Figure 4: Rad51 RNAi treatment caused a loss of mitochondrial membrane potential (ΔΨm) and impaired mitochondrial ATP production. | Scientific Reports

Figure 4: Rad51 RNAi treatment caused a loss of mitochondrial membrane potential (ΔΨm) and impaired mitochondrial ATP production.

From: The role of Rad51 in safeguarding mitochondrial activity during the meiotic cell cycle in mammalian oocytes

Figure 4

(A) Abnormal mitochondrial distribution was found in Rad51-silenced MI oocytes. GFP (a–d) or Rad51 (e–h) dsRNA was injected into MI oocytes that were precultured in M16 medium containing MitoTracker (mitochondria, red) for 30 minutes and then stained with an antibody against α-Tubulin (green). Cellular DNA was also stained (blue), and the cells were imaged by LSCM. The scale bars indicate 20 μm. (B) Effect of Rad51 on ΔΨm. ΔΨm in Rad51-silenced MI oocytes indicated by changes in RITC and FITC intensity, which were measured by LSCM as detailed in the Materials and Methods section. The scale bars indicate 20 μm. (C) Graphic representation of the results shown in (B). The data are presented as the mean ± SEM. The asterisk represents statistical significance at p < 0.05 as determined by a paired Student’s t-test. (D) Effects of Rad51 down-regulation on oocyte ATP levels. Reduction in Rad51 expression impaired mitochondrial ATP production. The data are presented as the mean ± SEM. The asterisk represents statistical significance at p < 0.01. (E) Rad51 RNAi treatment suppressed mitochondrial Mtnd6 mRNA expression. The data are presented as the mean ± SEM. The asterisk represents statistical significance at p < 0.01.

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