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Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [RNA-Seq]

ABSTRACT: Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [RNA-Seq]

PROVIDER: PRJNA985566 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24967616_1.fastq.gz	Fastqsanger.gz
	SRR24967616_2.fastq.gz	Fastqsanger.gz
	SRR24967617_1.fastq.gz	Fastqsanger.gz
	SRR24967617_2.fastq.gz	Fastqsanger.gz
	SRR24967618_1.fastq.gz	Fastqsanger.gz

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Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [RNA-Seq]

2023-11-15 | GSE235213 | GEO

Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [MEDIP-seq]

Project description:Background: Neonicotinoids, a widely used class of insecticide that used is agriculture to control insect’s population, are serious public concern. Objectives: In this study, we examined the capacity of a neonicotinoid, thiacloprid (thia) to induce transgenerational effects in the male mice. Methods: The pregnant outbred Swiss female mice were exposed to thia at embryonic days E6.5 to E15.5 using “0”, and “6” mg/kg/day doses. The genome-wide analysis of DNA methylation analysis showed that differentially methylated regions (DMRs) are located at the promoters and enhancers of many important developmental genes. Notably, DMRs were largely overlapping the germ cell reprograming responsive gene (GRRs) and super-enhancer elements found to be active in ES cells, testis or brain.

2023-11-15 | GSE234861 | GEO

Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice

Project description:Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice

| PRJNA985562 | ENA

Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [MEDIP-seq]

Project description:Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice [MEDIP-seq]

| PRJNA983361 | ENA

Ancestral gestational exposure to widely used neonicotinoid thiacloprid leads to global DNA methylation alterations in spermatozoa in three generations of male mice

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-11-15 | GSE235215 | GEO

Molecular effects of neonicotinoid thiacloprid in honey bees (Apis mellifera)

Project description:Molecular effects of neonicotinoid thiacloprid in honey bees (Apis mellifera)

| PRJNA599219 | ENA

Use of the synergist piperonyl butoxide slows the development of insecticide resistance in the whitefly Bemisia tabaci

Project description:In the current study we examined the speed of resistance development in the silverleaf whitefly, Bemisia tabaci, after selection with either a neonicotinoid (thiacloprid) or pyrethroid (alpha-cypermethrin) insecticide alone or in combination with PBO. We used one control sample with no selection, 2 samples for neonicotinoid (thiacloprid) and Pyrethroid treatment and 2 samples for neonicotinoid (thiacloprid) + PBO and Pyrethroid + PBO treatments. The findings of this study demonstrate that PBO used in combination with certain insecticides can suppress the development of resistance in a laboratory setting.

2016-05-02 | E-MTAB-4601 | biostudies-arrayexpress

Epigenetic Effects Promoted by Neonicotinoid Thiacloprid Exposure.

Project description:BackgroundNeonicotinoids, a widely used class of insecticide, have attracted much attention because of their widespread use that has resulted in the decline of the bee population. Accumulating evidence suggests potential animal and human exposure to neonicotinoids, which is a cause of public concern.ObjectivesIn this study, we examined the effects of a neonicotinoid, thiacloprid (thia), on the male reproductive system.MethodsThe pregnant outbred Swiss female mice were exposed to thia at embryonic days E6.5 to E15.5 using "0," "0.06," "0.6," and "6" mg/kg/day doses. Adult male progeny was analyzed for morphological and cytological defects in the testes using hematoxylin and eosin (H&E) staining. We also used immunofluorescence, Western blotting, RT-qPCR and RNA-seq techniques for the analyses of the effects of thia on testis.ResultsWe found that exposure to thia causes a decrease in spermatozoa at doses "0.6" and "6" and leads to telomere defects at all tested doses. At doses "0.6" and "6," thia exposure leads to an increase in meiotic pachytene cells and a decrease in lumen size, these changes were accompanied by increased testis-to-body weight ratios at high dose. By using RNA-seq approach we found that genes encoding translation, ATP production, ATP-dependent proteins and chromatin-modifying enzymes were deregulated in testes. In addition, we found that exposure to thia results in a decrease in H3K9me3 levels in spermatocytes. The changes in H3K9me3 were associated with a dramatic increase in activity of retroelements.ConclusionOur study suggests that gestational exposure to thia affects epigenetic mechanisms controlling meiosis which could lead to deleterious effects on male spermatogenesis.

| S-EPMC8290843 | biostudies-literature

Alteration in mRNA expression in hippocampus and next-generation effects due to paternal exposure to the neonicotinoid pesticide clothianidin

Project description:Accumulating evidence suggests that paternal environmental factors have epigenetic effects on sperm and influence offspring. Neonicotinoid pesticides, which are widely used around the world, are known to affect offspring phenotypes through maternal exposure in mice, but the effect of the paternal exposure remains unknown.The main purpose of this study was to estimate the neurobehavioral effects on offspring mice resulting from paternal exposure to the neonicotinoid pesticide clothianidin (CLO).Hippocampal RNA sequence data revealed that paternal CLO exposure altered the expression of genes related to the nervous system in male offspring, affecting pathways such as axonal guidance signaling, synaptogenesis signaling pathway, and calcium signaling.

2024-11-07 | GSE281282 | GEO

Transgenerational epigenetic effects imposed by neonicotinoid thiacloprid exposure.

Project description:Neonicotinoids are a widely used class of insecticides that are being applied in agricultural fields. We examined the capacity of a neonicotinoid, thiacloprid (thia), to induce transgenerational effects in male mice. Pregnant outbred Swiss female mice were exposed to thia at embryonic days E6.5-E15.5 using different doses. Testis sections were used for morphology analysis, ELISAs for testosterone level analysis, RT-qPCR and RNA-seq for gene expression analysis, MEDIP-seq and MEDIP-qPCR techniques for DNA methylation analysis, and Western blot for a protein analysis. The number of meiotic double-strand breaks and the number of incomplete synapsed chromosomes were higher in the thia 6-treated group of F3 males. Genome-wide analysis of DNA methylation in spermatozoa revealed that differentially methylated regions were found in all three generations at the promoters of germ cell reprogramming responsive genes and many superenhancers that are normally active in embryonic stem cells, testis, and brain. DNA methylation changes induced by thia exposure during embryonic period are preserved through several generations at important master regulator regions.

| S-EPMC10654101 | biostudies-literature

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