Prostate H3K4me3 ChIP-seq and the transgenerational effects of pesticide chlordecone on prostate
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PROVIDER: PRJNA557706 | ENA |
REPOSITORIES: ENA
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Project description:The environmental factors such as pesticides could affect the developmental processes and cause the phenotypic changes. Moreover, the changes could be transferred to a subsequent generation via gametes. In this project we studied whether the pesticide chlordecone could cause the developmental effects and cause the transgenerational inheritance in outbred mouse strain (Swiss). Mice were treated during development (E6.5-E15.5) at dose 100 µg/kg/day and the progeny of exposed mice (F1) were crossed for three generations. The prostate of the first (F1) and third generation males (F3) were used for RNA-seq-analysis. We used three biological replicates for each condition.
2021-04-01 | GSE135200 | GEO
Project description:The transgenerational effects of pesticide chlordecone on prostate
| PRJNA557708 | ENA
Project description:Exposure to pesticide chlordecone is associated with high risk of prostate cancer.We hypothesised that changes in histone H3K4me3 could be involved in pathological processes in prostate induced by chlordecone. We exposed mice to chlordecone during embryonic development (E6.5-E15.5) and we analysed F1 progeny male epigenetic H3K4me3 marks in prostate tissue, as well as H3K4me3 in the prostate of F3 progeny to reveal the transgenerational effects resulting from the ancestral exposure to CD. We performed ChIP using H3K4me3 commercial antibody (Merck Millipore, 07-473) and pooled prostate tissues from 4 mice. DNA-protein complex was immunoprecipitated, eluted and DNA purified.
2021-04-01 | GSE135199 | GEO
Project description:The environmental factors such as pesticides could affect the developmental processes and cause the phenotypic changes. Moreover, the changes could be transferred to a subsequent generation via gametes. In this project we studied whether the pesticide chlordecone could cause the developmental effects and cause the transgenerational inheritance in outbred mouse strain. Mice were treated during development at dose 100 µg/kg/day and the progeny of exposed mice were crossed for three generations. The testes of the third generations males were used for anti-H3K4me3 ChiP-seq analysis. We used two biological replicates for each condition.
2018-07-10 | GSE86439 | GEO
Project description:RNA seq project designed to understand the role of pesticide on transription of mRNA in the testis. We treated adult female mice with chlordecone with doses 0 (control), 100 Xg/kg/day and 1 mg/kg/day during gestation period E6- E15. Male born from Chlordecone- treated mice were crossed for a three generations. The testes from F3 generations were taken for mRNA extraction. For mRNA extraction we used columb. Three biological replicates used for each condition . We hypothesize that chlordecone cause changes in mRNA due to transgenerational effect of pesticides (Skinner et al, Science 2005). The changes in expression of certain genes can help us understand the effect of pesticides on many tissues. Number of sample :9 samples. We require Paired End sequencing and number of reads equal or more than 25M tags, strand specific sequencing
2018-07-10 | GSE86438 | GEO
Project description:Transgenerational effect of Chlordecone
| PRJNA341868 | ENA
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-04-01 | GSE135201 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a M-bM-^@M-^\pesticide mixtureM-bM-^@M-^] (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures. Methylated sperm DNA was isolated from rats ancestrally exposed to pesticides (Pip). Three independent samples from the treatment group were obtained. Differential DNA methylation between treatment groups was determined using Nimblegen microarrays. Treated samples were paired with control samples and hybridized together on arrays (Pip1/Cip1, Pip2/Cip2, and Pip3/Cip3), resulting in three arrays for the treatment.
2014-07-22 | E-GEOD-59554 | biostudies-arrayexpress
Project description:Permethrin and N,N-diethyl-meta-toluamide (DEET) are the pesticides and insect repellent most commonly used by humans. These pesticides have been shown to promote the epigenetic transgenerational inheritance of disease in rats. The current study was designed as an epigenome-wide association study (EWAS) to identify potential sperm differential DNA methylation regions (DMRs) for specific transgenerational disease. Outbred Sprague Dawley gestating female rats (F0) were exposed to the pesticide combination including Permethrin and DEET. Their great-grand offspring (F3) were only transgenerationally exposed to pesticides. The transgenerational adult male rat sperm were collected from individuals with single and multiple diseases and compared to non-diseased animals to identify DMRs associated with transgenerational disease transmission. The exposure of gestating female rats to a permethrin and DEET pesticide combination promoted testis disease, prostate disease, kidney disease, and the presence of multiple disease in the subsequent great-grand offspring F3 generation. Interestingly, the majority of the disease specific sperm DMR associated genes were previously found to be linked to relevant disease specific genes.
2020-11-12 | GSE158254 | GEO
Project description:Environmental compounds are known to promote epigenetic transgenerational inheritance of disease. The current study was designed to determine if a “pesticide mixture” (pesticide permethrin and insect repellent N,N-Diethyl-meta-toluamide, DEET) promotes epigenetic transgenerational inheritance of disease and associated DNA methylation epimutations in sperm. Gestating F0 generation female rats were exposed during fetal gonadal sex determination and the incidence of disease evaluated in F1 and F3 generations. There were significant increases in the incidence of total diseases in animals from pesticide lineage F1 and F3 generation animals. Pubertal abnormalities, testis disease, and ovarian disease (primordial follicle loss and polycystic ovarian disease) were increased in F3 generation animals. Analysis of the pesticide lineage F3 generation sperm epigenome identified 363 differential DNA methylation regions (DMR) termed epimutations. Observations demonstrate that a pesticide mixture (permethrin and DEET) can promote epigenetic transgenerational inheritance of adult onset disease and potential sperm epigenetic biomarkers for ancestral environmental exposures.
2014-07-22 | GSE59554 | GEO