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Copper ions impair zebrafish skeletal myofibrillogenesis via epigenetic regulation. | LitMetric

Copper ions impair zebrafish skeletal myofibrillogenesis via epigenetic regulation.

FASEB J

College of Fisheries, Key Laboratory of Freshwater Animal Breeding, Ministry of Agriculture, Huazhong Agricultural University, Wuhan, China.

Published: July 2021

AI Article Synopsis

  • Unbalanced copper levels in zebrafish embryos lead to developmental issues in muscle formation, characterized by reduced muscle fiber markers and irregular muscle structure.
  • Copper stress affects gene expression related to muscle development, particularly downregulating smyd1b and altering key histone modifications (H3K4me3) associated with muscle fiber specification.
  • Research reveals that hyper-methylation of the smyd5 gene contributes to muscle defects under copper stress, with findings suggesting that copper disrupts muscle development through epigenetic changes rather than affecting copper transporters directly.

Article Abstract

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. Additionally, whole genome DNA methylation sequencing unveiled that the gene smyd5 exhibited significant promoter hyper-methylation and increased expression in Cu stressed embryos, and the ectopic expression of smyd5 in zebrafish embryos also induced the myofibrils specification defects as those observed in Cu stressed embryos. Moreover, Cu was shown to suppress myofibrils specification and smyd1b promoter transcriptional activity directly independent of the integral function of copper transporter cox17 and atp7b. All these data may shed light on the linkage of unbalanced copper homeostasis with specific gene promoter methylation and epigenetic histone protein modification as well as the resultant signaling transduction and the myofibrillogenesis defects.

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Source
http://dx.doi.org/10.1096/fj.202100183RDOI Listing

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