scholarly journals Rapid evolution and strain turnover in the infant gut microbiome

2021 ◽  
Author(s):  
Daisy W. Chen ◽  
Nandita R. Garud
Keyword(s):  
Gut Microbiome ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
Rapid Evolution ◽  
Fold Increase ◽  
Metagenomic Data ◽  
Ecological Change ◽  
De Novo Mutations ◽  
Evolutionary Changes ◽  
Infant Gut Microbiome

While the ecological dynamics of the infant gut microbiome have been intensely studied, relatively little is known about the evolutionary dynamics in the infant gut microbiome. Here we analyze longitudinal fecal metagenomic data from >700 infants and their mothers over the first year of life and find that the evolutionary dynamics in infant gut microbiomes are distinct from that of adults. We find evidence for almost 100-fold increase in the rate of evolution and strain turnover in the infant gut compared to healthy adults, with the mother-infant transition at delivery being a particularly dynamic period in which gene loss dominates. Within a few months after birth, these dynamics stabilize, and gene gains become increasingly frequent as the microbiome matures. We furthermore find that evolutionary changes in infants show signatures of being seeded by a mixture of de novo mutations and transmissions of pre-evolved lineages from the broader family. Several of these evolutionary changes occur in parallel in multiple infants, highlighting candidate genes that may play important roles in the development of the infant gut microbiome. Our results point to a picture of a volatile infant gut microbiome characterized by rapid evolutionary and ecological change in the early days of life.

scholarly journals Rapid evolution of piRNA-mediated silencing of an invading transposable element was driven by abundant de novo mutations

2019 ◽  
Author(s):  
Shuo Zhang ◽  
Erin S. Kelleher
Keyword(s):  
Transposable Element ◽  
Small Rnas ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
Rapid Evolution ◽  
De Novo Mutations ◽  
Element Insertion ◽  
Pirna Cluster ◽  
Genomic Regions ◽  
First Time

ABSTRACTThe regulation of transposable element (TE) activity by small RNAs is a ubiquitous feature of germlines. However, despite the obvious benefits to the host in terms of ensuring the production of viable gametes and maintaining the integrity of the genomes they carry, it remains controversial whether TE regulation evolves adaptively. We examined the emergence and evolutionary dynamics of repressor alleles after P-elements invaded the Drosophila melanogaster genome in the mid 20th century. In many animals including Drosophila, repressor alleles are produced by transpositional insertions into piRNA clusters, genomic regions encoding the Piwi-interacting RNAs (piRNAs) that regulate TEs. We discovered that ∼94% of recently collected isofemale lines in the Drosophila Genetic Reference Panel (DGRP) contain at least one P-element insertion in a piRNA cluster, indicating that repressor alleles are produced by de novo insertion at an exceptional rate. Furthermore, in our sample of ∼200 genomes, we uncovered no fewer than 80 unique P-element insertion alleles in at least 15 different piRNA clusters. Finally, we observe no footprint of positive selection on P-element insertions in piRNA clusters, suggesting that the rapid evolution of piRNA-mediated repression in D. melanogaster was driven primarily by mutation. Our results reveal for the first time how the unique genetic architecture of piRNA production, in which numerous piRNA clusters can encode regulatory small RNAs upon transpositional insertion, facilitates the non-adaptive rapid evolution of repression.

scholarly journals Eco-evolutionary dynamics

2009 ◽  
Vol 364 (1523) ◽  
pp. 1483-1489 ◽  
Author(s):  
F. Pelletier ◽  
D. Garant ◽  
A.P. Hendry
Keyword(s):  
Time Scale ◽  
Evolutionary Dynamics ◽  
Evolutionary Change ◽  
Ecological Change ◽  
Evolutionary Changes ◽  
Microevolutionary Change ◽  
Theoretical Developments ◽  
Rapid Evolutionary Change

Evolutionary ecologists and population biologists have recently considered that ecological and evolutionary changes are intimately linked and can occur on the same time-scale. Recent theoretical developments have shown how the feedback between ecological and evolutionary dynamics can be linked, and there are now empirical demonstrations showing that ecological change can lead to rapid evolutionary change. We also have evidence that microevolutionary change can leave an ecological signature. We are at a stage where the integration of ecology and evolution is a necessary step towards major advances in our understanding of the processes that shape and maintain biodiversity. This special feature about ‘eco-evolutionary dynamics’ brings together biologists from empirical and theoretical backgrounds to bridge the gap between ecology and evolution and provide a series of contributions aimed at quantifying the interactions between these fundamental processes.

scholarly journals Adaptive phenotypic plasticity stabilizes evolution in fluctuating environments

2021 ◽  
Author(s):  
Alexander M Lalejini ◽  
Austin J Ferguson ◽  
Nkrumah A Grant ◽  
Charles Ofria
Keyword(s):  
Phenotypic Plasticity ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
Evolutionary Change ◽  
Adaptive Plasticity ◽  
Natural Environments ◽  
Selective Sweeps ◽  
De Novo Mutations ◽  
Environmental Fluctuations ◽  
Adaptive Phenotypic Plasticity

