely through massive horizontal gene
transfer (HGT). At a certain point, however, life made a transition to the
modern era of individuality and vertical descent. Here we present a minimal
model for this hypothesized "Darwinian transition." The model suggests that
HGT-dominated dynamics may have been intermittently interrupted by
selection-driven processes during which genotypes became fitter and decreased
their inclination toward HGT. Stochastic switching in the population dynamics
with three-point (hypernetwork) interactions may have destabilized the
HGT-dominated collective state and led to the emergence of vertical descent and
the first well-defined species in early evolution. A nonlinear analysis of a
stochastic model dynamics covering key features of evolutionary processes (such
as selection, mutation, drift and HGT) supports this view. Our findings thus
suggest a viable route from early collective evolution to the start of
individuality and vertical Darwinian evolution, enabling the emergence of the
first species.Comment: 9 pages, 5 figures, under review at Physical Review
Phase Diagrams of Quasispecies Theory with Recombination and Horizontal Gene Transfer
We consider how transfer of genetic information between individuals
influences the phase diagram and mean fitness of both the Eigen and the
parallel, or Crow-Kimura, models of evolution. In the absence of genetic
transfer, these physical models of evolution consider the replication and point
mutation of the genomes of independent individuals in a large population. A
phase transition occurs, such that below a critical mutation rate an
identifiable quasispecies forms. We generalize these models of quasispecies
evolution to include horizontal gene transfer. We show how transfer of genetic
information changes the phase diagram and mean fitness and introduces
metastability in quasispecies theory, via an analytic field theoretic mapping.Comment: 5 pages, 1 figure, to appear in Physics Review Letter
The influence of horizontal gene transfer on the mean fitness of unicellular populations in static environments
This paper develops a mathematical model describing the influence that
conjugation-mediated Horizontal Gene Transfer (HGT) has on the
mutation-selection balance in an asexually reproducing population of
unicellular, prokaryotic organisms. It is assumed that mutation-selection
balance is reached in the presence of a fixed background concentration of
antibiotic, to which the population must become resistant in order to survive.
We analyze the behavior of the model in the limit of low and high
antibiotic-induced first-order death rate constants, and find that the highest
mean fitness is obtained at low rates of bacterial conjugation. As the rate of
conjugation crosses a threshold, the mean fitness decreases to a minimum, and
then rises asymptotically to a limiting value as the rate of conjugation
becomes infinitely large. However, this limiting value is smaller than the mean
fitness obtained in the limit of low conjugation rate. This dependence of the
mean fitness on the conjugation rate is fairly small for the parameter ranges
we have considered, and disappears as the first-order death rate constant due
to the presence of antibiotic approaches zero. For large values of the
antibiotic death rate constant, we have obtained an analytical solution for the
behavior of the mean fitness that agrees well with the results of simulations.
The results of this paper suggest that conjugation-mediated HGT has a slightly
deleterious effect on the mean fitness of a population at mutation-selection
balance. Therefore, we argue that HGT confers a selective advantage by allowing
for faster adaptation to a new or changing environment. The results of this
paper are consistent with the observation that HGT can be promoted by
environmental stresses on a population.Comment: 27 pages, 4 figure
Biological applications of the theory of birth-and-death processes
In this review, we discuss the applications of the theory of birth-and-death
processes to problems in biology, primarily, those of evolutionary genomics.
