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

Mutation
Zebrafish/genetics*
Zebrafish/metabolism
Copper/metabolism
Copper/toxicity*
Reactive Oxygen Species/metabolism
Animals, Genetically Modified*
Homozygote
Ion Transport
Transcriptome/drug effects*
Animals
Oxidative Stress/drug effects*
Oxidative Stress/genetics
Embryo, Nonmammalian/drug effects*
Embryo, Nonmammalian/metabolism

(all 15)

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

Gene	Fish	Conditions	Stage	Anatomy	Assay	Figure
acta2	AB	standard conditions	Day 5	swim bladder mesenchyme	ISH	Fig. 7
acta2	AB	chemical treatment by environment: copper(2+)	Day 5	swim bladder mesenchyme	ISH	Fig. 7
acta2	AB	standard conditions	Day 5	swim bladder mesenchyme	ISH	Fig. 6
acta2	AB	chemical treatment by environment: copper(2+)	Day 5	swim bladder mesenchyme	ISH	Fig. 6
acta2	AB	standard conditions	Day 5	whole organism	RTPCR	Fig. 6
acta2	AB	standard conditions	Day 5	whole organism	RTPCR	Fig. 7
acta2	AB	chemical treatment by environment: copper(2+)	Day 5	whole organism	RTPCR	Fig. 6
acta2	AB	chemical treatment by environment: copper(2+)	Day 5	whole organism	RTPCR	Fig. 7
acta2	cox17^hza2/hza2 (AB)	standard conditions	Day 5	swim bladder mesenchyme	ISH	Fig. 7
acta2	cox17^hza2/hza2 (AB)	chemical treatment by environment: copper(2+)	Day 5	swim bladder mesenchyme	ISH	Fig. 7

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Phenotype

Fish	Conditions	Stage	Phenotype	Figure
AB	chemical treatment by environment: copper(2+)	Prim-5	hemoglobin biosynthetic process increased occurrence, abnormal	Fig. 5
AB	chemical treatment by environment: copper(2+)	Prim-5	intermediate cell mass of mesoderm hbbe3 expression increased amount, abnormal	Fig. 5
AB	chemical treatment by environment: copper(2+)	Prim-5	whole organism reactive oxygen species increased amount, abnormal	Fig. 5
AB	chemical treatment by environment: copper(2+)	Prim-5	whole organism reactive oxygen species increased amount, normal	Fig. 5
AB	chemical treatment by environment: copper(2+)	Prim-25	swim bladder bud pbx1a expression decreased amount, abnormal	Fig. 7
AB	chemical treatment by environment: copper(2+)	Prim-25	swim bladder bud pbx1a expression decreased amount, abnormal	Fig. 6
AB	chemical treatment by environment: copper(2+)	Prim-25	whole organism mnx1 expression decreased amount, abnormal	Fig. 7
AB	chemical treatment by environment: copper(2+)	Prim-25	whole organism mnx1 expression decreased amount, abnormal	Fig. 6
AB	chemical treatment by environment: copper(2+)	Prim-25	whole organism pbx1a expression decreased amount, abnormal	Fig. 7
AB	chemical treatment by environment: copper(2+)	Prim-25	whole organism pbx1a expression decreased amount, abnormal	Fig. 6

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Mutations / Transgenics

Allele	Construct	Type	Affected Genomic Region
hza2		Insertion	cox17
hza3		Small Deletion	cox17

Human Disease / Model

Sequence Targeting Reagents

Target	Reagent	Reagent Type
cox17	CRISPR1-cox17	CRISPR

Fish

Fish
AB
cox17^hza2/hza2 (AB)
cox17^hza3/hza3 (AB)
WT

Antibodies

Orthology

Engineered Foreign Genes

Mapping

Sun et al., 2019 ZDB-PUB-191031-4 PMID:31662245

Transcriptional profiles and copper stress responses in zebrafish cox17 mutants

Sun et al., 2019

ZDB-PUB-191031-4
PMID:31662245