Transcriptional profiling of a novel mutant resistant to imidacloprid and DDT
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ABSTRACT:
ORGANISM(S): Drosophila melanogaster
PROVIDER: GSE28560 | GEO | 2012/06/28
SECONDARY ACCESSION(S): PRJNA139041
REPOSITORIES: GEO
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Project description:Deep-sequencing analysis of mRNA expression differences between imidacloprid and DDT resistant mutant line and iso31 (w1118) susceptible line have been obtained. A total of 357 transcripts were found to be differently expressed, with 150 upregulated and 207 downregulated genes in the resistant line. Analysis of poly(A)+ RNA from one resistant mutant and one iso31 (w1118) susceptible (control) sample
2012-06-27 | E-GEOD-28560 | biostudies-arrayexpress
Project description:Transcriptional profiling of three Anopeheles arabiensis strains: (i) DDT resistant mosquitoes from the city of Bobo Dioulasso (ii) mosquitoes from Bobo Dioulasso not exposed to DDT (iii) a laboratory DDT-susceptible strain.
2012-07-30 | E-MTAB-1224 | biostudies-arrayexpress
Project description:Resistance to chemical insecticides including pyrethroids, the main insecticide class used against mosquitoes, led to a regain of interest for neonicotinoids. In this context, the present study aims at characterizing the molecular basis of neonicotinoid resistance in the mosquito Aedes aegypti. Resistance mechanisms were studied by combining transcriptomic and genomic data obtained from a laboratory strain selected at the larval stage for 30 generations with imidacloprid (Imida-R line). After thirty generations of selection, larvae of Imida-R line showed a 8-fold increased resistance to imidacloprid and a significant cross-tolerance to the pyrethroids permethrin and deltamethrin. Cross-resistance to pyrethroids was only observed in adults when larvae were previously exposed to imidacloprid suggesting a low but inducible expression of resistance alleles at the adult stage. Resistance of the Imida-R line was associated with a slower larval development time in females. Multiple detoxification enzymes were over-transcribed in larvae in association with resistance including the P450s CYP6BB2, CYP9M9 and CYP6M11 previously associated with pyrethroid resistance. Some of them together with their redox partner NADPH P450 reductase were also affected by non-synonymous mutations associated with resistance. Combining genomic and transcriptomic data allowed identifying promoter variations associated with the up-regulation of CYP6BB2 in the resistant line. Overall, these data confirm the key role of P450s in neonicotinoid resistance in Ae. aegypti and their potential to confer cross-resistance to pyrethroids, raising concerns about the use of neonicotinoids for resistance management in this mosquito species.
2021-05-07 | GSE174009 | GEO
Project description:This microarray study aimed at comparing constitutive gene expression levels between an Aedes aegypti insecticide-resistant strain (Imida-R) selected at the larval stage with the neonicotinoid insecticide imidacloprid for 10 generations and the parental strain (Bora-Bora) susceptible to all insecticides. Strains comparison was performed at both larval (4th stage larvae) and adult (3 days-old adults females, non-blood fed) stages.
2012-03-31 | E-MTAB-616 | biostudies-arrayexpress
Project description:The endocrine disrupting chemical o,p'-DDT can affect reproductive organs, tissues and cells in several species. Treatment of human endometrial endothelial cells (HEEC) with 50 µM o,p'-DDT decreased the cell proliferation compared to the control. Microarray analyses revealed that o,p'-DDT affected biological processes such as the cell cycle, cell division, defence response and lipid and steroid metabolism, in cellular components such as the plasma membrane and chromosomes, with molecular functions involved in signalling, receptor and cytokine activity, confirming the results of the proliferation assay. The present study supports our previous findings of decreased proliferation and increased cell death in response to o,p'-DDT, and may offer important clues in the deduction of the mechanisms of action of o,p'-DDT. Keywords: Exposure analysis
2007-10-10 | GSE9252 | GEO
Project description:The endocrine disrupting chemical o,p'-DDT can affect reproductive organs, tissues and cells in several species. Treatment of human endometrial endothelial cells (HEEC) with 50 µM o,p'-DDT decreased the cell proliferation compared to the control. Microarray analyses revealed that o,p'-DDT affected biological processes such as the cell cycle, cell division, defence response and lipid and steroid metabolism, in cellular components such as the plasma membrane and chromosomes, with molecular functions involved in signalling, receptor and cytokine activity, confirming the results of the proliferation assay. The present study supports our previous findings of decreased proliferation and increased cell death in response to o,p'-DDT, and may offer important clues in the deduction of the mechanisms of action of o,p'-DDT. Keywords: Exposure analysis Two-condition experiments, o,p'-DDT-exposed vs. control HEEC, and individual control vs control