Insecticide resistance fitness costs in D. simulans
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB39894 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4467770_1.fastq.gz | Fastqsanger.gz | |||
| ERR4467770_2.fastq.gz | Fastqsanger.gz | |||
| ERR4467780_1.fastq.gz | Fastqsanger.gz | |||
| ERR4467780_2.fastq.gz | Fastqsanger.gz | |||
| ERR4467790_1.fastq.gz | Fastqsanger.gz |
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Project description:Synonymous mutations do not change the sequence of the polypeptide but they may still influence fitness. We investigated in Salmonella enterica how four synonymous mutations in the rpsT gene (encoding ribosomal protein S20) reduce fitness (i.e. growth rate) and the mechanisms by which this cost can be genetically compensated. The reduced growth rates of the synonymous mutants were correlated with reduced levels of the rpsT transcript and S20 protein. In an adaptive evolution experiment these fitness impairments could be compensated by mutations that either caused up-regulation of S20 through increased gene dosage (due to duplications), increased transcription of the rpsT gene (due to an rpoD mutation or mutations in rpsT), or increased translation from the rpsT transcript (due to rpsT mutations). We suggest that the reduced levels of S20 in the synonymous mutants result in production of a defective subpopulation of 30S subunits lacking S20 that reduce protein synthesis and bacterial growth and that the compensatory mutations restore S20 levels and the number of functional ribosomes. Our results demonstrate how specific synonymous mutations can cause substantial fitness reductions and that many different types intra- and extragenic compensatory mutations can efficiently restore fitness. Furthermore, our study highlights that also synonymous sites can be under strong selection, which may have implications for the use of dN/dS ratios as signature for selection.
2016-03-11 | PXD003495 | Pride
Project description:Transcripcional responses in three genotypes of Muzus persicae, each exhibiting different resistance mechanisms, in response to an anti.cholinesterase insecticide
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Project description:Illumina HiSeq 2500 technology was used to sequence the transcriptome of three Ethiopian field populations of An. arabiensis (Asendabo (ASN), Chewaka (CHW) and Tolay (TOL)) and two An. arabiensis strains (Sekoru (SEK, from Ethiopia) and Moz (MOZ, from Mozambique)). Both ASN, CHW and TOL were previously shown to be resistant against delamethrin and DDT, while the two An. arabiensis strains (SEK and MOZ) were both susceptible to deltamethrin and DDT (Alemayehu et al. 2017, DOI: 10.1186/s13071-017-2342-y; Witzig et al. 2013, DOI: 10.1038/hdy.2012.112). Differentially expressed genes (absolute fold change (FC) ≥ 2 and Benjamini-Hochberg adjusted p-value < 0.05) were determined between each insecticide resistant field population (ASN, CHW or TOL) and one of the insecticide susceptible strains (SEK or MOZ).
2019-03-20 | GSE121006 | GEO
Project description:Antimicrobial resistance (AMR) poses a threat to global health and the economy. Rifampicin resistant Mycobacterium tuberculosis accounts for a third of the global AMR burden. Gaining the upper hand on AMR requires a deeper understanding of the physiology of resistance. AMR often results in the erosion of normal cell function: a fitness cost. Identifying intervention points in the mechanisms underpinning the cost of resistance in M. tuberculosis could play a pivotal role in strengthening future treatment regimens. We used a collection of M. tuberculosis strains providing an evolutionary and phylogenetic snapshot of rifampicin resistance and subjected them to genome-wide transcriptomic and proteomic profiling to identify key perturbations of normal physiology. We found that a rifampicin resistance-conferring mutation in RpoB imparts considerable gene expression changes, many of which are mitigated by a compensatory mutation in RpoC. However, our data also provide evidence for pervasive epistasis: the same resistance mutation imposed a different fitness cost and functionally unrelated changes to gene expression in clinical strains from unrelated genetic backgrounds. Rather than functional changes in specific pathways, our data suggest that the fitness cost of rifampicin resistance stems from a misallocation of resources: the greater the departure from the wild type baseline proteome investment, the greater the fitness cost of rifampicin resistance in a given strain. We summarize these observations in the “Burden of Expression” hypothesis of fitness cost and provide evidence that it can be used for suppressing the emergence of rifampicin resistance.
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Project description:Transcripcional responses in three genotypes of Muzus persicae, each exhibiting different resistance mechanisms, in response to an anti.cholinesterase insecticide Two-condition experiment in threee different genotypes: Insecticide vs. acetone plus water. Genotypes S (exhibiting no resistance mechanism) Biological replicates: 3. Genotypes RS (resistant through a kdr sodium channel mutation) Biological replicates: 2. Genotypes MR (carrying kdr and MACE mutations) Biological replicates: 2.