The mathematical principles of the theory of these processes are briefly
described. Birth-and-death processes, with some straightforward additions such
as innovation, are a simple, natural formal framework for modeling a vast
variety of biological processes such as population dynamics, speciation, genome
evolution, including growth of paralogous gene families and horizontal gene
transfer, and somatic evolution of cancers. We further describe how empirical
data, e.g., distributions of paralogous gene family size, can be used to choose
the model that best reflects the actual course of evolution among different
versions of birth-death-and-innovation models. It is concluded that
birth-and-death processes, thanks to their mathematical transparency,
flexibility and relevance to fundamental biological process, are going to be an
indispensable mathematical tool for the burgeoning field of systems biology.Comment: 29 pages, 4 figures; submitted to "Briefings in Bioinformatics
Parallel compensatory evolution stabilizes plasmids across the parasitism-mutualism continuum
Plasmids drive genomic diversity in bacteria via horizontal gene transfer [1 and 2]; nevertheless, explaining their survival in bacterial populations is challenging [3]. Theory predicts that irrespective of their net fitness effects, plasmids should be lost: when parasitic (costs outweigh benefits), plasmids should decline due to purifying selection [4, 5 and 6], yet under mutualism (benefits outweigh costs), selection favors the capture of beneficial accessory genes by the chromosome and loss of the costly plasmid backbone [4]. While compensatory evolution can enhance plasmid stability within populations [7, 8, 9, 10, 11, 12, 13, 14 and 15], the propensity for this to occur across the parasitism-mutualism continuum is unknown. We experimentally evolved Pseudomonas fluorescens and its mercury resistance mega-plasmid, pQBR103 [ 16], across an environment-mediated parasitism-mutualism continuum. Compensatory evolution stabilized plasmids by rapidly ameliorating the cost of plasmid carriage in all environments. Genomic analysis revealed that, in both parasitic and mutualistic treatments, evolution repeatedly targeted the gacA/gacS bacterial two-component global regulatory system while leaving the plasmid sequence intact. Deletion of either gacA or gacS was sufficient to completely ameliorate the cost of plasmid carriage. Mutation of gacA/gacS downregulated the expression of ∼17% of chromosomal and plasmid genes and appears to have relieved the translational demand imposed by the plasmid. Chromosomal capture of mercury resistance accompanied by plasmid loss occurred throughout the experiment but very rarely invaded to high frequency, suggesting that rapid compensatory evolution can limit this process. Compensatory evolution can explain the widespread occurrence of plasmids and allows bacteria to retain horizontally acquired plasmids even in environments where their accessory genes are not immediately useful
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Impacts of florfenicol on the microbiota landscape and resistome as revealed by metagenomic analysis.
BACKGROUND:Drug-resistant fish pathogens can cause significant economic loss to fish farmers. Since 2012, florfenicol has become an approved drug for treating both septicemia and columnaris diseases in freshwater fish. Due to the limited drug options available for aquaculture, the impact of the therapeutical florfenicol treatment on the microbiota landscape as well as the resistome present in the aquaculture farm environment needs to be evaluated. RESULTS:Time-series metagenomic analyses were conducted to the aquatic microbiota present in the tank-based catfish production systems, in which catfish received standard therapeutic 10-day florfenicol treatment following the federal veterinary regulations. Results showed that the florfenicol treatment shifted the structure of the microbiota and reduced the biodiversity of it by acting as a strong stressor. Planctomycetes, Chloroflexi, and 13 other phyla were susceptible to the florfenicol treatment and their abundance was inhibited by the treatment. In contrast, the abundance of several bacteria belonging to the Proteobacteria, Bacteroidetes, Actinobacteria, and Verrucomicrobia phyla increased. These bacteria with increased abundance either harbor florfenicol-resistant genes (FRGs) or had beneficial mutations. The florfenicol treatment promoted the proliferation of florfenicol-resistant genes. The copy number of phenicol-specific resistance genes as well as multiple classes of antibiotic-resistant genes (ARGs) exhibited strong correlations across different genetic exchange communities (p < 0.05), indicating the horizontal transfer of florfenicol-resistant genes among these bacterial species or genera. Florfenicol treatment also induced mutation-driven resistance. Significant changes in single-nucleotide polymorphism (SNP) allele frequencies were observed in membrane transporters, genes involved in recombination, and