The revolt of the clay

Author(s):  
Arlin Stoltzfus

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.

2021 ◽  
Author(s):  
Kyle J. McCulloch ◽  
Aide Macias-Muñoz ◽  
Ali Mortazavi ◽  
Adriana D. Briscoe

AbstractColor vision modifications occur in animals via a process known as spectral tuning. In Heliconius butterflies, a genus-specific UVRh opsin duplication led to the evolution of UV color discrimination in Heliconius erato females, a rare trait among butterflies. In the H. melpomene and H. ismenius lineages, the UV2 receptor has been lost. Here we compare how loss of the UV2 photoreceptor has altered the visual system of these butterflies. We compare visual system evolution in three Heliconius butterfly species using a combination of intracellular recordings, ATAC-seq, and antibody staining. We identify several spectral tuning mechanisms including adaptive evolution of opsins, deployment of two types of filtering pigments, and co-expression of two distinct opsins in the same cell. Our data show that opsin gain and loss is driving rapid divergence in Heliconius visual systems via tuning of multiple spectral classes of photoreceptor in distinct lineages, potentially contributing to ongoing speciation in this genus.


Science ◽  
1991 ◽  
Vol 252 (5008) ◽  
pp. 971-974 ◽  
Author(s):  
M Neitz ◽  
J Neitz ◽  
G. Jacobs

mSphere ◽  
2016 ◽  
Vol 1 (4) ◽  
Author(s):  
Charlie Y. Mo ◽  
Sara A. Manning ◽  
Manuela Roggiani ◽  
Matthew J. Culyba ◽  
Amanda N. Samuels ◽  
...  

ABSTRACT Our antibiotic arsenal is becoming depleted, in part, because bacteria have the ability to rapidly adapt and acquire resistance to our best agents. The SOS pathway, a widely conserved DNA damage stress response in bacteria, is activated by many antibiotics and has been shown to play central role in promoting survival and the evolution of resistance under antibiotic stress. As a result, targeting the SOS response has been proposed as an adjuvant strategy to revitalize our current antibiotic arsenal. However, the optimal molecular targets and partner antibiotics for such an approach remain unclear. In this study, focusing on the two key regulators of the SOS response, LexA and RecA, we provide the first comprehensive assessment of how to target the SOS response in order to increase bacterial susceptibility and reduce mutagenesis under antibiotic treatment. The bacterial SOS response is a DNA damage repair network that is strongly implicated in both survival and acquired drug resistance under antimicrobial stress. The two SOS regulators, LexA and RecA, have therefore emerged as potential targets for adjuvant therapies aimed at combating resistance, although many open questions remain. For example, it is not well understood whether SOS hyperactivation is a viable therapeutic approach or whether LexA or RecA is a better target. Furthermore, it is important to determine which antimicrobials could serve as the best treatment partners with SOS-targeting adjuvants. Here we derived Escherichia coli strains that have mutations in either lexA or recA genes in order to cover the full spectrum of possible SOS activity levels. We then systematically analyzed a wide range of antimicrobials by comparing the mean inhibitory concentrations (MICs) and induced mutation rates for each drug-strain combination. We first show that significant changes in MICs are largely confined to DNA-damaging antibiotics, with strains containing a constitutively repressed SOS response impacted to a greater extent than hyperactivated strains. Second, antibiotic-induced mutation rates were suppressed when SOS activity was reduced, and this trend was observed across a wider spectrum of antibiotics. Finally, perturbing either LexA or RecA proved to be equally viable strategies for targeting the SOS response. Our work provides support for multiple adjuvant strategies, while also suggesting that the combination of an SOS inhibitor with a DNA-damaging antibiotic could offer the best potential for lowering MICs and decreasing acquired drug resistance. IMPORTANCE Our antibiotic arsenal is becoming depleted, in part, because bacteria have the ability to rapidly adapt and acquire resistance to our best agents. The SOS pathway, a widely conserved DNA damage stress response in bacteria, is activated by many antibiotics and has been shown to play central role in promoting survival and the evolution of resistance under antibiotic stress. As a result, targeting the SOS response has been proposed as an adjuvant strategy to revitalize our current antibiotic arsenal. However, the optimal molecular targets and partner antibiotics for such an approach remain unclear. In this study, focusing on the two key regulators of the SOS response, LexA and RecA, we provide the first comprehensive assessment of how to target the SOS response in order to increase bacterial susceptibility and reduce mutagenesis under antibiotic treatment.


