Controlling insecticide resistant clones of the aphid, Myzus persicae , using the entomopathogenic fungus Akanthomyces muscarius : Fitness cost of resistance under pathogen challenge

2021 ◽  
Author(s):  
Zoltan Erdos ◽  
David Chandler ◽  
Chris Bass ◽  
Ben Raymond
Keyword(s):  
Myzus Persicae ◽  
Entomopathogenic Fungus ◽  
Fitness Cost ◽  
Pathogen Challenge ◽  
Cost Of Resistance

scholarly journals The Fitness Cost of Mutations Associated with Human Immunodeficiency Virus Type 1 Drug Resistance Is Modulated by Mutational Interactions

2006 ◽  
Vol 81 (6) ◽  
pp. 3037-3041 ◽  
Author(s):  
Mian-er Cong ◽  
Walid Heneine ◽  
J. Gerardo García-Lerma
Keyword(s):  
Human Immunodeficiency Virus ◽  
Human Immunodeficiency Virus Type ◽  
Virus Type ◽  
Fitness Cost ◽  
Resistance Mutations ◽  
Drug Pressure ◽  
Critical Determinant ◽  
Immunodeficiency Virus ◽  
Cost Of Resistance

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.

scholarly journals Reversing resistance: different routes and common themes across pathogens

2017 ◽  
Vol 284 (1863) ◽  
pp. 20171619 ◽  
Author(s):  
Richard C. Allen ◽  
Jan Engelstädter ◽  
Sebastian Bonhoeffer ◽  
Bruce A. McDonald ◽  
Alex R. Hall
Keyword(s):  
Fitness Cost ◽  
Biological Processes ◽  
Short Supply ◽  
Compensatory Evolution ◽  
Wide Range ◽  
Different Types ◽  
Cost Of Resistance

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.

scholarly journals Interaction between the entomopathogenic fungus, Beauveria bassiana (Ascomycota: Hypocreales) and the parasitoid wasp, Aphidius colemani Viereck (Hymenoptera: Braconidae)

2013 ◽  
Vol 45 (1) ◽  
pp. 4 ◽  
Author(s):  
F. Emami ◽  
M. Alichi ◽  
K. Minaei
Keyword(s):  
Beauveria Bassiana ◽  
Myzus Persicae ◽  
Entomopathogenic Fungus ◽  
Green Peach Aphid ◽  
Parasitoid Wasp ◽  
Lethal Concentration ◽  
Aphidius Colemani ◽  
Parasitoid Development ◽  
Fungus Beauveria Bassiana ◽  
F1 Generation

The effect of the entomopathogenic fungus, <em>Beauveria bassiana</em>, on the biological characteristics of <em>Aphidius colemani</em>, a parasitoid of the green peach aphid, <em>Myzus persicae</em>, was studied under laboratory conditions. Third-instar nymphs of green peach aphid were infected with 5/3&times;105 conidia/mL of <em>B. bassiana</em>, which was determined to be the lethal concentration 50 dose. They were then offered to mated female parasitoids for 24 h at different intervals. Results showed that by prolonging the release intervals of parasitoids, the number of mummies and percent emergence of parasitoids were reduced. Moreover, production of male offspring increased in the F1 generation of parasitoids. The interference of <em>B. bassiana</em> with parasitoid development was also studied by first exposing the aphid hosts to the parasitoids for 24 h and subsequently spraying them with <em>B. bassiana</em> 24, 48, 72, and 96 h after exposure. Results showed that by prolonging fungal spraying intervals, the number of mummies and percent emergence of parasitoids were increased. It appeared that the best time for applying <em>B. bassiana</em> would be three to four days after parasitisation.

scholarly journals The genomic basis of adaptation to the fitness cost of rifampicin resistance in Pseudomonas aeruginosa

2016 ◽  
Vol 283 (1822) ◽  
pp. 20152452 ◽  
Author(s):  
Qin Qi ◽  
Macarena Toll-Riera ◽  
Karl Heilbron ◽  
Gail M. Preston ◽  
R. Craig MacLean
Keyword(s):  
Pseudomonas Aeruginosa ◽  
Antibiotic Resistance ◽  
Low Cost ◽  
Fitness Cost ◽  
Clinical Settings ◽  
Resistance Mutations ◽  
Beneficial Mutations ◽  
Cost Of Resistance ◽  
Compensatory Mutations ◽  
The Cost

Antibiotic resistance carries a fitness cost that must be overcome in order for resistance to persist over the long term. Compensatory mutations that recover the functional defects associated with resistance mutations have been argued to play a key role in overcoming the cost of resistance, but compensatory mutations are expected to be rare relative to generally beneficial mutations that increase fitness, irrespective of antibiotic resistance. Given this asymmetry, population genetics theory predicts that populations should adapt by compensatory mutations when the cost of resistance is large, whereas generally beneficial mutations should drive adaptation when the cost of resistance is small. We tested this prediction by determining the genomic mechanisms underpinning adaptation to antibiotic-free conditions in populations of the pathogenic bacterium Pseudomonas aeruginosa that carry costly antibiotic resistance mutations. Whole-genome sequencing revealed that populations founded by high-cost rifampicin-resistant mutants adapted via compensatory mutations in three genes of the RNA polymerase core enzyme, whereas populations founded by low-cost mutants adapted by generally beneficial mutations, predominantly in the quorum-sensing transcriptional regulator gene lasR . Even though the importance of compensatory evolution in maintaining resistance has been widely recognized, our study shows that the roles of general adaptation in maintaining resistance should not be underestimated and highlights the need to understand how selection at other sites in the genome influences the dynamics of resistance alleles in clinical settings.

Gossypol in cottonseed increases the fitness cost of resistance to Bt cotton in pink bollworm

2019 ◽  
Vol 126 ◽  
pp. 104914 ◽  
Author(s):  
Yves Carrière ◽  
Alex J. Yelich ◽  
Ben A. Degain ◽  
Virginia S. Harpold ◽  
Gopalan C. Unnithan ◽  
...  
Keyword(s):  
Pink Bollworm ◽  
Fitness Cost ◽  
Bt Cotton ◽  
Cost Of Resistance
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