The role of weak selection and high mutation rates in nearly neutral evolution

ABSTRACT Oenococcus oeni is an alcohol-tolerant, acidophilic lactic acid bacterium primarily responsible for malolactic fermentation in wine. A recent comparative genomic analysis of O. oeni PSU-1 with other sequenced lactic acid bacteria indicates that PSU-1 lacks the mismatch repair (MMR) genes mutS and mutL. Consistent with the lack of MMR, mutation rates for O. oeni PSU-1 and a second oenococcal species, O. kitaharae, were higher than those observed for neighboring taxa, Pediococcus pentosaceus and Leuconostoc mesenteroides. Sequence analysis of the rpoB mutations in rifampin-resistant strains from both oenococcal species revealed a high percentage of transition mutations, a result indicative of the lack of MMR. An analysis of common alleles in the two sequenced O. oeni strains, PSU-1 and BAA-1163, also revealed a significantly higher level of transition substitutions than were observed in other Lactobacillales species. These results suggest that the genus Oenococcus is hypermutable due to the loss of mutS and mutL, which occurred with the divergence away from the neighboring Leuconostoc branch. The hypermutable status of the genus Oenococcus explains the observed high level of allelic polymorphism among known O. oeni isolates and likely contributed to the unique adaptation of this genus to acidic and alcoholic environments.

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NEUTRAL EVOLUTION AND MUTATION RATES OF SEQUENTIAL DYNAMICAL SYSTEMS

Advances in Complex Systems ◽

10.1142/s0219525904000275 ◽

2004 ◽

Vol 07 (03n04) ◽

pp. 395-418

Author(s):

H. S. MORTVEIT ◽

C. M. REIDYS

Keyword(s):

Dynamical Systems ◽

Mutation Rate ◽

Distance Measure ◽

Neutral Evolution ◽

Mutation Rates ◽

Combinatorial Properties ◽

Labeled Graph ◽

Sequential Dynamical Systems ◽

Natural Way ◽

Independent Probability

In this paper we study the evolution of sequential dynamical systems [Formula: see text] as a result of the erroneous replication of the SDS words. An [Formula: see text] consists of (a) a finite, labeled graph Y in which each vertex has a state, (b) a vertex labeled sequence of functions (Fvi,Y), and (c) a word w, i.e. a sequence (w1,…,wk), where each wi is a Y-vertex. The function Fwi,Y updates the state of vertex wi as a function of the states of wi and its Y-neighbors and leaves the states of all other vertices fixed. The [Formula: see text] over the word w and Y is the composed map: [Formula: see text]. The word w represents the genotype of the [Formula: see text] in a natural way. We will randomly flip consecutive letters of w with independent probability q and study the resulting evolution of the [Formula: see text]. We introduce combinatorial properties of [Formula: see text] which allow us to construct a new distance measure [Formula: see text] for words. We show that [Formula: see text] captures the similarity of corresponding [Formula: see text]. We will use the distance measure [Formula: see text] to study neutrality and mutation rates in the evolution of words. We analyze the structure of neutral networks of words and the transition of word populations between them. Furthermore, we prove the existence of a critical mutation rate beyond which a population of words becomes essentially randomly distributed, and the existence of an optimal mutation rate at which a population maximizes its mutant offspring.

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The Role of Reticulate Evolution in Creating Innovation and Complexity

International Journal of Evolutionary Biology ◽

10.1155/2012/418964 ◽

2012 ◽

Vol 2012 ◽

pp. 1-10 ◽

Cited By ~ 11

Author(s):

Kristen S. Swithers ◽

Shannon M. Soucy ◽

J. Peter Gogarten

Keyword(s):

Metabolic Pathways ◽

Driving Forces ◽

Reticulate Evolution ◽

Neutral Evolution ◽

Ecological Niches ◽

Eukaryotic Evolution ◽

New Host ◽

Whole Genome Duplications ◽

Genome Duplications

Reticulate evolution encompasses processes that conflict with traditional Tree of Life efforts. These processes, horizontal gene transfer (HGT), gene and whole-genome duplications through allopolyploidization, are some of the main driving forces for generating innovation and complexity. HGT has a profound impact on prokaryotic and eukaryotic evolution. HGTs can lead to the invention of new metabolic pathways and the expansion and enhancement of previously existing pathways. It allows for organismal adaptation into new ecological niches and new host ranges. Although many HGTs appear to be selected for because they provide some benefit to their recipient lineage, other HGTs may be maintained by chance through random genetic drift. Moreover, some HGTs that may initially seem parasitic in nature can cause complexity to arise through pathways of neutral evolution. Another mechanism for generating innovation and complexity, occurring more frequently in eukaryotes than in prokaryotes, is gene and genome duplications, which often occur through allopolyploidizations. We discuss how these different evolutionary processes contribute to generating innovation and complexity.

