PDF(Pubmed)
Abstract：
UNASSIGNED: The resurgence of Anopheles funestus, a dominant vector of human malaria in western Kenya was partly attributed to insecticide resistance. However, evidence on the molecular basis of pyrethroid resistance in western Kenya is limited. Noncoding RNAs (ncRNAs) form a vast class of RNAs that do not code for proteins and are ubiquitous in the insect genome. Here, we demonstrated that multiple ncRNAs could play a potential role in An. funestusresistance to pyrethroid in western Kenya.
UNASSIGNED: Anopheles funestus mosquitoes were sampled by aspiration methods in Bungoma, Teso, Siaya, Port Victoria and Kombewa in western Kenya. The F1 progenies were exposed to deltamethrin (0.05%), permethrin (0.75%), DDT (4%) and pirimiphos-methyl (0.25%) following WHO test guidelines. A synergist assay using piperonyl butoxide (PBO) (4%) was conducted to determine cytochrome P450s\' role in pyrethroid resistance. RNA-seq was conducted on a combined pool of specimens that were resistant and unexposed, and the results were compared with those of the FANG susceptible strain. This approach aimed to uncover the molecular mechanisms underlying pyrethroid resistance.
UNASSIGNED: Pyrethroid resistance was observed in all the sites with an average mortality rate of 57.6%. Port Victoria had the highest level of resistance to permethrin (MR=53%) and deltamethrin (MR=11%) pyrethroids. Teso had the lowest level of resistance to permethrin (MR=70%) and deltamethrin (MR=87%). Resistance to DDT was observed only in Kombewa (MR=89%) and Port Victoria (MR=85%). A full susceptibility to P-methyl (0.25%) was observed in all the sites. PBO synergist assay revealed high susceptibility (>98%) to the pyrethroids in all the sites except for Port Victoria (MR=96%, n=100). Whole transcriptomic analysis showed that most of the gene families associated with pyrethroid resistance comprised non-coding RNAs (67%), followed by imipenemase (10%), cytochrome P450s (6%), cuticular proteins (5%), olfactory proteins (4%), glutathione S-transferases (3%), UDP-glycosyltransferases (2%), ATP-binding cassettes (2%) and carboxylesterases(1%).
UNASSIGNED: This study unveils the molecular basis of insecticide resistance in An. funestus in western Kenya, highlighting for the first time the potential role of non-coding RNAs in pyrethroid resistance. Targeting non-coding RNAs for intervention development could help in insecticide resistance management.
UNASSIGNED: Anopheles funestus mosquitoes were sampled by aspiration methods in Bungoma, Teso, Siaya, Port Victoria and Kombewa in western Kenya. The F1 progenies were exposed to deltamethrin (0.05%), permethrin (0.75%), DDT (4%) and pirimiphos-methyl (0.25%) following WHO test guidelines. A synergist assay using piperonyl butoxide (PBO) (4%) was conducted to determine cytochrome P450s\' role in pyrethroid resistance. RNA-seq was conducted on a combined pool of specimens that were resistant and unexposed, and the results were compared with those of the FANG susceptible strain. This approach aimed to uncover the molecular mechanisms underlying pyrethroid resistance.
UNASSIGNED: Pyrethroid resistance was observed in all the sites with an average mortality rate of 57.6%. Port Victoria had the highest level of resistance to permethrin (MR=53%) and deltamethrin (MR=11%) pyrethroids. Teso had the lowest level of resistance to permethrin (MR=70%) and deltamethrin (MR=87%). Resistance to DDT was observed only in Kombewa (MR=89%) and Port Victoria (MR=85%). A full susceptibility to P-methyl (0.25%) was observed in all the sites. PBO synergist assay revealed high susceptibility (>98%) to the pyrethroids in all the sites except for Port Victoria (MR=96%, n=100). Whole transcriptomic analysis showed that most of the gene families associated with pyrethroid resistance comprised non-coding RNAs (67%), followed by imipenemase (10%), cytochrome P450s (6%), cuticular proteins (5%), olfactory proteins (4%), glutathione S-transferases (3%), UDP-glycosyltransferases (2%), ATP-binding cassettes (2%) and carboxylesterases(1%).
UNASSIGNED: This study unveils the molecular basis of insecticide resistance in An. funestus in western Kenya, highlighting for the first time the potential role of non-coding RNAs in pyrethroid resistance. Targeting non-coding RNAs for intervention development could help in insecticide resistance management.
摘要：
背景Funestus按蚊的复活，肯尼亚西部人类疟疾的主要传播媒介部分归因于杀虫剂抗性。然而,肯尼亚西部拟除虫菊酯耐药性的分子基础证据有限。非编码RNA(ncRNA)形成了一类庞大的RNA,其不编码蛋白质并且在昆虫基因组中普遍存在。这里,我们证明了多个ncRNAs可以在An中发挥潜在作用。肯尼亚西部的Funestus对拟除虫菊酯的抗性。材料和方法采用抽吸方法在Bungoma采样按蚊，泰索,Siaya,肯尼亚西部的维多利亚港和Kombewa。F1后代暴露于溴氰菊酯(0.05%)，氯菊酯(0.75%)，DDT（4％）和甲基吡啶磷（0.25％）遵循WHO测试指南。使用胡椒基丁醚（PBO）（4％）进行增效剂测定，以确定细胞色素P450在拟除虫菊酯抗性中的作用。RNA-seq是在具有抗性和未暴露的样本的组合库上进行的，并与FANG易感菌株的结果进行了比较。该方法旨在揭示拟除虫菊酯抗性的分子机制。结果所有部位均出现拟除虫菊酯耐药,平均死亡率为57.6%。维多利亚港对氯菊酯（MR=53％）和溴氰菊酯（MR=11％）拟除虫菊酯的抗性最高。Teso对氯菊酯（MR=70％）和溴氰菊酯（MR=87％）的抗性最低。仅在Kombewa（MR=89％）和维多利亚港（MR=85％）中观察到对DDT的抗性。在所有位点观察到对P-甲基的完全敏感性(0.25%)。PBO增效剂分析显示，除维多利亚港外，所有地点对拟除虫菊酯的敏感性都很高（>98%）（MR=96%，n=100)。全转录组分析表明，大多数与拟除虫菊酯抗性相关的基因家族包含非编码RNA(67%)，其次是亚胺培酶(10%)，细胞色素P450（6%），角质层蛋白（5%），嗅觉蛋白（4%），谷胱甘肽S-转移酶（3％），UDP-糖基转移酶（2%），ATP结合盒(2%)和羧酸酯酶(1%)。结论本研究揭示了An杀虫剂抗性的分子基础。肯尼亚西部的funestus，首次强调了非编码RNA在拟除虫菊酯抗性中的潜在作用。针对非编码RNA进行干预开发可能有助于杀虫剂抗性管理。
