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Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [WGBS]

ABSTRACT: Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [WGBS]

PROVIDER: PRJNA758397 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15657162_1.fastq.gz	Fastqsanger.gz
	SRR15657162_2.fastq.gz	Fastqsanger.gz
	SRR15657163_1.fastq.gz	Fastqsanger.gz
	SRR15657163_2.fastq.gz	Fastqsanger.gz
	SRR15657164_1.fastq.gz	Fastqsanger.gz

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Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [WGBS]

Project description:Here, we describe environmental Cu2+ in promoting zebrafish (Danio rerio) developmental abnormalities in subsequent generation. This study for the first time demonstrated that: 1. Cu2+ induced alterations in sperm methylome could be passed down to offspring and cause developmental defects in the nervous and digestive system, even the Cu2+ concentration is at 10 μg/L, the National Quality Standards of fishery water (GB11607-89); 2. DNA methylomes of F0 sperms and F1 offspring were altered in a loci-specific manner and were correlated with transcriptional expression of genes which function importantly in the development of CNS, retina, and digestive system development during F1 embryogenesis; 3. Loci-specific hypoDMRs in the pmpcb promoter and loci-specific hyperDMRs in the crebl2 and tab2 promoters might show adaptive and harmful responses to Cu2+ stresses in next generational inheritance, respectively. Those data revealed that Cu2+ induced alterations in sperm methylome may be passed down to offspring and cause the embryonic developmental defects and the resulted inferior seeding, suggesting that environmental Cu2+ might pose a dramatic and long-lasting threat to the sustainability of fish population and even to humans with imbalanced copper homeostasis.

2022-08-27 | GSE182944 | GEO

Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish

Project description:Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish

| PRJNA758396 | ENA

Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [RNA-Seq]

Project description:Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [RNA-Seq]

| PRJNA758398 | ENA

Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [RNA-Seq]

2022-08-27 | GSE182945 | GEO

Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish

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

2022-08-27 | GSE182946 | GEO

Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation

Project description:Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

Project description:Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (scRNA-Seq)

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Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

Project description:Cystic fibrosis causes olfactory system defects by altering progenitor cell proliferation (Bulk RNA-Seq)

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Comparison of Corynebacterium glutamicum cultivated under copper starvation with copper sufficiency

Project description:To identify genes which are differentially expressed in Corynebacterium glutamicum in the absence of copper, we performed DNA microarray analyses of cells cultivated under copper starvation conditions compared to copper sufficiency.

2018-08-28 | GSE117530 | GEO

HF001-A: Gene expression patterns in the progression towards canine copper-associated chronic hepatitis

Project description:Copper is an essential trace element, but can become toxic when present in abundance. The severe effects of copper-metabolism imbalance are illustrated by the inherited disorders Wilson disease and Menkes disease. The Labrador retriever dog breed is a novel non-rodent model for copper-storage defects displaying identical phenotypic alterations and carrying mutations in genes known to be involved in copper transport. Besides disease initiation and progression of copper accumulation, the molecular mechanisms and pathways involved in copper accumulation and eventually progression towards copper associated chronic hepatitis still remains unclear. Using liver tissue of Labrador retrievers in different stages of copper-associated hepatitis, expression levels targeted at candidate genes as well as transcriptome microarrays, have shed light on involved molecular pathways. At the initial phase, viz. increased hepatic copper levels, transcriptomic alterations in livers revealed enrichment for cell adhesion, developmental, inflammatory, and cytoskeleton pathways. Upregulation of targeted MT1A and COMMD1 mRNA shows the livers first response to rising intrahepatic copper concentrations. In livers with copper-associated hepatitis mainly an activation of inflammatory pathways is detected. Once the hepatitis is in the chronic stage, transcriptional differences are found in cell adhesion adaptations and cytoskeleton remodelling. In view of the high similarities in hepatopathies between men and dog extrapolation of these dog data into human biomedicine seems feasible.

2017-05-02 | GSE86932 | GEO

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