FITNESS COST OF RESISTANCE TO CADMIUM IN THE LEAST KILLIFISH (HETERANDRIA FORMOSA)

10.1897/03-96 ◽  
2004 ◽  
Vol 23 (6) ◽  
pp. 1499 ◽  
Author(s):  
Lingtian Xie ◽  
Paul L. Klerks

2006 ◽  
Vol 81 (6) ◽  
pp. 3037-3041 ◽  
Author(s):  
Mian-er Cong ◽  
Walid Heneine ◽  
J. Gerardo García-Lerma

ABSTRACT It is generally accepted that the fitness cost of resistance mutations plays a role in the persistence of transmitted drug-resistant human immunodeficiency virus type 1 and that mutations that confer a high fitness cost are less able to persist in the absence of drug pressure. Here, we show that the fitness cost of reverse transcriptase (RT) mutations can vary within a 72-fold range. We also demonstrate that the fitness cost of M184V and K70R can be decreased or enhanced by other resistance mutations such as D67N and K219Q. We conclude that the persistence of transmitted RT mutants might range widely on the basis of fitness and that the modulation of fitness cost by mutational interactions will be a critical determinant of persistence.



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.



2018 ◽  
Vol 221 (7) ◽  
pp. jeb168609 ◽  
Author(s):  
Mike Fleuren ◽  
Johan L. van Leeuwen ◽  
Elsa M. Quicazan-Rubio ◽  
Remco P. M. Pieters ◽  
Bart J. A. Pollux ◽  
...  




Copeia ◽  
1984 ◽  
Vol 1984 (3) ◽  
pp. 720 ◽  
Author(s):  
Ron T. Cheong ◽  
Sabine Henrich ◽  
James A. Farr ◽  
Joseph Travis


Evolution ◽  
2009 ◽  
Vol 63 (5) ◽  
pp. 1341-1347 ◽  
Author(s):  
Jeff Leips ◽  
Jean M. L. Richardson ◽  
F. Helen Rodd ◽  
Joseph Travis




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