Fluctuating environmental conditions are ubiquitous in natural systems, and populations have evolved various strategies to cope with such fluctuations. The particular mechanisms that evolve profoundly influence subsequent evolutionary dynamics. One such mechanism is phenotypic plasticity, which is the ability of a single genotype to produce alternate phenotypes in an environmentally dependent context. Here, we use digital organisms (self-replicating computer programs) to investigate how adaptive phenotypic plasticity alters evolutionary dynamics and influences evolutionary outcomes in cyclically changing environments. Specifically, we examined the evolutionary histories of both plastic populations and non-plastic populations to ask: (1) Does adaptive plasticity promote or constrain evolutionary change? (2) Are plastic populations better able to evolve and then maintain novel traits? And (3), how does adaptive plasticity affect the potential for maladaptive alleles to accumulate in evolving genomes? We find that populations with adaptive phenotypic plasticity undergo less evolutionary change than non-plastic populations, which must rely on genetic variation from de novo mutations to continuously readapt to environmental fluctuations. Indeed, the non-plastic populations undergo more frequent selective sweeps and accumulate many more genetic changes. We find that the repeated selective sweeps in non-plastic populations drive the loss of beneficial traits and accumulation of maladaptive alleles via deleterious hitchhiking, whereas phenotypic plasticity can stabilize populations against environmental fluctuations. This stabilization allows plastic populations to more easily retain novel adaptive traits than their non-plastic counterparts. In general, the evolution of adaptive phenotypic plasticity shifted evolutionary dynamics to be more similar to that of populations evolving in a static environment than to non-plastic populations evolving in an identical fluctuating environment. All natural environments subject populations to some form of change; our findings suggest that the stabilizing effect of phenotypic plasticity plays an important role in subsequent adaptive evolution.

scholarly journals Parallel evolution of influenza across multiple spatiotemporal scales

eLife ◽  
2017 ◽  
Vol 6 ◽  
Author(s):  
Katherine S Xue ◽  
Terry Stevens-Ayers ◽  
Angela P Campbell ◽  
Janet A Englund ◽  
Steven A Pergam ◽  
...  
Keyword(s):  
Evolutionary Dynamics ◽  
De Novo ◽  
Parallel Evolution ◽  
Global Scale ◽  
De Novo Mutations ◽  
Small Set ◽  
Spatiotemporal Scales ◽  
H3n2 Influenza ◽  
Multiple Patients

Viral variants that arise in the global influenza population begin as de novo mutations in single infected hosts, but the evolutionary dynamics that transform within-host variation to global genetic diversity are poorly understood. Here, we demonstrate that influenza evolution within infected humans recapitulates many evolutionary dynamics observed at the global scale. We deep-sequence longitudinal samples from four immunocompromised patients with long-term H3N2 influenza infections. We find parallel evolution across three scales: within individual patients, in different patients in our study, and in the global influenza population. In hemagglutinin, a small set of mutations arises independently in multiple patients. These same mutations emerge repeatedly within single patients and compete with one another, providing a vivid clinical example of clonal interference. Many of these recurrent within-host mutations also reach a high global frequency in the decade following the patient infections. Our results demonstrate surprising concordance in evolutionary dynamics across multiple spatiotemporal scales.

scholarly journals Evolutionary dynamics and structural consequences of de novo beneficial mutations and mutant lineages arising in a constant environment

BMC Biology ◽  
2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Margie Kinnersley ◽  
Katja Schwartz ◽  
Dong-Dong Yang ◽  
Gavin Sherlock ◽  
Frank Rosenzweig
Keyword(s):  
High Frequency ◽  
High Throughput Sequencing ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
Allelic Diversity ◽  
Microbial Evolution ◽  
De Novo Mutations ◽  
Beneficial Mutations ◽  
Adaptive Mutations ◽  
The Impact

Abstract Background Microbial evolution experiments can be used to study the tempo and dynamics of evolutionary change in asexual populations, founded from single clones and growing into large populations with multiple clonal lineages. High-throughput sequencing can be used to catalog de novo mutations as potential targets of selection, determine in which lineages they arise, and track the fates of those lineages. Here, we describe a long-term experimental evolution study to identify targets of selection and to determine when, where, and how often those targets are hit. Results We experimentally evolved replicate Escherichia coli populations that originated from a mutator/nonsense suppressor ancestor under glucose limitation for between 300 and 500 generations. Whole-genome, whole-population sequencing enabled us to catalog 3346 de novo mutations that reached > 1% frequency. We sequenced the genomes of 96 clones from each population when allelic diversity was greatest in order to establish whether mutations were in the same or different lineages and to depict lineage dynamics. Operon-specific mutations that enhance glucose uptake were the first to rise to high frequency, followed by global regulatory mutations. Mutations related to energy conservation, membrane biogenesis, and mitigating the impact of nonsense mutations, both ancestral and derived, arose later. New alleles were confined to relatively few loci, with many instances of identical mutations arising independently in multiple lineages, among and within replicate populations. However, most never exceeded 10% in frequency and were at a lower frequency at the end of the experiment than at their maxima, indicating clonal interference. Many alleles mapped to key structures within the proteins that they mutated, providing insight into their functional consequences. Conclusions Overall, we find that when mutational input is increased by an ancestral defect in DNA repair, the spectrum of high-frequency beneficial mutations in a simple, constant resource-limited environment is narrow, resulting in extreme parallelism where many adaptive mutations arise but few ever go to fixation.

