FIGURE

Fig. 7

ID
ZDB-FIG-250304-7
Publication
Chen et al., 2025 - NDUFB7 mutations cause brain neuronal defects, lactic acidosis, and mitochondrial dysfunction in humans and zebrafish
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Fig. 7

Knockdown of Ndufb7 reduces the oxygen consumption rate.

We treated one-cell stage zebrafish embryos without or with indicated Ndufb7 translational-blocking morpholino oligonucleotides (tMO), and Ndufb7 mRNA or Mitoquinone mesylate (MitoQ) as described in Fig. 3, cultured to 24 hours post-fertilization, and subjected them to the measurement of oxygen consumption rate (OCR) using the Seahorse XFe24. A Graphical depiction illustrating the changes in mitochondrial respiration upon exposure to oligomycin (18.7 μM), carbonyl cyanide 4-(trifluoromethoxy) phenylhydrazone (FCCP; 8 μM), and rotenone/antimycin A (3.5 μM). In 203 min for each measurement cycle, each inhibitor was injected at a predetermined time point as indicated by a dotted line. The blue, orange, gray, and yellow curves represent the untreated, tMO-injected embryos and tMO with Ndufb7 RNA or MitoQ, respectively. Calculations were made to show B Basal respiration, C maximal respiration, and D adenosine triphosphate (ATP) production. The error bar indicates the standard deviation. Data from three independent experiments are presented, analyzed, and shown as described in Fig. 3. NS not significant; **p < 0.01.

Expression Data

Expression Detail
Antibody Labeling
Phenotype Data
Fish:
Condition:
Knockdown Reagent:
Observed In:
Stage: Prim-5

Phenotype Detail
Acknowledgments
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