| Autor: |
Decio P; Universidade Estadual Paulista (UNESP), Instituto de Biociências, Centro de Estudos de Insetos Sociais, Rio Claro, São Paulo, Brazil., Ustaoglu P; School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom.; MRC Centre for Molecular Bacteriology and Infection, and Department of Life Sciences, Imperial College London, Ground Floor, Flowers Building, South Kensington Campus, London, SW7 2AZ, UK., Roat TC; Universidade Estadual Paulista (UNESP), Instituto de Biociências, Centro de Estudos de Insetos Sociais, Rio Claro, São Paulo, Brazil., Malaspina O; Universidade Estadual Paulista (UNESP), Instituto de Biociências, Centro de Estudos de Insetos Sociais, Rio Claro, São Paulo, Brazil., Devaud JM; Research Center on Animal Cognition, Center for Integrative Biology, Toulouse University, CNRS, UPS, Toulouse, France., Stöger R; School of Biosciences, University of Nottingham, LE12 5RD, Nottingham/Sutton Bonington Campus, United Kingdom. reinhard.stoger@nottingham.ac.uk., Soller M; School of Biosciences, College of Life and Environmental Sciences, University of Birmingham, Edgbaston, Birmingham, B15 2TT, United Kingdom. m.soller@bham.ac.uk. |
| Abstrakt: |
Securing food supply for a growing population is a major challenge and heavily relies on the use of agrochemicals to maximize crop yield. It is increasingly recognized, that some neonicotinoid insecticides have a negative impact on non-target organisms, including important pollinators such as the European honeybee Apis mellifera. Toxicity of neonicotinoids may be enhanced through simultaneous exposure with additional pesticides, which could help explain, in part, the global decline of honeybee colonies. Here we examined whether exposure effects of the neonicotinoid thiamethoxam on bee viability are enhanced by the commonly used fungicide carbendazim and the herbicide glyphosate. We also analysed alternative splicing changes upon pesticide exposure in the honeybee. In particular, we examined transcripts of three genes: (i) the stress sensor gene X box binding protein-1 (Xbp1), (ii) the Down Syndrome Cell Adhesion Molecule (Dscam) gene and iii) the embryonic lethal/abnormal visual system (elav) gene, which are important for neuronal function. Our results showed that acute thiamethoxam exposure is not enhanced by carbendazim, nor glyphosate. Toxicity of the compounds did not trigger stress-induced, alternative splicing in the analysed mRNAs, thereby leaving dormant a cellular response pathway to these man-made environmental perturbations. |
