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Lead exposure induced transgenerational developmental neurotoxicity by altering genome methylation in Drosophila

ABSTRACT: Lead exposure induced transgenerational developmental neurotoxicity by altering genome methylation in Drosophila

PROVIDER: PRJNA1048433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27059600_1.fastq.gz	Fastqsanger.gz
	SRR27059600_2.fastq.gz	Fastqsanger.gz
	SRR27059601_1.fastq.gz	Fastqsanger.gz
	SRR27059601_2.fastq.gz	Fastqsanger.gz
	SRR27059602_1.fastq.gz	Fastqsanger.gz

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Lead exposure induced transgenerational developmental neurotoxicity by altering genome methylation in Drosophila

Project description:Heavy metal toxicity is a worldwide health problem. Lead exposure is of particular concern due to the adverse effects of low concentrations on cognitive development in children. Although the mechanism of lead neurotoxicity has been well studied, the analysis and molecular mechanism of the transgenerational effects of lead exposure-induced neurotoxicity are lacking. To address this, Drosophila, a powerful developmental animal model, was exposed to lead acetate. We found that Pb exposure during the developmental stage affected the neurodevelopment of F0 fruit flies, resulting in a loss of the correlation between the motor terminal area and muscle fiber area and the increased frequency of β-lobe midline crossing phenotype in Mushroom bodies. We also found that Pb exposure led to an increase in BRP expression, suggesting an increase in synaptic vesicle release sites and a decrease in synaptic vesicle protein SYN expression in F0 generation. This explained the results of our electrophysiological data that Pb exposure led to an increase in the amplitude of evoked excitatory junctional potential (EJP) and an increase in the frequency of spontaneous excitatory junctional potential (mEJP). Our results further confirmed that the developmental neurotoxicity of parental Pb exposure has a transgenerational effect. Neurodevelopmental defects, abnormalities in synaptic function, and repetitive behavior also were observed in the F3 offspring of F0 exposed to lead. Our Medip-seq analysis showed that Pb exposure altered the DNA methylation levels of many neurodevelopmentally associated genes (eg, hppy, nrg, baz, and spn) in the F3 offspring of the F0 generation with Pb exposure. Our findings suggest that epigenetic mechanisms may underlie the transgenerational inheritance of acquired phenotypic traits resulting from exposure to environmental factors.

2023-12-09 | GSE249281 | GEO

Mechanistic Insights into Lead Acetate-Induced Neurotoxicity Using RNA-Seq Analysis

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Effects of Developmental Lead Exposure on the Hippocampal Transcriptome.

Project description:In this study we analyzed the effects of lead-exposure up hippocampal gene expression in males and females exposed to 0ppm, 250ppm and 750ppm lead during two different developmental periods, perinatal (in utero through to weaning at PND21) and postnatal (PND0-PND45). All tissue was taken at PND 55. We used affymetrix Rat Gene 1.0ST arrays to obtain global gene expression data from each animal, with a group size of 4 for all conditions (Total number of Arrays = 40) Gene expression was profiled in hippocampus at no lead exposure (0ppm), 250ppm and 750 ppm lead exposure level at peinatal and postnaltal developmental period.

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Acephate Exposure Induces Transgenerational Ovarian Developmental Toxicity by Altering the Expression of Follicular Growth Markers in Female Rats

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Developmental Origins of Transgenerational Sperm DNA Methylation Epimutations Following Ancestral DDT Exposure

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.

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Developmental Origins of Transgenerational Sperm DNA Methylation Epimutations Following Ancestral Vinclozolin Exposure

Project description:Previously the agricultural fungicide vinclozolin was found to promote the transgenerational inheritance of sperm differential DNA methylation regions (DMRs) termed epimutations that help mediate this epigenetic inheritance. The current study was designed to investigate the developmental origins of the transgenerational DMRs during gametogenesis. Male control and vinclozolin lineage F3 generation rats were used as a source of embryonic day 16 (E16) prospermatogonia, postnatal day 10 (P10) spermatogonia, and adult pachytene spermatocytes, round spermatids, caput epididymal sperm, and caudal sperm. The DMRs between the control versus vinclozolin lineage samples were determined for each developmental stage. The top 100 statistically significant DMRs for each stage were compared and the developmental origins of the caudal epididymal sperm DMRs were assessed.

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Transgenerational effects of developmental neurotoxicity induced by exposure to a no-observed-adverse-effect level (NOAEL) of neonicotinoid pesticide clothianidin.

Project description:Neonicotinoid pesticides (NNs) transfer rapidly from mother to offspring, which exhibit neurobehavioral effects. However, no studies have investigated NNs' transgenerational effects. We exposed F0 generation mice (mothers) to a no-observed-adverse-effect level (NOAEL) of clothianidin (CLO) during gestation and lactation, and examined the adult neurobehavioral effects of three generations of offspring (F1, F2, F3). F1 had lower birth weight, decreased locomotor activity, and increased anxiety-like behavior. In F2, body weight was affected, and there was a decreasing trend in locomotor activity and an increasing trend in anxiety-like behavior. In F3, locomotor activity tended to increase. Thus, even when only the mothers were exposed, the effects of CLOs were still observed in F1, F2, and F3 but the effects became smaller.

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