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. 2025 Jan 12;16(1):69.
doi: 10.3390/insects16010069.

Involvement of Inwardly Rectifying Potassium (Kir) Channels in the Toxicity of Flonicamid to Drosophila melanogaster

Xuan Liu  1 , Yuying Gao  1 , Tengfei Liu  1 , Hailiang Guo  1 , Jizu Qiao  1 , Jianya Su  1
Affiliations

Involvement of Inwardly Rectifying Potassium (Kir) Channels in the Toxicity of Flonicamid to Drosophila melanogaster

Xuan Liu et al. Insects. .

Abstract

Inwardly rectifying potassium (Kir) channels regulate essential physiological processes in insects and have been identified as potential targets for developing new insecticides. Flonicamid has been reported to inhibit Kir channels, disrupting the functions of salivary glands and renal tubules. However, the precise molecular target of flonicamid remains debated. It is unclear whether flonicamid directly targets Kir channels or acts on other sites involved in the activation of transient receptor potential vanilloid (TRPV) channels. In this study, we observed that flonicamid is more toxic to flies than its metabolite, flumetnicam. This higher toxicity is difficult to reconcile if nicotinamidase is the active target, as flonicamid does not inhibit nicotinamidase. An alternative explanation is that flonicamid and flumetnicam may have distinct targets or act on multiple targets. Furthermore, reducing the expression of three individual Kir genes in the salivary glands of D. melanogaster significantly decreased the flies' susceptibility to both flonicamid and flumetnicam. The double knockdown of Kir1 with Kir3 or Kir2 with Kir3 further reduced the flies' sensitivity to both compounds. These findings confirm the involvement of Kir channels in mediating the toxic effects of flonicamid on flies. Overall, this study offers new insights into the physiological roles of insect Kir channels and flonicamid toxicity.

Keywords: flonicamid; flumetnicam; inwardly rectifying potassium channels; molecular target.

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Conflict of interest statement

The authors declare no conflicts of interest. The founding sponsors had no role in the design of the study, the collection, analysis, or interpretation of data, in the writing of the manuscript or in the decision to publish the results.

Figures

Figure 1
Figure 1
The apparatus for toxicity assay of flonicamid on fly adults.
Figure 2
Figure 2
The toxicities of flonicamid and its metabolite to w1118 fly. (A) The time course changes in mortalities of w1118 fly exposed to flonicamid. (B) The comparison of lethal toxicities between flonicamid and its metabolite. Asterisk represents significant difference between treatments (p < 0.05).
Figure 3
Figure 3
The susceptibilities of D. melanogaster with Kir knockdown in salivary glands to flonicamid. (A–C) represent the susceptibilities of fly with knockdown of Kir1, Kir2, and Kir3, respectively. (D) represents the susceptibilities with double knockdown of Kir1 and Kir3. (E) represents the susceptibilities with double knockdown of Kir2 and Kir3. Asterisks represent significant differences (p < 0.05).
Figure 4
Figure 4
The susceptibilities of D. melanogaster with Kir knockdown in salivary glands to flumetnicam. (A–C) represent fly’s susceptibilities after knockdown of Kir1, Kir2, and Kir3, respectively. (D) represents the susceptibilities with double knockdown of Kir1 and Kir3. (E) represents the susceptibilities with double knockdown of Kir2 and Kir3. Asterisks represent significant difference (p < 0.05).
Figure 5
Figure 5
Effects of Kir channels on ovarian development in D. melanogaster. (A) Knockdown of Kir genes significantly reduced ovariole numbers compared to the control group with statistical differences indicated by different letters (one-way ANOVA with Dunnett’s test, p < 0.0001). The F1 offsprings of Nos-Gal4 and w1118 were used as the control. (B) Knockdown of Kir genes led to a marked decrease in ovary size. Scale bar: 100 μm. The F1 offsprings of nanos-Gal4 and w1118 were used as the control.
Figure 6
Figure 6
Effects of Kir expression on egg production and hatchability in D. melanogaster. (A–C) show the effects on egg production following knockdown of Kir1, Kir2, and Kir3, respectively. (D–F) depict the effects on hatchability following knockdown of Kir1, Kir2, and Kir3, respectively. The F1 offsprings of Nos-Gal4 and w1118 were used as the control (CK). Asterisk indicates significant difference (Student’s t-test, p < 0.05).
Figure 7
Figure 7
Effect of flonicamid on ovarian development in D. melanogaster. (A) Effect of flonicamid on ovarole numbers. ** indicates significant differences (Student’s t-test, p < 0.01). (B) Effect of flonicamid on ovary size compared to the control (w1118). Scale bar: 100 μm.
Figure 8
Figure 8
Effect of flonicamid on egg production (A) and hatchability (B) in D. melanogaster. ** and **** represent significant difference at the levels of 0.01 and 0.0001 (Student’s t-test), respectively. The horizonal lines represent the mean and their 95% FLs, respectively.
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