Methoxyfenozide resistance of the housefly,<i>Musca domestica</i>L. (Diptera: Muscidae): cross-resistance patterns, stability and associated fitness costs

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BACKGROUND The house fly, Musca domestica L. (Diptera: Muscidae) is an important public health pest that serves as a carrier for pathogens transmitting various diseases of man and animals. It is well known for rapid resistance development to insecticides applied for its chemical control. Chlorantraniliprole, an anthranilic diamide, a ryanodine receptor agonist, is a promising agent for the integrated pest management of various insect pests. To design a retrospective resistance management strategy, life history traits of the chlorantraniliprole laboratory‐selected (CTPR‐SEL) and unselected counterpart (UNSEL) sub‐populations of a field strain and their reciprocal crosses were studied. RESULTS After eight generations of consecutive selection with chlorantraniliprole, a 750‐fold resistance level when compared to a susceptible strain and a 124‐fold resistance level when compared to the UNSEL strain had developed in CTPR‐SEL. Very low cross resistance to bifenthrin but no cross resistance to spinosad and fipronil was observed in the CTPR‐SEL strain. Results of the fitness traits suggest that the CTPR‐SEL has a lower relative fitness (0.34), reduced fecundity, a decrease in eggs hatchability, lower biotic potential and net reproductive rate as compared to the UNSEL strain. Interestingly, chlorantraniliprole resistance was unstable in the CTPR‐SEL. CONCLUSIONS Fitness costs associated with chlorantraniliprole resistance suggest that the efficacy of this insecticide could be preserved for a prolonged duration of time by alternating its use with insecticides having dissimilar modes of action and no cross resistance. When cross‐resistance is absent, a sequence of two insecticides is expected to be more durable than a mixture unless the population's h2 of resistance to the mixture is less than half of the mean of the population's h2 of resistance to the two individual components of the mixture. Unstable chlorantraniliprole resistance could also help to sustain its efficacy by being withdrawn from usage for some period of time. © 2019 Society of Chemical Industry

Section: Discussionsupporting

confidence: 83%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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House fly resistance to chlorantraniliprole: cross resistance patterns, stability and associated fitness costs

Shah

Shad

2019

Self Cite

“…Usually, resistant populations are less competitive; they have a higher mortality rate, longer developmental duration, and lower fecundity. For example, methoxyfenozide‐resistant Musca domestica had a reduced relative fitness (0.31), with a lower hatching ability, a smaller number of next‐generation larvae, a lower intrinsic rate of natural increase and a lower biotic potential than a susceptible strain . Similarly, the development of resistance led to high fitness costs for spirotetramat‐selected Phenacoccus solenopsis .…”

Section: Discussionmentioning

confidence: 99%

The feeding behavior and life history changes in imidacloprid‐resistant Aphis gossypii glover (Homoptera: Aphididae)

Wang

Rui

et al. 2019

BACKGROUND Imidacloprid (IMI) is a major neonicotinoid insecticide used to control Aphis gossypii Glover. However, resistance to IMI developed rapidly in A. gossypii. The feeding behavior and life history changes associated with IMI resistance were studied in A. gossypii. RESULTS The resistant population with a point mutation (R81T) in the nAChR β1 subunit showed an IMI resistance ratio of 58.12. This IMI‐resistant A. gossypii became more active in finding an appropriate position for feeding. They made more intercellular apoplastic stylet pathway events (C) than the susceptible population. Moreover, the probing and feeding behavior of two aphid populations were dramatically altered by IMI. The phloem ingestion (E2) duration was significantly longer for IMI‐resistant aphids on IMI‐treated plants (WDI: 208.70 ± 17.38 min) than on control plants (WDI: 133.80 ± 16.37 min). However, IMI statistically reduced the ability of susceptible aphids to find and feed from the phloem. The number and duration of phloem‐related activities were sharply decreased for the susceptible aphids treated with IMI. In addition, the resistant population showed an increased relative fitness of 1.36. The fecundity of IMI‐resistant adults was dramatically higher than that of the susceptible population. This difference also led to an increase in the net reproductive rate (R0) for the IMI‐resistant A. gossypii. CONCLUSIONS Imidacloprid provoked phloem‐feeding more rapidly and effectively in IMI‐resistant A. gossypii, but significantly suppressed the feeding of susceptible A. gossypii. Therefore, the resistance to IMI can result in stimulated feeding and fecundity and subsequent population outbreaks, which make the control of IMI‐resistant A. gossypii more challenging. © 2019 Society of Chemical Industry

Dissecting the roles of FTZ‐F1 in larval molting and pupation, and the sublethal effects of methoxyfenozide on Helicoverpa armigera

Zhang

Liu

et al. 2020

BACKGROUND In holometabolous insects, the major developmental transitions – larval molting and pupation – are triggered by a pulse of 20‐hydroxyecdysone (20E) and coordinated by juvenile hormone. Methoxyfenozide (MF), an ecdysteroid agonist, represents a new class of insect growth regulators and is effective against lepidopteran pests. Fushi‐tarazu factor 1 (FTZ‐F1) is an ecdysone‐inducible transcription factor. To date, the effect of MF on 20E‐response genes remains unclear, and we speculate the involvement of FTZ‐F1 in MF's growth regulating effect. RESULTS MF at LC25 and LC10 caused severe ecdysis failure in Helicoverpa armigera, extended their larval duration, lowered their pupal weight, and reduced the respiratory, pupation and emergence rates. Furthermore, sublethal doses of MF inhibited ecdysteroidogenesis and lowered the intrinsic 20E titer, but showed an inductive effect on 20E‐response genes including HaFTZ‐F1. HaFTZ‐F1, predominantly expressed in larval epidermis, was markedly upregulated before or right after larval ecdysis, and maintained a high level in prepupal stage. Knockdown of HaFTZ‐F1 in 4th‐instar larvae severely impaired larval ecdysis, whereas its knockdown in final‐instar larvae caused abnormal pupation. Moreover, knocking down HaFTZ‐F1 downregulated three critical ecdysteroidogenesis genes, lowered 20E titer, and suppressed the expression of 20E receptors and 20E‐response genes. The introduction of 20E into HaFTZ‐F1‐RNAi larvae partly relieved the negative effects on the 20E‐induced signaling cascade. CONCLUSION Our findings reveal the adverse effects of sublethal doses of MF on the development of H. armigera and elucidate the resulting perturbations on the 20E‐induced signaling cascade; we propose that HaFTZ‐F1 regulates ecdysis and pupation by mediating 20E titer and its signaling pathway. © 2020 Society of Chemical Industry