scholarly journals Mutation rates and the evolution of germline structure

2016 ◽  
Vol 371 (1699) ◽  
pp. 20150137 ◽  
Author(s):  
Aylwyn Scally
Keyword(s):  
Mutation Rate ◽  
De Novo ◽  
Active Role ◽  
Paternal Age ◽  
State Transitions ◽  
De Novo Mutations ◽  
Evolutionary Changes ◽  
Sequencing Studies ◽  
Paternal Age Effect ◽  
Stem Cell State

Genome sequencing studies of de novo mutations in humans have revealed surprising incongruities in our understanding of human germline mutation. In particular, the mutation rate observed in modern humans is substantially lower than that estimated from calibration against the fossil record, and the paternal age effect in mutations transmitted to offspring is much weaker than expected from our long-standing model of spermatogenesis. I consider possible explanations for these discrepancies, including evolutionary changes in life-history parameters such as generation time and the age of puberty, a possible contribution from undetected post-zygotic mutations early in embryo development, and changes in cellular mutation processes at different stages of the germline. I suggest a revised model of stem-cell state transitions during spermatogenesis, in which ‘dark’ gonial stem cells play a more active role than hitherto envisaged, with a long cycle time undetected in experimental observations. More generally, I argue that the mutation rate and its evolution depend intimately on the structure of the germline in humans and other primates. This article is part of the themed issue ‘Dating species divergences using rocks and clocks'.

scholarly journals A two-tiered model for simulating the ecological and evolutionary dynamics of rapidly evolving viruses, with an application to influenza

2010 ◽  
Vol 7 (50) ◽  
pp. 1257-1274 ◽  
Author(s):  
Katia Koelle ◽  
Priya Khatri ◽  
Meredith Kamradt ◽  
Thomas B. Kepler
Keyword(s):  
Influenza A ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
Sequence Data ◽  
Nucleotide Composition ◽  
Sequence Length ◽  
Influenza B ◽  
Model Parameters ◽  
De Novo Mutations ◽  
Estimation Of Model Parameters

Understanding the epidemiological and evolutionary dynamics of rapidly evolving pathogens is one of the most challenging problems facing disease ecologists today. To date, many mathematical and individual-based models have provided key insights into the factors that may regulate these dynamics. However, in many of these models, abstractions have been made to the simulated sequences that limit an effective interface with empirical data. This is especially the case for rapidly evolving viruses in which de novo mutations result in antigenically novel variants. With this focus, we present a simple two-tiered ‘phylodynamic’ model whose purpose is to simulate, along with case data, sequence data that will allow for a more quantitative interface with observed sequence data. The model differs from previous approaches in that it separates the simulation of the epidemiological dynamics (tier 1) from the molecular evolution of the virus's dominant antigenic protein (tier 2). This separation of phenotypic dynamics from genetic dynamics results in a modular model that is computationally simpler and allows sequences to be simulated with specifications such as sequence length, nucleotide composition and molecular constraints. To illustrate its use, we apply the model to influenza A (H3N2) dynamics in humans, influenza B dynamics in humans and influenza A (H3N8) dynamics in equine hosts. In all three of these illustrative examples, we show that the model can simulate sequences that are quantitatively similar in pattern to those empirically observed. Future work should focus on statistical estimation of model parameters for these examples as well as the possibility of applying this model, or variants thereof, to other host–virus systems.

scholarly journals Multiple mechanisms drive genomic adaptation to extreme O2 levels in Drosophila melanogaster

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Arya Iranmehr ◽  
Tsering Stobdan ◽  
Dan Zhou ◽  
Huiwen Zhao ◽  
Sergey Kryazhimskiy ◽  
...  
Keyword(s):  
Drosophila Melanogaster ◽  
Evolutionary Dynamics ◽  
De Novo ◽  
De Novo Mutations ◽  
Multiple Alleles ◽  
Adaptive Mechanisms ◽  
Genomic Adaptation ◽  
Soft Selective Sweeps ◽  
Analyze Time Series ◽  
Insight Into

AbstractTo detect the genomic mechanisms underlying evolutionary dynamics of adaptation in sexually reproducing organisms, we analyze multigenerational whole genome sequences of Drosophila melanogaster adapting to extreme O2 conditions over an experiment conducted for nearly two decades. We develop methods to analyze time-series genomics data and predict adaptive mechanisms. Here, we report a remarkable level of synchronicity in both hard and soft selective sweeps in replicate populations as well as the arrival of favorable de novo mutations that constitute a few asynchronized sweeps. We additionally make direct experimental observations of rare recombination events that combine multiple alleles on to a single, better-adapted haplotype. Based on the analyses of the genes in genomic intervals, we provide a deeper insight into the mechanisms of genome adaptation that allow complex organisms to survive harsh environments.

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