scholarly journals Integrating ecology and evolution to study hypothetical dynamics of algal blooms and Muller’s ratchet using Evolvix

Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  

Algal blooms have been the subject of considerable research as they occur over various spatial and temporal scales and can produce toxins that disrupt their ecosystem. Algal blooms are often governed by nutrient availability however other limitations exist. Algae are primary producers and therefore subject to predation which can keep populations below levels supported by nutrient availability. If algae as prey mutate to gain the ability to produce toxins deterring predators, they may increase their survival rates and form blooms unless other factors counter their effective increase in growth rate. Where might such mutations come from? Clearly, large populations of algae will repeatedly experience mutations knocking-out DNA repair genes, increasing mutation rates, and with them the chance of acquiring de-novo mutations producing a toxin against predators. We investigate this hypothetical scenario by simulation in the Evolvix modeling language. We modeled a sequence of steps that in principle can allow a typical asexual algal population to escape predation pressure and form a bloom with the help of mutators. We then turn our attention to the unavoidable side effect of generally increased mutation rates, many slightly deleterious mutations. If these accumulate at sufficient speed, their combined impact on fitness might place upper limits on the duration of algal blooms. These steps are required: (1) Random mutations result in the loss of DNA repair mechanisms. (2) Increased mutation rates make it more likely to acquire the ability to produce toxins by altering metabolism. (3) Toxins deter predators providing algae with growth advantages that can mask linked slightly deleterious mutational effects. (4) Reduced predation pressure enables blooms if algae have sufficient nutrients. (5) Lack of recombination results in the accumulation of slightly deleterious mutations as predicted by Muller’s ratchet. (6) If fast enough, deleterious mutation accumulation eventually leads to mutational meltdown of toxic blooming algae. (7) Non-mutator algal populations are not affected due to ongoing predation pressure. Our simulation models integrate ecological continuous-time dynamics of predator-prey systems with the population genetics of a simplified Muller’s ratchet model using Evolvix. Evolvix maps these models to Continuous-Time Markov Chain models that can be simulated deterministically or stochastically depending on the question. The current model is incomplete; we plan to investigate many parameter combinations to produce a more robust model ensemble with stable links to reasonable parameter estimates. However, our model already has several intriguing features that may allow for the eventual development of observation methods for monitoring ecosystem health. Our work also highlights a growing need to simulate integrated models combining ecological processes, multi-level population dynamics, and evolutionary genetics in a single computational run.

2017 ◽  
Author(s):  
Sarah Northey ◽  
Courtney Hove ◽  
Justine Kao ◽  
Jon Ide ◽  
Janel McKinney ◽  
...  

Algal blooms have been the subject of considerable research as they occur over various spatial and temporal scales and can produce toxins that disrupt their ecosystem. Algal blooms are often governed by nutrient availability however other limitations exist. Algae are primary producers and therefore subject to predation which can keep populations below levels supported by nutrient availability. If algae as prey mutate to gain the ability to produce toxins deterring predators, they may increase their survival rates and form blooms unless other factors counter their effective increase in growth rate. Where might such mutations come from? Clearly, large populations of algae will repeatedly experience mutations knocking-out DNA repair genes, increasing mutation rates, and with them the chance of acquiring de-novo mutations producing a toxin against predators. We investigate this hypothetical scenario by simulation in the Evolvix modeling language. We modeled a sequence of steps that in principle can allow a typical asexual algal population to escape predation pressure and form a bloom with the help of mutators. We then turn our attention to the unavoidable side effect of generally increased mutation rates, many slightly deleterious mutations. If these accumulate at sufficient speed, their combined impact on fitness might place upper limits on the duration of algal blooms. These steps are required: (1) Random mutations result in the loss of DNA repair mechanisms. (2) Increased mutation rates make it more likely to acquire the ability to produce toxins by altering metabolism. (3) Toxins deter predators providing algae with growth advantages that can mask linked slightly deleterious mutational effects. (4) Reduced predation pressure enables blooms if algae have sufficient nutrients. (5) Lack of recombination results in the accumulation of slightly deleterious mutations as predicted by Muller’s ratchet. (6) If fast enough, deleterious mutation accumulation eventually leads to mutational meltdown of toxic blooming algae. (7) Non-mutator algal populations are not affected due to ongoing predation pressure. Our simulation models integrate ecological continuous-time dynamics of predator-prey systems with the population genetics of a simplified Muller’s ratchet model using Evolvix. Evolvix maps these models to Continuous-Time Markov Chain models that can be simulated deterministically or stochastically depending on the question. The current model is incomplete; we plan to investigate many parameter combinations to produce a more robust model ensemble with stable links to reasonable parameter estimates. However, our model already has several intriguing features that may allow for the eventual development of observation methods for monitoring ecosystem health. Our work also highlights a growing need to simulate integrated models combining ecological processes, multi-level population dynamics, and evolutionary genetics in a single computational run.


