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Fig. 7 | Molecular Neurodegeneration

Fig. 7

From: A partial Drp1 knockout improves autophagy flux independent of mitochondrial function

Fig. 7

Generation and characterization of Drp1 heterozygous global knockout (Drp1+/−) mice. (A) Schematic diagram illustrating the targeting strategy for generating different types of Drp1-deficient mice using the “knockout-first” technology. The KO-first allele is flexible and can produce reporter knockouts, conditional knockouts, and null alleles following exposure to site-specific recombinases Cre and Flp to delete Exon 2 of the Dnm1l gene. (B) representative genotyping results of Drp1+/− versus WT controls. (C) qPCR and (D) immunoblotting confirmed the reduction of mRNA and protein levels of Drp1 in the Drp1+/− mice in different brain regions (cortex, hippocampus, and ventral midbrain). (E, F) Weekly measurement showed no differences in body weight and length between Drp1+/− and WT littermates during the developmental stage, n = 66 WT (44M & 22 F), and 63 Drp1+/− (33M & 30 F). (G) No differences in locomotor activity (P = 0.4066 for distance travelled, P = 0.1671 for resting time, P = 0.3282 for speed, n = 11 WT, n = 9 Drp1+/−), as well as learning and memory test (P = 0.6736, n = 18/group) between genotypes. (H) Stereological counting of DA neurons in the SNpc show no differences between genotypes (data represent Mean ± SEM, n = 6). Statistical comparison was performed using either independent t-test or Two-Way ANOVA.

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