Copper ions impair zebrafish skeletal myofibrillogenesis via epigenetic regulation.

Unbalanced copper (Cu ) homeostasis is associated with the developmental defects of vertebrate myogenesis, but the underlying molecular mechanisms remain elusive. In this study, it was found that Cu stressed zebrafish embryos and larvae showed reduced locomotor speed as well as loose and decreased myofibrils in skeletal muscle, coupled with the downregulated expression of muscle fiber markers mylpfa and smyhc1l and the irregular arrangement of myofibril and sarcomere. Meanwhile, the Cu stressed zebrafish embryos and larvae also showed significant reduction in the expression of H3K4 methyltransferase smyd1b transcripts and H3K4me3 protein as well as in the binding enrichment of H3K4me3 on gene mylpfa promoter in skeletal muscle cells, suggesting that smyd1b-H3K4me3 axis mediates the Cu -induced myofibrils specification defects.

Copper stress induces zebrafish central neural system myelin defects via WNT/NOTCH-hoxb5b signaling and pou3f1/fam168a/fam168b DNA methylation.

Unbalanced copper (Cu) homeostasis is associated with neurological development defects and diseases. However, the molecular mechanisms remain elusive. Here, central neural system (CNS) myelin defects and the down-regulated expression of WNT/NOTCH signaling and its down-stream mediator hoxb5b were observed in Cu stressed zebrafish larvae.

Common responses of fish embryos to metals: an integrated analysis of transcriptomes and methylomes in zebrafish embryos under the stress of copper ions or silver nanoparticles.

Recently, the responses of embryos to Cu or AgNP stresses have been investigated, but few studies have been performed on the common responses of embryos to both Cu and AgNPs, the same kind of stressor metal. In this study, a large number of commonly down-regulated and up-regulated differentially expressed genes (DEGs) were revealed in both Cu- and AgNP-stressed embryos. The down-regulated DEGs were enriched in myosin complex and muscle structure development, ion transport and metal ion binding, transmission of nerve impulses, etc.

Silver nanoparticles impair zebrafish skeletal and cardiac myofibrillogenesis and sarcomere formation.

Metal nanoparticles from industries contaminate the environment and affect the normal development of fish even human health. However, little is known about their biological effects on fish embryogenesis and the potential mechanisms. In this study, zebrafish embryos exposed to/injected with silver nanopaticles (AgNPs) exhibited shorter body, reduced heartbeats, and dysfunctional movements.

Mechanisms of silver_nanoparticles induced hypopigmentation in embryonic zebrafish.

Silver_nanoparticles (AgNPs) have been reported to inhibit specification of erythroid cells and to induce spinal cord deformities and cardiac arrhythmia in vertebrates, but have not been implicated in development of neural crest (NC) and pigment cells in an in vivo model yet. In current study, down-regulated expressions of NC genes pax7 and foxd3, melanophore genes mitfa and dct, and xanthophore gene gch2 in AgNPs-exposed embryos were revealed by microarray, qRT-PCR and whole-mount in situ hybridization (WISH). Then, the down-regulated expressions of melanophore genes mitfa and dct but not xanthophore gene gch2 in AgNPs-exposed embryos were found to be recovered by melanogenesis agonists palmitic acid and dibutyryl cyclic AMP (dbcAMP).