Fall armyworm is a polyphagous migratory pest. Insecticides are used as major components of integrated pest management to control the pest, however, full dependence on insecticides has made the pest evolve resistance to most insecticide classes. The involvement of voltage-gated sodium channels in the excitation of cells makes them a primary target site of a large number of synthetic and naturally occurring neurotoxins. Consequently, it is imperative to delineate the molecular determinants that mediate interactions between insecticides with voltage-gated sodium channels. The present study sought to identify residues involved in the binding of these insecticides and to demarcate the most efficacious insecticides depending on their binding affinity to the voltage-gated sodium channels. The study took an in-silico approach to identify docking sites on voltage-gated sodium channels along with the interactions between known insecticides and specific amino acids on the voltage-gated sodium channels. The homology of the Spodoptera frugiperda voltage-gated sodium channels was developed to predict the binding sites of different known insecticides that target the insect. The current study identified amino acid residues that insecticides could target to enhance their effectiveness against the fall armyworm. Insecticides that do not target voltage-gated sodium channels also showed interactions with this channel, indicating the possibility of a different mode of action that could be confirmed by experimental studies. Our findings can direct efforts that monitor for mutations that result in insecticide resistance given that new interacting residues were identified. These findings can enable better management of resistance when it develops.
Background Pseudomonas aeruginosa is an opportunistic pathogen associated with numerous nosocomial infections that are difficult to treat as a result of natural resistance to various antibiotics, particularly because of biofilm formation. The purpose of this study was to determine the distribution of biofilm formation genes in sequences of this opportunistic pathogen and their association with different ecological niches. In total, 13 genes responsible for biofilm formation by P. aeruginosa were identified and used in the study. They were clustered into seven categories based on the role they play in the biofilm formation process. The study also analyzed 185 complete genome sequences of P. aeruginosa strains retrieved from the NCBI and IPCD databases. These were classified into 14 categories based on the ecological niches they occupy. Results Phylogenetic analyses of the biofilm formation genes indicated a strong co-evolution of a majority of these genes, n=10 . Exceptions were the genes fliC, algD, and algU which may have been exchanged by horizontal gene transfer or evolved faster than the other genes of this functional group as they are more important in terms of a proper response of the biofilm formation to specific environmental stimuli in different habitats. The BLAST Ring Image Generator (BRIG) analysis was used to visualize the distribution of biofilm formation genes between different strains of P. aeruginosa . Conclusions fliC, algD, and algU genes were identified as potential targets for antibiofilm therapies. These findings could inform the development of antibiofilm therapies that target processes mediated by these genes. Also, this study provides useful information that can guide the direction of future research.
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