Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation

Authors: Alburaki, Mohamed; Madella, Shayne; Cook, Steven

Submitted to: Scientific Reports
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 2/20/2023
Publication Date: 3/9/2023
Citation: Alburaki, M., Madella, S., Cook, S.C. 2023. Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation. Scientific Reports. 13. Article 3931. https://doi.org/10.1038/s41598-023-30264-0.
DOI: https://doi.org/10.1038/s41598-023-30264-0

Interpretive Summary: Regulation of antioxidant genes is a complex process honey bees undertake to alleviate toxicity. Other factors affect this process and may amplify the effect of pesticides on bees. In this study, we tested how ambient temperature interlinks with the toxicological effect of imidacloprid. We found that bees subjected to non-optimal temperature are more susceptible to imidacloprid. Moreover, this study showed that major developmental genes are also involved in the detoxification process as well as other poorly characterized genes.

Technical Abstract: In this study, we conducted a transcriptional analysis of five honey bee genes to examine their functional involvement vis-à-vis ambient temperatures and exposure to imidacloprid. In a 15-day cage experiment, three cohorts of one-day-old sister bees emerged in incubators, were distributed into cages, and maintained at three different temperatures (26 °C, 32 °C, 38 °C). Each cohort was fed a protein patty and three concentrations of imidacloprid-tainted sugar (0 ppb, 5 ppb and 20 ppb) ad libitum. Honey bee mortality, syrup and patty consumption were monitored daily over 15 days. Bees were sampled every three days for a total of five time points. RT-qPCR was used to longitudinally assess gene regulation of Vg, mrjp1, Rsod, AChE-2 and Trx-1 using RNA extracted from whole bee bodies. Kaplan–Meier models show that bees kept at both non-optimal temperatures (26 °C and 38 °C) were more susceptible to imidacloprid, with significantly higher mortality (P'<'0.001 and P'<'0.01, respectively) compared to the control. At 32 °C, no differences in mortality (P'='0.3) were recorded among treatments. In both imidacloprid treatment groups and the control, the expression of Vg and mrjp1 was significantly downregulated at 26 °C and 38 °C compared to the optimal temperature of 32 °C, indicating major influence of ambient temperature on the regulation of these genes. Within the ambient temperature groups, both imidacloprid treatments exclusively downregulated Vg and mrjp1 at 26 °C. AChE-2 and the poorly characterized Rsod gene were both consistently upregulated at the highest temperature (38 °C) compared to the ideal temperature (32 °C) in all treatment groups. Trx-1 showed no effect to both temperature and imidacloprid treatments and was regulated in an age-related manner. Overall, our results indicate that ambient temperatures amplify imidacloprid toxicity and affect honey bee gene regulation.