Inference on Arthropod Demographic Parameters: Computational Advances Using R

Maia, A. de H. N.; Pazianotto, Ricardo Antonio De Almeida; Luiz, A. J. B.; Marinho-Prado, J. S.; Pervez, Ahmad

doi:10.1603/ec13222

Cited by 29 publications

(22 citation statements)

References 27 publications

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“…Th e following data were used to construct age specifi c survival and fecundity, and to calculate fertility life table (FLT) parameters: the pivotal age for the female age class in units of time (x), the number of individuals dying during the age interval x (d x ), the total number of female eggs laid in age class x (l x m x ), the proportion of population surviving to age x (l x ), the number of female off spring per female aged x per day (m x ), the net reproductive or replacement rate (R 0 ), the intrinsic rate of increase (r m ), the fi nite rate of increase (λ), the mean generation time (TG), and the doubling time (DT) of the population (Southwood 1978) for each cultivar, the period of development and survival of immature stages, longevity, and daily fecundity. A computer program with the code sheet of lifetable.r in the open source, a free soft ware programming environment R version 3.0.3 (R Development Core Team 2014), developed by Maia et al (2000Maia et al ( , 2014, was used to calculate and compare between FLT parameters of thrips population on cultivars.…”

Section: Discussionmentioning

confidence: 99%

Biological parameters of onion thrips, Thrips tabaci Lindeman on onion cultivars

Moraiet¹,

Ansari²,

Basri³

2017

Journal of Plant Protection Research

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Biological parameters of the onion thrips, Thrips tabaci Lindeman were studied on the following onion (Allium cepa L.) cultivars: Nasik Red Plus N-53, Onion Dr-301 (Krishna), Onion White, and Nasik Red, at 25±1 o C and 65±5% RH. Signifi cant (p < 0.05) diff erences were found in the life stages and fertility life tables on diff erent cultivars except in the pupal stages. More information about the biological parameters of T. tabaci on onion cultivars can help in designing Integrated Pest Management programs for onion thrips.

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Section: Discussionmentioning

confidence: 99%

Biological parameters of onion thrips, Thrips tabaci Lindeman on onion cultivars

Moraiet¹,

Ansari²,

Basri³

2017

Journal of Plant Protection Research

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“…Differences between the introgressed lines were determined using Tukey's HSD test at a 95% confidence level. Life table analysis was performed based on the lifetable R script . The intrinsic rate of increase (rm) was calculated with the equation

\sum_{x = x 0}^{Ωg} e ‐ rmlxmx = 1

where lx is the proportion of females surviving to age x and mx is the mean number of female progeny per adult female at age x.…”

Section: Methodsmentioning

confidence: 99%

“…Life table analysis was performed based on the lifetable R script. 44 The intrinsic rate of increase (rm) was calculated with the equation The finite rate of increase and doubling time were inferred from the equations: LM = erm and DT = ln 2 rm . Variance for the life table parameters was estimated using the jackknife resampling method.…”

Section: Oviposition and Adult Longevitymentioning

confidence: 99%

Identification and characterization of new mutations in mitochondrial cytochrome b that confer resistance to bifenazate and acequinocyl in the spider mite Tetranychus urticae

Fotoukkiaii

Tan

Xue

et al. 2019

Pest Management Science

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BACKGROUND In spider mites, mutations in the mitochondrial cytochrome b Qo pocket have been reported to confer resistance to the Qo inhibitors bifenazate and acequinocyl. In this study, we surveyed populations of the two‐spotted spider mite Tetranychus urticae for mutations in cytochrome b, linked newly discovered mutations with resistance and assessed potential pleiotropic fitness costs. RESULTS We identified two novel mutations in the Qo site: G132A (equivalent to G143A in fungi resistant to strobilurins) and G126S + A133T (previously reported to cause bifenazate and acequinocyl resistance in Panonychus citri). Two T. urticae strains carrying G132A were highly resistant to bifenazate but not acequinocyl, whereas a strain with G126S + A133T displayed high levels of acequinocyl resistance, but only moderate levels of bifenazate resistance. Bifenazate and acequinocyl resistance were inherited maternally, providing strong evidence for the involvement of these mutations in the resistance phenotype. Near isogenic lines carrying G132A revealed several fitness penalties in T. urticae; a lower net reproductive rate (R0), intrinsic rate of increase (rm) and finite rate of increase (LM); a higher doubling time (DT); and a more male‐biased sex ratio. CONCLUSIONS Several lines of evidence were provided to support the causal role of newly discovered cytochrome b mutations in bifenazate and acequinocyl resistance. Because of the fitness costs associated with the G132A mutation, resistant T. urticae populations might be less competitive in a bifenazate‐free environment, offering opportunities for resistance management. © 2019 Society of Chemical Industry

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“…The analysis of life‐history raw data of the different lines was based on the lifetable R script (Maia, Pazianotto, Luiz, Marinho‐Prado, & Pervez, 2014). Specifically, line name, female ID, age, and number of eggs laid per female at each oviposition date, proportion of female offspring and ISS were used as input.…”

Section: Methodsmentioning

confidence: 99%

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider mite Tetranychus urticae

Bajda

Riga

Wybouw

et al. 2018

Evolutionary Applications

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The frequency of insecticide/acaricide target‐site resistance is increasing in arthropod pest populations and is typically underpinned by single point mutations that affect the binding strength between the insecticide/acaricide and its target‐site. Theory predicts that although resistance mutations clearly have advantageous effects under the selection pressure of the insecticide/acaricide, they might convey negative pleiotropic effects on other aspects of fitness. If such fitness costs are in place, target‐site resistance is thus likely to disappear in the absence of insecticide/acaricide treatment, a process that would counteract the spread of resistance in agricultural crops. Hence, there is a great need to reliably quantify the various potential pleiotropic effects of target‐site resistance point mutations on arthropod fitness. Here, we used near‐isogenic lines of the spider mite pest Tetranychus urticae that carry well‐characterized acaricide target‐site resistance mutations to quantify potential fitness costs. Specifically, we analyzed P262T in the mitochondrial cytochrome b, the combined G314D and G326E substitutions in the glutamate‐gated chloride channels, L1024V in the voltage‐gated sodium channel, and I1017F in chitin synthase 1. Five fertility life table parameters and nine single‐generation life‐history traits were quantified and compared across a total of 15 mite lines. In addition, we monitored the temporal resistance level dynamics of populations with different starting frequency levels of the chitin synthase resistant allele to further support our findings. Three target‐site resistance mutations, I1017F and the co‐occurring G314D and G326E mutations, were shown to significantly and consistently alter certain fitness parameters in T. urticae. The other two mutations (P262T and L1024V) did not result in any consistent change in a fitness parameter analyzed in our study. Our findings are discussed in the context of the global spread of T. urticae pesticide resistance and integrated pest management.

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Inference on Arthropod Demographic Parameters: Computational Advances Using R

Cited by 29 publications

References 27 publications

Biological parameters of onion thrips, Thrips tabaci Lindeman on onion cultivars

Biological parameters of onion thrips, Thrips tabaci Lindeman on onion cultivars

Identification and characterization of new mutations in mitochondrial cytochrome b that confer resistance to bifenazate and acequinocyl in the spider mite Tetranychus urticae

Fitness costs of key point mutations that underlie acaricide target‐site resistance in the two‐spotted spider mite Tetranychus urticae

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