Abstract
Somatic cells can be reprogrammed into a pluripotent cellular state similar to that of embryonic stem cells. Given the significant physiological differences between the somatic and pluripotent cells, cell reprogramming is associated with a profound reorganization of the somatic phenotype at all levels. The remodeling of mitochondrial morphology is one of these dramatic changes that somatic cells have to undertake during cell reprogramming. Somatic cells transform their tubular and interconnected mitochondrial network to the fragmented and isolated organelles found in pluripotent stem cells early during cell reprogramming. Accordingly, mitochondrial fission, the process whereby the mitochondria divide, plays an important role in the cell reprogramming process. Here, we present an overview of the importance of mitochondrial fission in both cell reprogramming and cellular transformation.
Highlights
Mitochondria and their movement as organelles were described for the first time 100 years ago [1]
The observed changes in both mitochondrial morphology and metabolism seem to be key for cell reprogramming and during the early events of tumorigenesis
Published data suggest a close parallelism between the stochastic phase of cell reprogramming and cellular transformation [105]
Summary
Mitochondria and their movement as organelles were described for the first time 100 years ago [1]. The molecular machinery that controls the fission and fusion processes includes proteins that are either localized in mitochondrial membranes or recruited to the surface of these organelles in response to different stimuli. Drp is activated in the cytosol by posttranslational modifications in response to different stimuli and recruited to the mitochondrial surface by its interaction with protein adapters [28, 29]. It has been shown that ER projections wrap mitochondria around the areas where fragmentation of these organelles takes place These ERmitochondria contacts are not Drp1-dependent, but rather enhance the recruitment of the GTPase to these focal points [57, 58]. A profission role for ganglioside-induced differentiationassociated protein 1 (Gdap1) has been proposed, as Gdap favors the formation of ER-mitochondria contacts in certain neural cell types and its overexpression leads to fragmented mitochondria [59,60,61]
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