1978 ◽  
Vol 32 (3) ◽  
pp. 289-293 ◽  
Author(s):  
R. Heller ◽  
J. Maynard Smith

SUMMARYThe accumulation of deleterious mutations in a finite diploid selfing population is investigated. It is shown that the conditions for accumulation are very similar to those for the accumulation of mutations in an asexual population by ‘Muller's ratchet’. The ratchet is likely to operate in both types of population if there is a large class of slightly deleterious mutations.


Genetics ◽  
1998 ◽  
Vol 149 (4) ◽  
pp. 2135-2146 ◽  
Author(s):  
Carl T Bergstrom ◽  
Jonathan Pritchard

Abstract Several features of the biology of mitochondria suggest that mitochondria might be susceptible to Muller's ratchet and other forms of evolutionary degradation: Mitochondria have predominantly uniparental inheritance, appear to be nonrecombining, and have high mutation rates producing significant deleterious variation. We demonstrate that the persistence of mitochondria may be explained by recent data that point to a severe “bottleneck” in the number of mitochondria passing through the germline in humans and other mammals. We present a population-genetic model in which deleterious mutations arise within individual mitochondria, while selection operates on assemblages of mitochondria at the level of their eukaryotic hosts. We show that a bottleneck increases the efficacy of selection against deleterious mutations by increasing the variance in fitness among eukaryotic hosts. We investigate both the equilibrium distribution of deleterious variation in large populations and the dynamics of Muller's ratchet in small populations. We find that in the absence of the ratchet, a bottleneck leads to improved mitochondrial performance and that, over a longer time scale, a bottleneck acts to slow the progression of the ratchet.


mBio ◽  
2016 ◽  
Vol 7 (3) ◽  
Author(s):  
Mizue Naito ◽  
Teresa E. Pawlowska

ABSTRACT   Heritable endobacteria, which are transmitted from one host generation to the next, are subjected to evolutionary forces that are different from those experienced by free-living bacteria. In particular, they suffer consequences of Muller’s ratchet, a mechanism that leads to extinction of small asexual populations due to fixation of slightly deleterious mutations combined with the random loss of the most-fit genotypes, which cannot be recreated without recombination. Mycoplasma-related endobacteria (MRE) are heritable symbionts of fungi from two ancient lineages, Glomeromycota (arbuscular mycorrhizal fungi) and Mucoromycotina . Previous studies revealed that MRE maintain unusually diverse populations inside their hosts and may have been associated with fungi already in the early Paleozoic. Here we show that MRE are vulnerable to genomic degeneration and propose that they defy Muller’s ratchet thanks to retention of recombination and genome plasticity. We suggest that other endobacteria may be capable of raising similar defenses against Muller’s ratchet.


Genetics ◽  
1987 ◽  
Vol 116 (1) ◽  
pp. 161-167
Author(s):  
William R Rice

ABSTRACT A new model for the evolution of reduced genetic activity of the Y sex chromosome is described. The model is based on the process of genetic hitchhiking. It is shown that the Y chromosome can gradually lose its genetic activity due to the fixation of deleterious mutations that are linked with other beneficial genes. Fixation of deleterious Y-linked mutations generates locus-specific selection for dosage tolerance and/or compensation. The hitchhiking effect is most pronounced when operating in combination with an alternative model, Muller's ratchet. It is shown, however, that the genetic hitchhiking mechanism can operate under conditions where Muller's ratchet is ineffective.


