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Mejia-Jaramillo, A. M.

Publications and source records attributed to Mejia-Jaramillo, A. M..

3 recordsLinked to original sources

Resistance to Pyrethroids in Aedes aegypti: Insights into Transcriptomic Response to Different Insecticide Concentrations Transcriptomic responses of Aedes aegypti to insecticide concentrations

Insecticide spraying is a common strategy for controlling dengue outbreaks, but its effectiveness is compromised by the development of resistance in mosquito populations. In this study, we subjected a strain of Aedes aegypti known for its exceptional ability to develop resistance to controlled permethrin and lambda-cyhalothrin insecticides pressure using two different concentrations. We analyzed resistance mechanisms that are enhanced at each concentration and used RNA sequencing to identify transcripts specifically associated with these exposure levels. Our objective was to uncover the molecular mechanisms triggered by different insecticide concentrations and to distinguish responses between type I and type II pyrethroids, which differ in chemical structure. Our results showed that kdr mutations confer only moderate levels of resistance, as do detoxifying enzymes. For lambda-cyhalothrin, we identified genes involved in the electron transport chain, mitochondrial function, and overall responses to oxidative stress. tRNA transcripts were also upregulated, along with mitochondrial and stress-response transcripts, suggesting a metabolic shift, particularly toward maintaining homeostasis under oxidative stress. These changes point to mechanisms that sustain resistance to this type II insecticide beyond direct detoxification in this population. On the contrary, permethrin induced marked overexpression of cuticle genes, CYP450 genes (especially CYP4), and Odorant Binding Proteins. These expression patterns, together with metabolic enzymes, point to detoxification, reduced penetration, or even sequestration of insecticide, all of which intensify with increasing concentrations. This overregulation of genes suggests an integrated response complemented by classical metabolic detoxification and accompanied by overregulation of mitochondrial complexes. We showed that despite the shared mode of action of the insecticides permethrin and lambda-cyhalothrin, they elicit distinct responses in this Ae. aegypti population. We also showed that the transcriptomic response depends on insecticide concentration and may modulate insecticide tolerance. This article advances understanding of the complexity of pyrethroid resistance in Aedes aegypti and underscores the importance of considering both the insecticide type and the concentration used in vector control programs. Author summaryAedes aegypti mosquitoes transmit dengue and other arboviruses, being a major public health problem in tropical regions like Colombia, where control relies on pyrethroid insecticide spraying. Based on reports of inconsistent results in the field due to different effects of insecticide concentrations, we recreated variable doses by exposing a resistant Colombian Aedes aegypti strain to low (LC25) and high (LC75) concentrations of permethrin (type I) and lambda-cyhalothrin (type II) to identify concentration-dependent resistance mechanisms. Using genetic mutation analysis, enzyme activity assays, and RNA sequencing, we identified the molecular mechanisms these mosquitoes use to survive. Knockdown resistance (kdr) and detoxification enzymes contributed to some extent to resistance but varied by insecticide type and concentration. RNAseq identified that lambda-cyhalothrin upregulated genes for mitochondrial energy production, oxidative stress defense, immune signaling, and transfer RNAs, facilitating homeostasis under chemical stressors. Permethrin instead upregulated genes for cuticle thickening, cytochrome P450 enzymes, and odorant-binding proteins, which are associated with improved penetration barriers, and metabolic breakdown that intensified with higher concentrations. This reveals pyrethroid resistance as complex beyond classic mechanisms, as even low field doses favor stress tolerance or physical defenses to evade sprays. We detected transcripts that improve survival at high concentrations and could be selected in these mosquitoes. Carefully selecting the type of pyrethroid to be used and the dose should be an important factor in vector control. This optimizes current interventions, prolongs their efficacy, and aids researchers in modeling resistance to protect communities.

bioinformatics↗

The role of the Trypanosoma cruzi enzyme L-threonine 3-dehydrogenase in combating stressful environments

Trypanosoma cruzi is a digenetic parasite that undergoes various transformations to complete its life cycle. Changes between hosts and vectors involve exposure to stressful environments, for which it has developed different strategies to cope with such stress. L-threonine 3-dehydrogenase (TDH) is a key enzyme in trypanosome metabolism, and several studies have shown that inhibiting TDH affects parasite survival. To understand the role of TDH in T. cruzi, we investigated its expression in different benznidazole (Bz)-resistant clones and overexpressed it in a Bz-susceptible clone. After overexpressing TDH and exposing it to reactive oxygen species (ROS), alkylating agents, and drugs such as Bz, we evaluated certain biological parameters. Our results show that TDH led to higher survival rates when exposed to H2O2 and increased tolerance to Bz. Moreover, the parasites were able to infect more cells, and their mitochondrial membrane potential ({Psi}m) remained unchanged, both of which are linked to higher tolerance to ROS. Finally, parasites overexpressing TDH were less vulnerable to genetic damage caused by agents such as MMS and gamma radiation. Overall, our results demonstrate that TDH, a key enzyme in threonine metabolism, helps combat stressful environments and, under certain experimental conditions, supports the survival of parasites.

molecular biology↗

Transcriptomic analysis of benznidazole-resistant Trypanosoma cruzi clone reveals nitroreductase I-independent resistance mechanisms

The enzyme nitroreductase I (NTRI) has been implicated as the primary gene responsible for resistance to benznidazole (Bz) and nifurtimox in Trypanosoma cruzi. However, Bz-resistant T. cruzi field isolates carrying the wild-type NTR-I enzyme suggest that additional mechanisms independent of this enzyme may contribute to the resistance phenotype. To investigate these alternative mechanisms, in this paper, we pressured a Trypanosoma cruzi clone with a high Bz concentration over several generations to select Bz-resistant clones. Surprisingly, we found a highly drug-resistant clone carrying a wild-type NTRI. However, the knockout of this gene using CRISPR-Cas9 in the sensitive clone showed that NTRI indeed induces resistance to Bz and supports the idea that the resistant one exhibits mechanisms other than NTRI. To explore these new mechanisms, we performed an RNA-seq analysis, which revealed genes involved in metabolic pathways related to oxidative stress, energy metabolism, membrane transporters, DNA repair, and protein synthesis. Our results support the idea that resistance to benznidazole is a multigenic trait. A Deeper understanding of these genes is essential for developing new drugs to treat Chagas disease.

bioinformatics↗