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

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 i...

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Main Authors: Mohamed Alburaki, Shayne Madella, Steven C. Cook
Format: Article
Language:English
Published: Nature Portfolio 2023-03-01
Series:Scientific Reports
Online Access:https://doi.org/10.1038/s41598-023-30264-0
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author Mohamed Alburaki
Shayne Madella
Steven C. Cook
author_facet Mohamed Alburaki
Shayne Madella
Steven C. Cook
author_sort Mohamed Alburaki
collection DOAJ
description 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.
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spelling doaj.art-cff81cc6ce384130ae214fa4e4a73e932023-03-22T10:57:50ZengNature PortfolioScientific Reports2045-23222023-03-0113111510.1038/s41598-023-30264-0Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulationMohamed Alburaki0Shayne Madella1Steven C. Cook2USDA-ARS Bee Research LaboratoryUSDA-ARS Bee Research LaboratoryUSDA-ARS Bee Research LaboratoryAbstract 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.https://doi.org/10.1038/s41598-023-30264-0
spellingShingle Mohamed Alburaki
Shayne Madella
Steven C. Cook
Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
Scientific Reports
title Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
title_full Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
title_fullStr Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
title_full_unstemmed Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
title_short Non-optimal ambient temperatures aggravate insecticide toxicity and affect honey bees Apis mellifera L. gene regulation
title_sort non optimal ambient temperatures aggravate insecticide toxicity and affect honey bees apis mellifera l gene regulation
url https://doi.org/10.1038/s41598-023-30264-0
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