2013-01-01 | E-GEOD-37310 | biostudies-arrayexpress
Project description:Purpose: Next-generation transcriptome sequencing was done to understand host and eukaryotic microbiome changes in gene expression in association with defined insecticide selection pressures. The specific goal of this research was to understand whole-body physiological responses in German cockroaches and associated microbiota, at the metatranscriptome level, to defined insecticide selection pressures. Methods: We used the insecticide indoxacarb as the selecting insecticide, which is an important bait active ingredient for cockroach control. Six generations of selection with indoxacarb bait produced a strain with substantial (>20x) resistance relative to inbred control lines originating from the same parental stock. Results: Metatranscriptome sequencing revealed 1123 significantly differentially expressed genes in > two of three statistical models (81 upregulated and 1042 downregulated; FDR p<0.001; log2FC of +/- 1). The majority of upreglated genes were from the host cockroach while the majority of downregulated genes were from associated viruses and the eukaryotic microbiome. Conclusions: We show here significant impacts by insecticide selection on not only host stress-respnses like detoxification, but also on clearace of microbial parasites, pathogens, commensals and/or symbionts.
2021-12-07 | GSE188950 | GEO
Project description:Bioinsecticides and transgenic crops based on the bacterial pathogen Bacillus thuringiensis (Bt) can effectively control diverse agricultural insect pests, nevertheless, insect resistance evolution without causing obvious fitness costs has seriously eroded the sustainable use of these Bt products. Recently, we have discovered that an increased titer of juvenile hormone (JH) favors an insect host (Plutella xylostella) to enhance fitness whilst resisting the Bt pathogen, however, the underlying regulatory mechanisms of the increased JH titer is obscure. Here, we define the involvement of N6-methyladenosine (m6A) RNA modification in modulating the availability of JH in this process. Specifically, we found that two m6A methyltransferase subunit genes, PxMettl3 and PxMettl14, repressed the expression of a key JH-degrading enzyme JH esterase (JHE) to induce an increased JH titer, mitigating the fitness costs associated with a robust defense against the Bt pathogen. This study identifies an as-yet uncharacterized m6A-mediated epigenetic regulator of insect hormones for maintaining fitness during pathogen defense and unveils an emerging Bt resistance-related m6A methylation atlas in insects, which further expands the functional landscape of m6A modification and showcases the pivotal role of epigenetic regulation in host-pathogen interactions.
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Project description:Protein profiles of insecticide resistance Ae. aegypti in Penang island, Malaysia
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Project description:This experiment was used to determine the effect of a botanical insecticide upon gene expression profiles in Drosophila melanogaster. Adult female Drosophila (oregon-R strain) were treated with an ethylacetate extract of Piper nigrum (Piperaceae) seeds formulated in 99% ethanol. Treatment was topical, using a Potter's tower to administer a total of 2 mL of a 0.9mg/mL concentration. Control treatment was identical except flies were treated with 99% ethanol as a solvent control. Gene expression was studied four hours post-treatment. Keywords: insecticide response, stress-response
2006-01-24 | GSE3032 | GEO
Project description:The goal of this study is to proactively assess the risk of insecticide resistance development by determining susceptibility of field-collected D. suzukii and their response to insecticide treatment at the transcriptome level using next-generation sequencing technology. Methods:LC50 values were calculated for zeta-cypermethrin, spinosad, malathion treated D. suzukii field-collected and lab-reared populations. LC50 dosage survived and untreated (10 individuals per replicate) field-collected and lab reared D.suzukii transcript profiles were generated by RNA sequencing, in triplicate, using Illumina NextSeq 500. The 24 samples (paired-end reads, including replicates) were independently mapped onto the D. suzukii genome (SpottedWingFlybase v.1) by using TopHat followed by Cufflinks to estimate the expression values of the transcripts in FPKM (Fragments Per Kilobase per Million mapped reads) with the Cuffdiff 2 default geometric normalization. Differentially expressed genes (FDR < 0.05 after Benjamini-Hochberg correction for multiple-testing) were identified for insecticide-treated or untreated control for either (1) lab-reared populations or (2) field-collected populations. Results: As an approach to proactively assess the risk of insecticide resistance development, we determined the LC50 (lethal concentration, 50%) values of commonly used insecticides zeta-cypermethrin, spinosad, and malathion against laboratory-reared and field-collected D. suzukii populations. The LC50 values were significantly higher in field-collected populations when compared to lab-reared populations, indicating that field populations are less susceptible to these insecticides. Furthermore, we used RNA sequencing to analyze the response of D. suzukii at the transcriptome level upon treatment with the same three insecticide classes that are used in our bioassays. We identified differentially expressed genes (DEGs) in D. suzukii that survived LD50 doses of zeta-cypermethrin, spinosad, and malathion and gene classes that are overrepresented in DEGs. We observed that a high number of significantly DEGs are involved in detoxification and reduced cuticular penetration, especially in field population, thus providing potential molecular mechanisms for the higher LC50 values for field-collected population. Conclusion: Our study identified a high number of metabolic detoxification genes that are induced in field-collected D. suzukii upon insecticide treatment and a high degree of overlap when examining the lists of genes that are induced when D. suzukii is treated with three commonly used insecticides. Based on our results, we conclude that there is a substantial risk of insecticide resistance and cross-resistance development in D. suzukii in the field.
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