scholarly journals Investigating the presence of compensatory evolution in dicamba resistant IAA16 mutated kochia ( Bassia scoparia ) †

2020 ◽  
Author(s):  
Chenxi Wu ◽  
Marta Paciorek ◽  
Kang Liu ◽  
Sherry LeClere ◽  
Alejandro Perez‐Jones ◽  
...  

Genetics ◽  
2000 ◽  
Vol 154 (2) ◽  
pp. 909-921 ◽  
Author(s):  
John Parsch ◽  
John M Braverman ◽  
Wolfgang Stephan

Abstract A novel method of RNA secondary structure prediction based on a comparison of nucleotide sequences is described. This method correctly predicts nearly all evolutionarily conserved secondary structures of five different RNAs: tRNA, 5S rRNA, bacterial ribonuclease P (RNase P) RNA, eukaryotic small subunit rRNA, and the 3′ untranslated region (UTR) of the Drosophila bicoid (bcd) mRNA. Furthermore, covariations occurring in the helices of these conserved RNA structures are analyzed. Two physical parameters are found to be important determinants of the evolution of compensatory mutations: the length of a helix and the distance between base-pairing nucleotides. For the helices of bcd 3′ UTR mRNA and RNase P RNA, a positive correlation between the rate of compensatory evolution and helix length is found. The analysis of Drosophila bcd 3′ UTR mRNA further revealed that the rate of compensatory evolution decreases with the physical distance between base-pairing residues. This result is in qualitative agreement with Kimura's model of compensatory fitness interactions, which assumes that mutations occurring in RNA helices are individually deleterious but become neutral in appropriate combinations.



Genetics ◽  
1996 ◽  
Vol 144 (1) ◽  
pp. 419-426 ◽  
Author(s):  
Wolfgang Stephan

Abstract A two-locus model is presented to analyze the evolution of compensatory mutations occurring in stems of RNA secondary structures. Single mutations are assumed to be deleterious but harmless (neutral) in appropriate combinations. In proceeding under mutation pressure, natural selection and genetic drift from one fitness peak to another one, a population must therefore pass through a valley of intermediate deleterious states of individual fitness. The expected time for this transition is calculated using diffusion theory. The rate of compensatory evolution, kc, is then defined as the inverse of the expected transition time. When selection against deleterious single mutations is strong, kc, depends on the recombination fraction r between the two loci. Recombination generally reduces the rate of compensatory evolution because it breaks up favorable combinations of double mutants. For complete linkage, kc, is given by the rate at which favorable combinations of double mutantS are produced by compensatory mutation. For r > 0, kc, decreases exponentially with r. In contrast, kc, becomes independent of r for weak selection. We discuss the dynamics of evolutionary substitutions of compensatory mutants in relation to Wright'S shifting balance theory of evolution and use our results to analyze the substitution process in helices of mRNA secondary structures.



2009 ◽  
Vol 9 (1) ◽  
pp. 106 ◽  
Author(s):  
WR Harcombe ◽  
R Springman ◽  
JJ Bull


2017 ◽  
Vol 284 (1863) ◽  
pp. 20171619 ◽  
Author(s):  
Richard C. Allen ◽  
Jan Engelstädter ◽  
Sebastian Bonhoeffer ◽  
Bruce A. McDonald ◽  
Alex R. Hall

Resistance spreads rapidly in pathogen or pest populations exposed to biocides, such as fungicides and antibiotics, and in many cases new biocides are in short supply. How can resistance be reversed in order to prolong the effectiveness of available treatments? Some key parameters affecting reversion of resistance are well known, such as the fitness cost of resistance. However, the population biological processes that actually cause resistance to persist or decline remain poorly characterized, and consequently our ability to manage reversion of resistance is limited. Where do susceptible genotypes that replace resistant lineages come from? What is the epidemiological scale of reversion? What information do we need to predict the mechanisms or likelihood of reversion? Here, we define some of the population biological processes that can drive reversion, using examples from a wide range of taxa and biocides. These processes differ primarily in the origin of revertant genotypes, but also in their sensitivity to factors such as coselection and compensatory evolution that can alter the rate of reversion, and the likelihood that resistance will re-emerge upon re-exposure to biocides. We therefore argue that discriminating among different types of reversion allows for better prediction of where resistance is most likely to persist.



2016 ◽  
Vol 6 (3) ◽  
pp. e1179074 ◽  
Author(s):  
Ellie Harrison ◽  
Calvin Dytham ◽  
James P. J. Hall ◽  
David Guymer ◽  
Andrew J. Spiers ◽  
...  




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