in genes with primary functions of a resistance phenotype. CONCLUSIONS:The therapeutical level of florfenicol treatment significantly altered the microbiome and resistome present in catfish tanks. Both intra-population and inter-population horizontal ARG transfer was observed, with the intra-population transfer being more common. The oxazolidinone/phenicol-resistant gene optrA was the most prevalent transferred ARG. In addition to horizontal gene transfer, bacteria could also acquire florfenicol resistance by regulating the innate efflux systems via mutations. The observations made by this study are of great importance for guiding the strategic use of florfenicol, thus preventing the formation, persistence, and spreading of florfenicol-resistant bacteria and resistance genes in aquaculture
How the other half lives: CRISPR-Cas's influence on bacteriophages
CRISPR-Cas is a genetic adaptive immune system unique to prokaryotic cells
used to combat phage and plasmid threats. The host cell adapts by incorporating
DNA sequences from invading phages or plasmids into its CRISPR locus as
spacers. These spacers are expressed as mobile surveillance RNAs that direct
CRISPR-associated (Cas) proteins to protect against subsequent attack by the
same phages or plasmids. The threat from mobile genetic elements inevitably
shapes the CRISPR loci of archaea and bacteria, and simultaneously the
CRISPR-Cas immune system drives evolution of these invaders. Here we highlight
our recent work, as well as that of others, that seeks to understand phage
mechanisms of CRISPR-Cas evasion and conditions for population coexistence of
phages with CRISPR-protected prokaryotes.Comment: 24 pages, 8 figure
Unrelated toxin-antitoxin systems cooperate to induce persistence.
Persisters are drug-tolerant bacteria that account for the majority of bacterial infections. They are not mutants, rather, they are slow-growing cells in an otherwise normally growing population. It is known that the frequency of persisters in a population is correlated with the number of toxin-antitoxin systems in the organism. Our previous work provided a mechanistic link between the two by showing how multiple toxin-antitoxin systems, which are present in nearly all bacteria, can cooperate to induce bistable toxin concentrations that result in a heterogeneous population of slow- and fast-growing cells. As such, the slow-growing persisters are a bet-hedging subpopulation maintained under normal conditions. For technical reasons, the model assumed that the kinetic parameters of the various toxin-antitoxin systems in the cell are identical, but experimental data indicate that they differ, sometimes dramatically. Thus, a critical question remains: whether toxin-antitoxin systems from the diverse families, often found together in a cell, with significantly different kinetics, can cooperate in a similar manner. Here, we characterize the interaction of toxin-antitoxin systems from many families that are unrelated and kinetically diverse, and identify the essential determinant for their cooperation. The generic architecture of toxin-antitoxin systems provides the potential for bistability, and our results show that even when they do not exhibit bistability alone, unrelated systems can be coupled by the growth rate to create a strongly bistable, hysteretic switch between normal (fast-growing) and persistent (slow-growing) states. Different combinations of kinetic parameters can produce similar toxic switching thresholds, and the proximity of the thresholds is the primary determinant of bistability. Stochastic fluctuations can spontaneously switch all of the toxin-antitoxin systems in a cell at once. The spontaneous switch creates a heterogeneous population of growing and non-growing cells, typical of persisters, that exist under normal conditions, rather than only as an induced response. The frequency of persisters in the population can be tuned for a particular environmental niche by mixing and matching unrelated systems via mutation, horizontal gene transfer and selection
Quasispecies Theory for Evolution of Modularity
Biological systems are modular, and this modularity evolves over time and in
different environments. A number of observations have been made of increased
modularity in biological systems under increased environmental pressure. We
here develop a quasispecies theory for the dynamics of modularity in
populations of these systems. We show how the steady-state fitness in a
randomly changing environment can be computed. We derive a fluctuation
dissipation relation for the rate of change of modularity and use it to derive
a relationship between rate of environmental changes and rate of growth of
modularity. We also find a principle of least action for the evolved modularity
at steady state. Finally, we compare our predictions to simulations of protein
evolution and find them to be consistent.Comment: 21 pages, 4 figures; presentation reordered; to appear in Phys. Rev.
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