2018 ◽  
Author(s):  
Logan Chipkin ◽  
Peter Olofsson ◽  
Ryan C. Daileda ◽  
Ricardo B. R. Azevedo

AbstractAsexual populations are expected to accumulate deleterious mutations through a process known as Muller’s Ratchet. Lynch, Gabriel, and colleagues have proposed that the Ratchet eventually results in a vicious cycle of mutation accumulation and population decline that drives populations to extinction. They called this phenomenon mutational meltdown. Here, we analyze the meltdown using a multitype branching process model where, in the presence of mutation, populations are doomed to extinction. We find that extinction occurs more quickly in small populations, experiencing a high deleterious mutation rate, and mutations with more severe deleterious effects. The effects of mutational parameters on extinction time in doomed populations differ from those on the severity of Muller’s Ratchet in populations of constant size. We also 1nd that mutational meltdown, although it does occur in our model, does not determine extinction time. Rather, extinction time is determined by the expected impact of deleterious mutations on fitness.


2015 ◽  
Author(s):  
David Castellano ◽  
Marta Coronado ◽  
Jose Campos ◽  
Antonio Barbadilla ◽  
Adam Eyre-Walker

It is known that rates of mutation and recombination vary across the genome in many species. Here we investigate whether these factors affect the rate at which genes undergo adaptive evolution both individually and in combination and quantify the degree to which Hill-Robertson interference (HRi) impedes the rate of adaptive evolution. To do this we compiled a dataset of 6,141 autosomal protein coding genes from Drosophila, for which we have polymorphism data from D. melanogaster and divergence out to D. yakuba. We estimated the rate of adaptive evolution using a derivative of the McDonald-Kreitman test that controls for the slightly deleterious mutations. We find that the rate of adaptive amino acid substitution is positively correlated to both the rates of recombination and mutation. We also find that these correlations are robust to controlling for each other, synonymous codon bias and gene functions related to immune response and testes. We estimate that HRi reduces the rate of adaptive evolution by ~27%. We also show that this fraction depends on a gene's mutation rate; genes with low mutation rates lose ~11% of their adaptive substitutions while genes with high mutation rates lose ~43%. In conclusion, we show that the mutation rate and the rate of recombination, are important modifiers of the rate of adaptive evolution in Drosophila.


2020 ◽  
Author(s):  
Marco Colnaghi ◽  
Nick Lane ◽  
Andrew Pomiankowski

ABSTRACTProkaryotes generally reproduce clonally but can also acquire new genetic material via lateral gene transfer (LGT). Like sex, LGT can prevent the accumulation of deleterious mutations predicted by Muller’s ratchet for asexual populations. This similarity between sex and LGT raises the question why did eukaryotes abandon LGT in favor of sexual reproduction? Understanding the limitations of LGT provides insight into this evolutionary transition. We model the evolution of a haploid population undergoing LGT at a rate λ and subjected to a mutation rate μ. We take into account recombination length, L, and genome size, g, neglected by previous theoretical models. We confirm that LGT counters Muller’s ratchet by reducing the rate of fixation of deleterious mutations in small genomes. We then demonstrate that this beneficial effect declines rapidly with genome size. Populations with larger genomes are subjected to a faster rate of fixation of deleterious mutations and become more vulnerable to stochastic frequency fluctuations. Muller’s ratchet therefore generates a strong constraint on genome size. Importantly, we show that the degeneration of larger genomes can be resisted by increases in the recombination length, the average number of contiguous genes drawn from the environment for LGT. Large increases in genome size, as in early eukaryotes, are only possible as L reaches the same order of magnitude as g. This requirement for recombination across the whole genome can explain the strong selective pressure towards the evolution of sexual cell fusion and reciprocal recombination during early eukaryotic evolution – the origin of meiotic sex.


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