Mugenzi Leon M J, Tekoh Theofelix A, Ntadoun Stevia T, Chi Achille D, Gadji Mahamat, Menze Benjamin D, Tchouakui Magellan, Irving Helen, Wondji Murielle J, Weedall Gareth D, Hearn Jack, Wondji Charles S
LSTM Research Unit, Centre for Research in Infectious Diseases (CRID), Yaoundé, Cameroon.
Department of Biochemistry and Molecular Biology, Faculty of Science University of Buea, Buea, Cameroon.
PLoS Genet. 2024 Jul 29;20(7):e1011344. doi: 10.1371/journal.pgen.1011344. eCollection 2024 Jul.
Deciphering the evolutionary forces controlling insecticide resistance in malaria vectors remains a prerequisite to designing molecular tools to detect and assess resistance impact on control tools. Here, we demonstrate that a 4.3kb transposon-containing structural variation is associated with pyrethroid resistance in central/eastern African populations of the malaria vector Anopheles funestus. In this study, we analysed Pooled template sequencing data and direct sequencing to identify an insertion of 4.3kb containing a putative retro-transposon in the intergenic region of two P450s CYP6P5-CYP6P9b in mosquitoes of the malaria vector Anopheles funestus from Uganda. We then designed a PCR assay to track its spread temporally and regionally and decipher its role in insecticide resistance. The insertion originates in or near Uganda in East Africa, where it is fixed and has spread to high frequencies in the Central African nation of Cameroon but is still at low frequency in West Africa and absent in Southern Africa. A marked and rapid selection was observed with the 4.3kb-SV frequency increasing from 3% in 2014 to 98% in 2021 in Cameroon. A strong association was established between this SV and pyrethroid resistance in field populations and is reducing pyrethroid-only nets' efficacy. Genetic crosses and qRT-PCR revealed that this SV enhances the expression of CYP6P9a/b but not CYP6P5. Within this structural variant (SV), we identified putative binding sites for transcription factors associated with the regulation of detoxification genes. An inverse correlation was observed between the 4.3kb SV and malaria parasite infection, indicating that mosquitoes lacking the 4.3kb SV were more frequently infected compared to those possessing it. Our findings highlight the underexplored role and rapid spread of SVs in the evolution of insecticide resistance and provide additional tools for molecular surveillance of insecticide resistance.
破解控制疟疾媒介中杀虫剂抗性的进化力量,仍然是设计分子工具以检测和评估抗性对控制工具影响的先决条件。在此,我们证明一个含有4.3kb转座子的结构变异与东非/中非地区疟疾媒介冈比亚按蚊群体中的拟除虫菊酯抗性相关。在本研究中,我们分析了混合模板测序数据和直接测序,以确定在来自乌干达的疟疾媒介冈比亚按蚊的两个P450基因CYP6P5 - CYP6P9b的基因间区域插入了一个含有假定逆转座子的4.3kb片段。然后,我们设计了一种PCR检测方法来追踪其在时间和区域上的传播,并解读其在杀虫剂抗性中的作用。该插入起源于东非的乌干达或其附近地区,在那里它是固定存在的,并已在中非国家喀麦隆以高频率传播,但在西非频率仍然较低,在南非则不存在。在喀麦隆观察到显著且快速的选择,4.3kb - SV频率从2014年的3%增加到2021年的98%。在野外群体中,该结构变异与拟除虫菊酯抗性之间建立了强关联,并且正在降低仅使用拟除虫菊酯蚊帐的效果。遗传杂交和定量逆转录PCR显示,该结构变异增强了CYP6P9a/b的表达,但未增强CYP6P5的表达。在这个结构变异(SV)中,我们确定了与解毒基因调控相关的转录因子的假定结合位点。观察到4.3kb SV与疟原虫感染之间呈负相关,表明缺乏4.3kb SV的蚊子比拥有它的蚊子更频繁地被感染。我们的研究结果突出了结构变异在杀虫剂抗性进化中未被充分探索的作用和快速传播,并为杀虫剂抗性的分子监测提供了额外的工具。