Cross-resistance, stability, and fitness cost of resistance to imidacloprid in Musca domestica L., (Diptera: Muscidae)

2014 ◽  
Vol 114 (1) ◽  
pp. 247-255 ◽  
Author(s):  
Naeem Abbas ◽  
Hussnain Khan ◽  
Sarfraz Ali Shad
Keyword(s):  
Musca Domestica ◽  
Fitness Cost ◽  
Cross Resistance ◽  
Cost Of Resistance ◽  
Resistance Stability

Characterization of indoxacarb resistance in Phenacoccus solenopsis Tinsley (Homoptera: Pseudococcidae): Cross-resistance, stability and fitness cost

2015 ◽  
Vol 18 (4) ◽  
pp. 779-785 ◽  
Author(s):  
Muhammad Babar Shahzad Afzal ◽  
Sarfraz Ali Shad ◽  
Esteban Basoalto ◽  
Masood Ejaz ◽  
Jose Eduardo Serrao
Keyword(s):  
Fitness Cost ◽  
Cross Resistance ◽  
Phenacoccus Solenopsis ◽  
Resistance Stability

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 Characterization of resistance and fitness cost of Descurainia sophia L. populations from Henan and Xinjiang, China

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Dongzhi Li ◽  
Lanfen Xie ◽  
Pei Zhang ◽  
Runqiang Liu ◽  
Mingwang Shi ◽  
...  
Keyword(s):  
Fitness Cost ◽  
Cross Resistance ◽  
Homozygous Mutation ◽  
Susceptible Population ◽  
Relative Growth Rates ◽  
Wheat Field ◽  
Production Region ◽  
Descurainia Sophia ◽  
Mutation Type ◽  
Tribenuron Methyl

AbstractDescurainia sophia L. is a notorious weed in winter wheat field and has serious resistance to tribenuron-methyl. Xinjiang is a main wheat production region in China with no information on D. sophia resistance to tribenuron-methyl. Here, resistance levels of D. sophia populations to tribenuron-methyl from Xinjiang and Henan were investigated. In addition, homozygous mutation subpopulations of high resistant D. sophia populations from Xinjiang and Henan were generated and then cross-resistance and fitness cost were determined. Results showed that 5 out of 31 populations from Xinjiang developed resistance to tribenuron-methyl, including two high resistant populations (X30 and X31). While 10 out of 11 populations from Henan showed resistance to tribenuron-methyl, including three high resistant populations (H5, H6 and H7). X30 and X31 shared the same mutation type of Pro197Thr in ALS1, while the mutation type of ALS1 in H5, H6 and H7 were Pro197Ser, Pro197His and Pro197Ala, respectively. The homozygous mutation subpopulations (SX30, SX31, SH5, SH6, SH7) showed cross-resistance to flucarbazone-sodium, bensulfuron methyl and flumetsulam. Under monoculture condition, relative growth rates of SX30, SX31 were higher than susceptible population (SX13), while that in SH5, SH6, SH7 were almost same with SX13. When mix planted with SX13, SX30 and SX31 displayed weaker competitiveness than SX13, while SH5, SH6, SH7 showed stronger competitiveness than SX13. The results suggested that D. sophia from Xinjiang had low resistance frequency to tribenuron-methyl and the high resistant populations had fitness costs.

scholarly journals Insecticide Resistant Strains of House Flies (Musca domestica) Show Limited Cross-Resistance to Chlorfenapyr

2004 ◽  
Vol 29 (2) ◽  
pp. 124-126 ◽  
Author(s):  
Jeffrey G. Scott ◽  
Cheryl A. Leichter ◽  
Frank D. Rinkevich
Keyword(s):  
Musca Domestica ◽  
Cross Resistance ◽  
House Flies ◽  
Resistant Strains

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.

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