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Fig. 5 | BMC Biology

Fig. 5

From: GATD3A, a mitochondrial deglycase with evolutionary origins from gammaproteobacteria, restricts the formation of advanced glycation end products

Fig. 5

GATD3A influences mitochondrial dynamics. A 1,2-dicarbonyl slot blot immunoreactivity pulse-chase assay and cellular morphology of glyoxal (GO)-treated Gatd3a+/+ or Gatd3a−/− MEFs. GAPDH is used as a loading control (p = *<0.05, two-tailed Student’s t test, n = 4, +SEM). B Oxygen consumption rate is decreased in Gatd3a/ mouse embryonic fibroblasts (MEFs) compared to wildtype. Treatment with methylglyoxal (0.2 mM) for 24 h prior to assay exacerbates observed phenotype in knockout cells. Data is normalized to cell number (p = *<0.05, p = *<0.01, two-tailed Student’s t test, n = 3 biological replicates, N = 4 technical replicates per plate, N = 3 replicates per genotype, error bars ±SEM). C Mitochondrial morphology is not significantly disrupted in Gatd3a/ MEFs (N = 21 per genotype, two-tailed Welch’s t-test, lines represent mean value, extended data in Additional file 1, Fig. S4B). D Overexpression of GATD3A in Gatd3a+/+ MEFs leads to reduced mitochondrial content and fragmented mitochondrial network (N = 21 per condition, p = ****<0.0001, ***<0.001, two-tailed Welch’s t-test, lines represent mean value)

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