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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
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 | GSE182945 | GEO
Project description:Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish
| PRJNA758396 | ENA
Project description:Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [WGBS]
| PRJNA758397 | ENA
Project description:Parental copper stress induces offspring developmental defects by altering DNA methylation in zebrafish [RNA-Seq]
| PRJNA758398 | ENA
Project description:BACKGROUND:The disorder of copper homeostasis is linked with disease and developmental defects, and excess copper_nanoparticles (CuNPs) and ion (Cu2+) will induce developmental malformation and disease in organisms. However, little knowledge is available regarding its potential regulation mechanisms, and little study links excess copper with retinal developmental malformation and disease. METHODS:Embryos were stressed with copper (CuNPs and Cu2+), and cell proliferation and apoptosis assays, reactive oxygen species (ROS) and endoplasmic reticulum (ER) signaling detections, and genetic mutants cox17-/- and atp7a-/- application, were used to evaluate copper induced retinal developmental malformation and the underlying genetic and biological regulating mechanisms. RESULTS:Copper reduced retinal cells and down-regulated expression of retinal genes, damaged the structures of ER and mitochondria in retinal cells, up-regulated unfold protein responses (UPR) and ROS, and increased apoptosis in copper-stressed retinal cells. The copper induced retinal defects could be significantly neutralized by ROS scavengers reduced Glutathione (GSH) & N-acetylcysteine (NAC) and ER stress inhibitor 4- phenylbutyric acid (PBA). Blocking the transportation of copper to mitochondria, or to trans-Golgi network and to be exported into plasma, by deleting gene cox17 or atp7a, could alleviate retinal developmental defects in embryos under copper stresses. CONCLUSIONS:This is probably the first report to reveal that copper nanoparticles and ions induce retinal developmental defects via upregulating UPR and ROS, leading to apoptosis in zebrafish embryonic retinal cells. Integrated function of copper transporter (Cox17 and Atp7a) is necessary for copper induced retinal defects.
| S-EPMC7071659 | biostudies-literature
Project description:A major hurdle in using complex systems for drug screening is the difficulty of defining the mechanistic targets of small molecules. The zebrafish provides an excellent model system for juxtaposing developmental phenotypes with mechanism discovery using organism genetics. We carried out a phenotype-based screen of uncharacterized small molecules in zebrafish that produced a variety of chemically induced phenotypes with potential genetic parallels. Specifically, kalihinol F caused an undulated notochord, defects in pigment formation, hematopoiesis, and neural development. These phenotypes were strikingly similar to the zebrafish mutant, calamity, an established model of copper deficiency. Further studies into the mechanism of action of kalihinol F revealed a copper-chelating activity. Our data support this mechanism of action for kalihinol F and the utility of zebrafish as an effective system for identifying therapeutic and target pathways.
| S-EPMC3715381 | biostudies-literature
Project description:Selenium (Se) leaches into water from agricultural soils and from storage sites for coal fly ash. Se toxicity causes population and community level effects in fishes and birds. We used the laboratory aquarium model fish, Japanese medaka (Oryzias latipes), an asynchronous breeder, to determine aspects of uptake in adults and resultant developmental toxicity in their offspring. The superior imaging properties of the model enabled detailed descriptions of phenotypic alterations not commonly reported in the existing Se literature. Adult males and females in treatment groups were exposed, separately and together, to a dry diet spiked with 0, 12.5, 25, or 50 μg/g (dry weight) seleno-L-methionine (SeMet) for 6 days, and their embryo progeny collected for 5 days, maintained under controlled conditions and observed daily for hatchability, mortality and/or developmental toxicity. Sites of alteration included: craniofacial, pericardium and abdomen (Pc/Ab), notochord, gall bladder, spleen, blood, and swim bladder. Next, adult tissue Se concentrations (liver, skeletal muscle, ovary and testis) were determined and compared in treatment groups of bred and unbred individuals. No significant difference was found across treatment groups at the various SeMet concentrations; and, subsequent analysis compared exposed vs. control in each of the treatment groups at 10 dpf. Increased embryo mortality was observed in all treatment groups, compared to controls, and embryos had a decreased hatching rate when both parents were exposed. Exposure resulted in significantly more total altered phenotypes than controls. When altered phenotypes following exposure of both parents were higher than maternal only exposure, a male role was suggested. The comparisons between treatment groups revealed that particular types of phenotypic change may be driven by the sex of the exposed parent. Additionally, breeding reduced Se concentrations in some adult tissues, specifically the liver of exposed females and skeletal muscle of exposed males. Detailed phenotypic analysis of progeny from SeMet exposed parents should inform investigations of later life stages in an effort to determine consequences of early life exposure.
| S-EPMC4698014 | biostudies-literature
Project description:The persistence of reef building corals is threatened by human-induced environmental change. Maintaining coral reefs into the future requires not only the survival of adults, but also the influx of recruits to promote genetic diversity and retain cover following adult mortality. Few studies examine the linkages among multiple life stages of corals, despite a growing knowledge of carryover effects in other systems. We provide a novel test of coral parental conditioning to ocean acidification (OA) and tracking of offspring for 6 months post-release to better understand parental or developmental priming impacts on the processes of offspring recruitment and growth. Coral planulation was tracked for 3 months following adult exposure to high pCO2 and offspring from the second month were reciprocally exposed to ambient and high pCO2 for an additional 6 months. Offspring of parents exposed to high pCO2 had greater settlement and survivorship immediately following release, retained survivorship benefits during 1 and 6 months of continued exposure, and further displayed growth benefits to at least 1 month post release. Enhanced performance of offspring from parents exposed to high conditions was maintained despite the survivorship in both treatments declining in continued exposure to OA. Conditioning of the adults while they brood their larvae, or developmental acclimation of the larvae inside the adult polyps, may provide a form of hormetic conditioning, or environmental priming that elicits stimulatory effects. Defining mechanisms of positive acclimatization, with potential implications for carry over effects, cross-generational plasticity, and multi-generational plasticity, is critical to better understanding ecological and evolutionary dynamics of corals under regimes of increasing environmental disturbance. Considering environmentally-induced parental or developmental legacies in ecological and evolutionary projections may better account for coral reef response to the chronic stress regimes characteristic of climate change.
| S-EPMC7423898 | biostudies-literature
Project description:The alpha regulator subunit B'' of protein phosphatase 2 (PPP2R3A), a regulatory subunit of protein phosphatase 2A (PP2A), was reported to present a special subcellular localization in cardiomyocytes and elevate in non-ischemia failing hearts. PPP2R3A has two transcriptions PR72 and PR130. PR72 acts as a negative regulator of the Wnt signaling cascade, while the Wnt signaling cascade plays a pivotal role in cardiac development. And PR130 was found to be involved in cardiac development of zebrafish in our previous study. Thus, to investigate the function of PR72 in heart, two stable pr72 knockout (KO) zebrafish lines were generated using Transcription Activator-Like Effector Nuclease (TALEN) technology. Homozygous pr72 KO fish struggled to survive to adulthood and exhibited cardiac developmental defects, including enlarged ventricular chambers, reduced cardiomyocytes and decreased cardiac function. And the defective sarcomere ultrastructure that affected mitochondria, I bands, Z lines, and intercalated disks was also observed. Furthermore, the abnormal heart looping was detected in mutants which could be rescued by injection with wild type pr72 mRNA. Additionally, it was found that Wnt effectors were elevated in mutants. Those indicated that deletion of pr72 in zebrafish interrupted cardiac development, probably through activation of the Wnt pathway.
| S-EPMC6258505 | biostudies-literature