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Faster than Neutral Evolution of Constrained Sequences: The Complex Interplay of Mutational Biases and Weak Selection

Genome Biology and Evolution ◽

10.1093/gbe/evr032 ◽

2011 ◽

Vol 3 ◽

pp. 383-395 ◽

Cited By ~ 26

Author(s):

David S. Lawrie ◽

Dmitri A. Petrov ◽

Philipp W. Messer

Keyword(s):

Neutral Evolution ◽

Weak Selection ◽

Complex Interplay

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exo1-Dependent Mutator Mutations: Model System for Studying Functional Interactions in Mismatch Repair

Molecular and Cellular Biology ◽

10.1128/mcb.21.15.5142-5155.2001 ◽

2001 ◽

Vol 21 (15) ◽

pp. 5142-5155 ◽

Cited By ~ 133

Author(s):

Neelam S. Amin ◽

My-Nga Nguyen ◽

Scott Oh ◽

Richard D. Kolodner

Keyword(s):

Mismatch Repair ◽

Copy Number ◽

Model System ◽

Mutation Rates ◽

Binding Region ◽

Functional Interactions ◽

Interaction Regions ◽

Overexpressed Gene ◽

Mmr Proteins

ABSTRACT EXO1 interacts with MSH2 and MLH1 and has been proposed to be a redundant exonuclease that functions in mismatch repair (MMR). To better understand the role of EXO1 in mismatch repair, a genetic screen was performed to identify mutations that increase the mutation rates caused by weak mutator mutations such as exo1Δ andpms1-A130V mutations. In a screen starting with anexo1 mutation, exo1-dependent mutator mutations were obtained in MLH1, PMS1, MSH2, MSH3, POL30 (PCNA),POL32, and RNR1, whereas starting with the weakpms1 allele pms1-A130V,pms1-dependent mutator mutations were identified inMLH1, MSH2, MSH3, MSH6, and EXO1. These mutations only cause weak MMR defects as single mutants but cause strong MMR defects when combined with each other. Most of the mutations obtained caused amino acid substitutions in MLH1 or PMS1, and these clustered in either the ATP-binding region or the MLH1-PMS1 interaction regions of these proteins. The mutations showed two other types of interactions: specific pairs of mutations showed unlinked noncomplementation in diploid strains, and the defect caused by pairs of mutations could be suppressed by high-copy-number expression of a third gene, an effect that showed allele and overexpressed gene specificity. These results support a model in which EXO1 plays a structural role in MMR and stabilizes multiprotein complexes containing a number of MMR proteins. A similar role is proposed for PCNA based on the data presented.

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Effects of Different Mutation Rates and Randomness on the Distribution of Linkage Disequilibrium

10.21203/rs.3.rs-1066165/v1 ◽

2021 ◽

Author(s):

Rong Zhang ◽

ZhiQiang Du

Keyword(s):

Linkage Disequilibrium ◽

Transition Matrix ◽

Complex Trait ◽

Mutation Rates ◽

Minor Role ◽

Effective Population ◽

Different Types ◽

A Minor ◽

Nucleotide Transition

Abstract Background Mutation has recently received much attention on its role in the evolution and genetics of complex trait. The linkage disequilibrium (LD) distribution can be affected by mutation as reported recently, in which the same mutation rates were adopted in the transition matrix. However, effects of different types, rates and randomness of mutation on LD distribution remain unexplored. Results Here, we considered in the transition matrix mutations at each locus to be of different types and rates (i.e. nucleotide transition or transversion treated differently), to examine how the LD distribution between two genetic loci was affected. After examining consecutively factors such as effective population size, recombination and selection, different mutation types and rates could further change the dynamics of LD distribution. However, at the current scale of mutation rate (weak at 10−9-10−8), mutation seemed to play only a minor role, compared to recombination and selection. A simple model further showed that mutation randomness increased the ruggedness of LD curves, which fluctuated around the steady state. Conclusions Taken together, different mutation rates and randomness could further disturb the dynamics of LD distribution. Our findings can help better understand the role of mutation in molecular evolution and complex trait genetics.

