PUBLICATION

Transcriptional profiles and copper stress responses in zebrafish cox17 mutants

Authors
Sun, H., Chen, M., Wang, Z., Zhao, G., Liu, J.X.
ID
ZDB-PUB-191031-4
Date
2019
Source
Environmental pollution (Barking, Essex : 1987)   256: 113364 (Journal)
Registered Authors
Liu, Jing-xia
Keywords
Copper stimulation responses, ROS, Transcriptome profiles, Wnt signaling, cox17 mutants
MeSH Terms
  • Animals
  • Animals, Genetically Modified*
  • Copper/metabolism
  • Copper/toxicity*
  • Embryo, Nonmammalian/drug effects*
  • Embryo, Nonmammalian/metabolism
  • Homozygote
  • Ion Transport
  • Mutation
  • Oxidative Stress/drug effects*
  • Oxidative Stress/genetics
  • Reactive Oxygen Species/metabolism
  • Transcriptome/drug effects*
  • Zebrafish/genetics*
  • Zebrafish/metabolism
PubMed
31662245 Full text @ Environ. Pollut.
Abstract
While Cox17 functions importantly in copper metalation of cytochrome c oxidase and integral mitochondrial architecture in vertebrates, rare studies have been performed regarding the developmental and physiological characters of vertebrate cox17 mutants. In this study, normal-like developmental phenotype was observed in both cox17Δ6-/- and cox17Δ4-/- homozygous zebrafish mutants, while gene ontology term and pathway analysis of the differentially expressed genes in both mutants showed enrichment in oxidoreductase activity, ion transport, histone methylation, MICOS complex, Wnt signaling, etc. This implied the occurrence of damage to the integral function of Cox17 and change of transcriptomes in the two mutants. Further qRT-PCR and WISH assays revealed the down-regulated expression of Wnt signaling and reduced expression of swim bladder marker genes in the two mutants. Moreover, copper stimulation induced no obvious increase in reactive oxygen species (ROS) or in the expression of hemoglobin marker genes, but further reduced the expression of swim bladder marker genes in the mutants. The integral data in this study suggest that: (1) cox17 mutants cannot activate the response of oxidoreductase to copper stimulation; (2) copper depends on the integral function of Cox17 to induce developmental defects in hemoglobin rather than swim bladder and (3) Wnt signaling but not ROS might mediate copper-induced swim bladder developmental defects in fish.
Genes / Markers
Figures
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Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes