ArticleFrontiers in microbiology2025
Elimination of
Article in Frontiers in microbiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Abstract
Introduction: The cotton aphid, Aphis gossypii Glover, is a globally significant agricultural pest that harbors diverse microbial symbionts. Beyond their well-known roles in nutrition, these microbial partners are increasingly recognized for their potential to modulate host detoxification pathways and influence insecticide susceptibility. While sulfoxaflor is a primary insecticide for controlling A. gossypii, the extent to which the predominant secondary symbiont, Arsenophonus, mediates susceptibility to this chemical remains largely unexplored. Methods: In this study, we investigated the role of Arsenophonus in modulating host sulfoxaflor susceptibility and the underlying molecular mechanisms. We established an Arsenophonus-infected A. gossypii line (A-infected) and an antibiotic-cured, Arsenophonus-deleted line (A-deleted). To ensure identical genetic backgrounds and eliminate residual antibiotic effects, the A-deleted line was maintained for 10 generations under antibiotic-free conditions, with symbiont status confirmed by PCR and 16S rRNA sequencing. We then compared sulfoxaflor susceptibility, analyzed protein levels of detoxification enzymes, performed comparative transcriptomic analysis, and validated key candidate genes using RNA interference (RNAi). Results and discussion: Bioassays revealed that the elimination of Arsenophonus significantly increased susceptibility to sulfoxaflor. This hypersensitivity was metabolically associated with reduced protein levels of mixed-function oxidases (MFOs) and glutathione S-transferases (GSTs). Comparative transcriptomic analysis identified multiple differentially expressed cytochrome P450 genes, including
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