2011 ◽  
Vol 279 (1727) ◽  
pp. 247-256 ◽  
Author(s):  
Bjørn Østman ◽  
Arend Hintze ◽  
Christoph Adami

Evolutionary adaptation is often likened to climbing a hill or peak. While this process is simple for fitness landscapes where mutations are independent, the interaction between mutations (epistasis) as well as mutations at loci that affect more than one trait (pleiotropy) are crucial in complex and realistic fitness landscapes. We investigate the impact of epistasis and pleiotropy on adaptive evolution by studying the evolution of a population of asexual haploid organisms (haplotypes) in a model of N interacting loci, where each locus interacts with K other loci. We use a quantitative measure of the magnitude of epistatic interactions between substitutions, and find that it is an increasing function of K . When haplotypes adapt at high mutation rates, more epistatic pairs of substitutions are observed on the line of descent than expected. The highest fitness is attained in landscapes with an intermediate amount of ruggedness that balance the higher fitness potential of interacting genes with their concomitant decreased evolvability. Our findings imply that the synergism between loci that interact epistatically is crucial for evolving genetic modules with high fitness, while too much ruggedness stalls the adaptive process.


2004 ◽  
Vol 07 (03n04) ◽  
pp. 395-418
Author(s):  
H. S. MORTVEIT ◽  
C. M. REIDYS

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.


1998 ◽  
Vol 46 (6) ◽  
pp. 697-702 ◽  
Author(s):  
Song-Kun Shyue ◽  
Stéphane Boissinot ◽  
Horacio Schneider ◽  
Iracilda Sampaio ◽  
Maria Paula Schneider ◽  
...  

2012 ◽  
Vol 12 (1) ◽  
pp. 252 ◽  
Author(s):  
Adérito L Monjane ◽  
Daniel Pande ◽  
Francisco Lakay ◽  
Dionne N Shepherd ◽  
Eric van der Walt ◽  
...  

2018 ◽  
Author(s):  
Juraj Bergman ◽  
Adam Eyre-Walker

AbstractA longstanding question in evolutionary biology is the relative contribution of large and small effect mutations to the adaptive process. We have investigated this question in proteins by estimating the rate of adaptive evolution between all pairs of amino acids separated by one mutational step using a McDonald-Kreitman type approach and genome-wide data from several Drosophila species. We find that the rate of adaptive evolution is higher amongst amino acids that are more similar. This is partly due to the fact that the proportion of mutations that are adaptive is higher amongst more similar amino acids. We also find that the rate of neutral evolution between amino acids is higher amongst similar amino acids. Overall our results suggest that both the adaptive and non-adaptive evolution of proteins is dominated by substitutions between amino acids that are more similar.


2018 ◽  
Author(s):  
Peter A. Lind ◽  
Eric Libby ◽  
Jenny Herzog ◽  
Paul B. Rainey

AbstractPredicting evolutionary change poses numerous challenges. Here we take advantage of the model bacterium Pseudomonas fluorescens in which the genotype-to-phenotype map determining evolution of the adaptive “wrinkly spreader” (WS) type is known. We present mathematical descriptions of three necessary regulatory pathways and use these to predict both the rate at which each mutational route is used and the expected mutational targets. To test predictions, mutation rates and targets were determined for each pathway. Unanticipated mutational hotspots caused experimental observations to depart from predictions but additional data led to refined models. A mismatch was observed between the spectra of WS-causing mutations obtained with and without selection due to low fitness of previously undetected WS-causing mutations. Our findings contribute toward the development of mechanistic models for forecasting evolution, highlight current limitations, and draw attention to challenges in predicting locus-specific mutational biases and fitness effects.Impact statementA combination of genetics, experimental evolution and mathematical modelling defines information necessary to predict the outcome of short-term adaptive evolution.


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