BACKGROUND Understanding the genetic basis of insect resistance to insecticides can help to implement insecticide resistance management (IRM) strategies. In this study, we selected a strain of Spodoptera frugiperda (J. E. Smith) (Lepidoptera: Noctuidae) resistant to chlorantraniliprole using the F2 screen method, characterized the inheritance of resistance and evaluated patterns of cross‐resistance to other diamide insecticides. RESULTS The chlorantraniliprole‐resistant strain (Chlorant‐R) was selected from a field‐collected population with an estimated allele frequency of 0.1316. The estimated median lethal concentration (LC50) values were 0.011 and 2.610 µg a.i. cm–2 for the susceptible (Sus) and Chlorant‐R strains, respectively, resulting in a resistance ratio (RR) of 237‐fold. The LC50 values of the reciprocal crosses were 0.155 and 0.164 µg a.i. cm–2, indicating that resistance is autosomally inherited. Resistance was characterized as incompletely recessive and monogenic at concentrations close to the recommended field rates of chlorantraniliprole. Survival of the resistant strain and heterozygous larvae in maize plants treated at the field rate was ∼ 60 (similar to the susceptible strain on untreated maize) and 15%, respectively. The Chlorant‐R strain showed low cross‐resistance to cyantraniliprole (RR ∼ 27‐fold) and very high cross‐resistance to flubendiamide (RR > 42 000‐fold). CONCLUSIONS The frequency of chlorantraniliprole resistance allele was moderately high in a field‐collected population of S. frugiperda. The inheritance of chlorantraniliprole resistance was characterized as autosomal, incompletely recessive and monogenic. S. frugiperda showed cross‐resistance to other diamide insecticides. These results provide essential information for the implementation of IRM programs to preserve the useful life of diamide insecticides for controlling S. frugiperda in Brazil. © 2019 Society of Chemical Industry

Based on genetic crosses, the inheritance pattern of lufenuron resistance in S. frugiperda was autosomal, incompletely recessive and polygenic. Implications of this finding to IRM are discussed in this paper.

BACKGROUNDThe use of spinosyn insecticides is one of the major control strategies of the fall armyworm, Spodoptera frugiperda (J. E. Smith) in Brazil. In this study, we selected a spinetoram‐resistant strain from a field‐population of S. frugiperda to characterize the inheritance of the resistance and cross‐resistance relationship between spinosyn insecticides.RESULTSThe values of LC50 (95% CI) obtained from concentration–response bioassays were 0.63 (0.55–0.73) μg spinetoram mL−1 for the susceptible strain (SUS), and 1170.96 (1041.61–1323.89) μg spinetoram mL−1 for the strain resistant to spinetoram (SPT‐R). These values resulted in a resistance ratio of 1844‐fold. The SPT‐R strain showed cross‐resistance with spinosad (resistance ratio = 1196‐fold). The reciprocal crosses showed LC50 values of 3.91 (2.97–5.84) and 5.37 (4.52–6.52) μg spinetoram mL−1, suggesting that the resistance of S. frugiperda to spinetoram is autosomal and incompletely recessive. The backcrosses of the F1 progeny with the SPT‐R strain suggest a resistance with polygenic effect. Estimates of the effective number of loci with equal contributions to the resistance effect were from 1.18 to 1.76, suggesting that resistance to spinetoram is associated with a few genes.CONCLUSIONThe inheritance pattern of resistance of S. frugiperda to spinetoram was characterized as autosomal, incompletely recessive and polygenic. Cross‐resistance between spinosyns was confirmed in S. frugiperda. The importance of this information for implementing insect resistance management strategies is discussed in this paper. © 2020 Society of Chemical Industry

BackgroundThe evolution of insecticide resistance in Spodoptera frugiperda (Lepidoptera: Noctuidae) has resulted in large economic losses and disturbances to the environment and agroecosystems. Resistance to lufenuron, a chitin biosynthesis inhibitor insecticide, was recently documented in Brazilian populations of S. frugiperda. Thus, we utilized large-scale cDNA sequencing (RNA-Seq analysis) to compare the pattern of gene expression between lufenuron-resistant (LUF-R) and susceptible (LUF-S) S. larvae in an attempt to identify the molecular basis behind the resistance mechanism(s) of S. frugiperda to this insecticide.ResultsA transcriptome was assembled using approximately 19.6 million 100 bp-long single-end reads, which generated 18,506 transcripts with a N50 of 996 bp. A search against the NCBI non-redundant database generated 51.1 % (9,457) functionally annotated transcripts. A large portion of the alignments were homologous to insects, with the majority (45 %) being similar to sequences of Bombyx mori (Lepidoptera: Bombycidae). Moreover, 10 % of the alignments were similar to sequences of various species of Spodoptera (Lepidoptera: Noctuidae), with 3 % of them being similar to sequences of S. frugiperda. A comparative analysis of the gene expression between LUF-R and LUF-S S. frugiperda larvae identified 940 differentially expressed transcripts (p ≤ 0.05, t-test; fold change ≥ 4). Six of them were associated with cuticle metabolism. Of those, four were overexpressed in LUF-R larvae. The machinery involved with the detoxification process was represented by 35 differentially expressed transcripts; 24 of them belonging to P450 monooxygenases, four to glutathione-S-transferases, six to carboxylases and one to sulfotransferases. RNA-Seq analysis was validated for a number of selected candidate transcripts by using quantitative real time PCR (qPCR).ConclusionsThe gene expression profile of LUF-R larvae of S. frugiperda differs from LUF-S larvae. In general, gene expression is much higher in resistant larvae when compared to the susceptible ones, particularly for those genes involved with pathways for xenobiotic detoxification, mainly represented by P450 monooxygenases transcripts. Our data indicate that enzymes involved with the detoxification process, and mostly the P450, are one of the resistance mechanisms employed by the LUF-R S. frugiperda larvae against lufenuron.Electronic supplementary materialThe online version of this article (doi:10.1186/s12864-015-2183-z) contains supplementary material, which is available to authorized users.

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