期刊
PESTICIDE BIOCHEMISTRY AND PHYSIOLOGY
卷 164, 期 -, 页码 73-84出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.pestbp.2019.12.009
关键词
Citrus red mite; Fenpyroximate; METI-I; Drosophila; CRISPR-Cas9; Target-site resistance; NDUFS7
资金
- Iran National Science Foundation [96003038]
- Research Foundation Flanders (FWO) [G009312N, G053815N]
- Research Council (ERC) under the European Union's Horizon 2020 research and innovation program [772026, 773902]
- Hellenic Foundation for Research and Innovation, HFRI
- ERANET, C-IPM [618110]
- European Research Council (ERC) [772026] Funding Source: European Research Council (ERC)
The citrus red mite, Panonychus citri, is a major pest on citrus all around the world. Mitochondrial Electron Transport Inhibitors of complex I (METI-I) acaricides such as fenpyroximate have been used extensively to control P. citri populations, which resulted in multiple reports of METI-I resistant populations in the field. In this study, biochemical and molecular mechanisms of fenpyroximate resistance were investigated in P. citri. Seven populations were collected from Northern provinces of Iran. Resistance ratios were determined and reached up to 75-fold in comparison to a fenpyroximate susceptible population. Cross-resistance to two additional METI-I acaricides, pyridaben and tebufenpyrad, was detected. PBO synergism experiments, in vivo enzyme assays and gene expression analysis suggest a minor involvement of cytochrome P450 monooxygenases in fenpyroximate resistance, which is in contrast with many reported cases for the closely related Tetranychus urticae. Next, we determined the frequency of a well-known mutation in the target-site of METI-Is, the PSST subunit, associated with METI-I resistance. Indeed, the H92R substitution was detected in a highly fenpyroximate resistant P. citri population. Additionally, a new amino acid substitution at a conserved site in the PSST subunit was detected, A94V, with higher allele frequencies in a moderately resistant population. Marker-assisted back-crossing in a susceptible background confirmed the potential involvement of the newly discovered A94V mutation in fenpyroximate resistance. However, introduction of the A94V mutation in the PSST homologue of D. melanogaster using CRISPR-Cas9 did not result in fenpyroximate resistant flies. In addition, differences in binding curves between METI-Is and complex I measured directly, in isolated transgenic and wildtype mitochondria preparations, could not be found.
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