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Population-level consequences of inheritable somatic mutations and the evolution of mutation rates in plants

10.1101/2020.09.29.318402 ◽

2020 ◽

Author(s):

Thomas Lesaffre

Keyword(s):

Life Expectancy ◽

Inbreeding Depression ◽

Life Histories ◽

Somatic Mutations ◽

Population Level ◽

Mutation Rates ◽

Deleterious Mutations

ABSTRACTInbreeding depression, that is the decrease in fitness of inbred relative to outbred individuals, was shown to increase strongly as life expectancy increases in plants. Because plants are thought to not have a separated germline, it was proposed that this pattern could be generated by somatic mutations accumulating during growth, since larger and more long-lived species have more opportunities for mutations to accumulate. A key determinant of the role of somatic mutations is the rate at which they occur, which likely differs between species because mutation rates may evolve differently in species with constrasting life-histories. In this paper, we study the evolution of the mutation rates in plants, and consider the population-level consequences of inheritable somatic mutations given this evolution. We show that despite substantially lower per year mutation rates, more long-lived species still tend to accumulate larger amounts of deleterious mutations because of higher per generation, leading to higher levels of inbreeding depression in these species. However, the magnitude of this increase depends strongly on how mutagenic meiosis is relative to growth.

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The revolt of the clay

Mutation, Randomness, and Evolution ◽

10.1093/oso/9780198844457.003.0009 ◽

2021 ◽

pp. 165-196

Author(s):

Arlin Stoltzfus

Keyword(s):

Local Adaptation ◽

Color Vision ◽

Adaptive Evolution ◽

Molecular Level ◽

Neutral Evolution ◽

Mutation Rates ◽

Spectral Tuning ◽

Evolution Of Resistance ◽

Altitude Adaptation

Chapter 9 presents an empirical case for the importance of mutational biases, based on studies of adaptation traced to the molecular level. Where Chapter 8 identified a variational cause of bias that does not depend on neutral evolution, absolute constraints, or high mutation rates, this chapter focuses on how quantitative biases in ordinary nucleotide mutations influence adaptive evolution. It uses published studies of parallel adaptation in nature and in the laboratory. The natural studies include both (1) cases of recent local adaptation, e.g., evolution of resistance to insecticides and herbicides, and (2) cases of fixed changes, e.g., altitude adaptation via changes in hemoglobins, spectral tuning of photoreceptors used in color vision, and so on. The results indicate that the kinds of changes that happen most often in adaptation are the kinds favored by simple biases in mutation, e.g., transition-transversion bias.

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The strength of the selection barrier between populations

Genetics Research ◽

10.1017/s001667230000464x ◽

2000 ◽

Vol 76 (2) ◽

pp. 179-185 ◽

Cited By ~ 2

Author(s):

KONSTANTIN V. PYLKOV ◽

LEV A. ZHIVOTOVSKY ◽

FREDDY BUGGE CHRISTIANSEN

Keyword(s):

Small Parameter ◽

Genetic Difference ◽

Weak Selection ◽

Approximate Analytical Expression ◽

Epistatic Interactions ◽

Linkage Disequilibria ◽

Donor Population ◽

Mean Fitness ◽

Two Populations

Genetic differences among populations exposed to selection form barriers against genetic exchange by mortality among hybrids. The strength of such a selection barrier, with which one (recipient) population reacts against immigration from another (donor) population, may be measured as the cumulative mean fitness of hybrids and their descendants relative to the fitness of the recipient population. Previous work analysed a case of weak selection with pairwise epistatic interactions by assuming small genetic distance between two populations in contact. The present study allows large genetic difference between the donor and recipient populations and considers weak multilocus selection with arbitrary epistatic interactions between two or more linked loci. An approximate analytical expression for the barrier strength is obtained as an expansion in which the strength of selection plays the role of a small parameter. It is shown that allele frequencies and gametic linkage disequilibria contribute in different ways to the strength of the selection barrier.

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