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Research Article

miR-30 Regulates Mitochondrial Fission through Targeting p53 and the Dynamin-Related Protein-1 Pathway

  • Jincheng Li equal contributor,

    equal contributor Contributed equally to this work with: Jincheng Li, Stefan Donath

    Affiliation: Department of Physiology, Shantou University School of Medicine, Shantou, China

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  • Stefan Donath equal contributor,

    equal contributor Contributed equally to this work with: Jincheng Li, Stefan Donath

    Affiliation: Franz-Volhard-Clinics, HELIOS Clinics GmBH, Berlin, Germany

    X
  • Yanrui Li mail,

    * ; peifli@uic.edu (PL)

    Affiliation: Department of Physiology, Shantou University School of Medicine, Shantou, China

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  • Danian Qin,

    Affiliation: Department of Physiology, Shantou University School of Medicine, Shantou, China

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  • Bellur S. Prabhakar,

    Affiliation: College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America

    X
  • Peifeng Li mail

    * ; peifli@uic.edu (PL)

    Affiliation: College of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America

    X
  • Published: January 08, 2010
  • DOI: 10.1371/journal.pgen.1000795

Reader Comments (1)

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Is it physiologically relevant?

Posted by tsoimp on 01 Feb 2010 at 22:39 GMT

The title is very eyes-catching but the link between miR-30 and Drp1 is not direct or insignificant.

As we all know that mitochondria fragments during apoptosis, therefore, anything that blocks or promotes apoptosis will affect mitochondria fission indirectly. Although mitochondria fission and apoptosis could be uncoupled, there is no data indicating that p53 regulates these two processes separately.

It's novel that Drp1 is a new trasncriptional target of p53. However, it is not shown whether this elevated Drp1 level by p53 during apoptosis is required for mitochondrial fission. The best experiment will be to test whether pDrp1-BS2-Drp1 (endogenous Drp1 promoter with p53 binding site mutated drives Drp1 expression) can rescue Drp1 RNAi phenotype. If elevated Drp1 level is essential for mitochondrial fission during apoptosis, this construct should not rescue the phenotype.

Therefore, if miR-30 regulates mitochondrial fission simply through regulating apoptosis by targeting p53, I don't think it provides significant advancement of our understanding on how apoptosis triggers mitochondria fission.

No competing interests declared.