Early ERK1/2 activation promotes DRP1-dependent mitochondrial fission necessary for cell reprogramming

Javier Prieto, Marian León, Xavier Ponsoda, Ramón Sendra, Roque Bort, Raquel Ferrer-Lorente, Angel Raya, Carlos López-García and Josema Torres ()
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Javier Prieto: Universidad de Valencia
Marian León: Universidad de Valencia
Xavier Ponsoda: Universidad de Valencia
Ramón Sendra: Universidad de Valencia
Roque Bort: Unidad de Hepatología Experimental, CIBERehd, Instituto de Investigación Sanitaria La Fe
Raquel Ferrer-Lorente: Centre de Medicina Regenerativa de Barcelona
Angel Raya: Centre de Medicina Regenerativa de Barcelona
Carlos López-García: Universidad de Valencia
Josema Torres: Universidad de Valencia

Nature Communications, 2016, vol. 7, issue 1, 1-13

Abstract: Abstract During the process of reprogramming to induced pluripotent stem (iPS) cells, somatic cells switch from oxidative to glycolytic metabolism, a transition associated with profound mitochondrial reorganization. Neither the importance of mitochondrial remodelling for cell reprogramming, nor the molecular mechanisms controlling this process are well understood. Here, we show that an early wave of mitochondrial fragmentation occurs upon expression of reprogramming factors. Reprogramming-induced mitochondrial fission is associated with a minor decrease in mitochondrial mass but not with mitophagy. The pro-fission factor Drp1 is phosphorylated early in reprogramming, and its knockdown and inhibition impairs both mitochondrial fragmentation and generation of iPS cell colonies. Drp1 phosphorylation depends on Erk activation in early reprogramming, which occurs, at least in part, due to downregulation of the MAP kinase phosphatase Dusp6. Taken together, our data indicate that mitochondrial fission controlled by an Erk-Drp1 axis constitutes an early and necessary step in the reprogramming process to pluripotency.

Date: 2016
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Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11124

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DOI: 10.1038/ncomms11124

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