pool. Biological replicates: 5 HEEC cultures, independently grown, exposed and harvested. One replicate per array. Dye-swaps for exposed and reference samples between replicates. variable = Exposure: o,p'-DDT-treated: Indiv1 s1 op-DDT Cy3, Indiv2 s19 op-DDT Cy3, Indiv3 s37 op-DDT Cy3, Indiv4 s55 op-DDT Cy5, Indiv5 s73 op-DDT Cy5 variable = Exposure: control: Indiv1 s2 control Cy5, Indiv2 s20 control Cy5, Indiv3 s38 control Cy5, Indiv4 s56 control Cy3, Indiv5 s74 control Cy3 variable = Exposure: individual control: Indiv1 s17 control Cy3, Indiv2 s35 control Cy5, Indiv3 s53 control Cy3, Indiv4 s71 control Cy5, Indiv5 s89 control Cy3 variable = Exposure: control pool: Pooled control s18/36/54/72/90 Cy5, Pooled control s18/36/54/72/90 Cy3, Pooled control s18/36/54/72/90 Cy5, Pooled control s18/36/54/72/90 Cy3, Pooled control s18/36/54/72/90 Cy5 repeat = Biological replicate: Indiv1 s1 op-DDT Cy3, Indiv1 s2 control Cy5, Indiv1 s17 control Cy3, sample 18 in Pooled control repeat = Biological replicate: Indiv2 s19 op-DDT Cy3, Indiv2 s20 control Cy5, Indiv2 s35 control Cy5, sample 36 in Pooled control repeat = Biological replicate: Indiv3 s37 op-DDT Cy3, Indiv3 s38 control Cy5, Indiv3 s53 control Cy3, sample 54 in Pooled control repeat = Biological replicate: Indiv4 s55 op-DDT Cy5, Indiv4 s56 control Cy3, Indiv4 s71 control Cy5, sample 72 in Pooled control repeat = Biological replicate: Indiv5 s73 op-DDT Cy5, Indiv5 s74 control Cy3, Indiv5 s89 control Cy3, sample 90 in Pooled control
2007-10-10 | E-GEOD-9252 | biostudies-arrayexpress
Project description:Transcriptional profiling of a novel mutant resistant to imidacloprid and DDT
| PRJNA139041 | ENA
Project description:Gestating F0 generational female rats were transiently exposed to DDT during fetal gonadal sex determination and the incidence of adult onset pathologies was assessed in the subsequent F1, F2, and F3 generations. In addition, sperm differential DNA methylation regions (DMRs) that were associated with specific pathologies in the F3 generation males were investigated. No pathology was observed in the F1 generation DDT lineage males or females compared with F1 generation controls (vehicle exposure). There was an increase of testis disease and early onset puberty in the F2 generation DDT lineage males. The F3 generation DDT males had significant increases in testis disease, prostate disease, and late onset puberty. The F3 generation DDT females had significant increases in ovarian and kidney disease. Both the F3 generation males and females had significant increases in the frequency of obesity and multiple disease. The F3 generation sperm was collected to examine DMRs for the ancestrally exposed DDT male population. Unique sets of DMRs were associated with late onset puberty, kidney disease, and multiple disease pathologies.
2018-07-31 | GSE114032 | GEO
Project description:In previous studies, the pesticide DDT was shown to promote the transgenerational inheritance of sperm differential DNA methylation regions (DMRs), also called epimutations, which can mediate this epigenetic inheritance. In the current study, the developmental origins of the transgenerational DMRs during gametogenesis have been investigated. Male control and DDT lineage F3 generation rats were used to isolate embryonic day 16 (E16) prospermatogonia, postnatal day 10 (P10) spermatogonia, adult pachytene spermatocytes, round spermatids, caput epididymal spermatozoa, and caudal sperm. The DMRs between the control versus DDT lineage samples were determined at each developmental stage. The top 100 statistically significant DMRs at each stage were compared and the developmental origins of the caudal epididymal sperm DMRs were assessed.
2019-01-19 | GSE121585 | GEO
Project description:Neonicotinoids are considered safe because of their low affinities to mammalian nicotinic acetylcholine receptors (nAChRs) relative to insect nAChRs. However, because of importance of nAChRs in mammalian brain development, there remains a need to establish the safety of chronic neonicotinoid exposures with regards to children’s health. Here we examined the effects of long-term (14 days) and low dose (1 μM) exposure of neuron-enriched cultures from neonatal rat cerebellum to nicotine and two neonicotinoids: acetamiprid and imidacloprid. Immunocytochemistry revealed no differences in the number or morphology of immature neurons or glial cells in any group versus untreated control cultures. However, a slight disturbance in Purkinje cell dendritic arborization was observed in the exposed cultures. Next we performed transcriptome analysis on total RNAs using microarrays, and identified significant differential expression (p < 0.05, q < 0.05, ≥1.5 fold) between control cultures versus nicotine-, acetamiprid-, or imidacloprid-exposed cultures in 34, 48, and 67 genes, respectively. Common to all exposed groups were nine genes essential for neurodevelopment, suggesting that chronic neonicotinoid exposure alters the transcriptome of the developing mammalian brain in a similar way to nicotine exposure. Our results highlight the need for further careful investigations into the effects of neonicotinoids in the developing mammalian brain.
2016-10-04 | GSE80653 | GEO