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Comment
. 2009 Jul 21;106(29):11825-6.
doi: 10.1073/pnas.0906430106. Epub 2009 Jul 15.

The Krebs cycle meets the cell cycle: mitochondria and the G1-S transition

Toren Finkel  1 , Paul M Hwang
Affiliations
Comment

The Krebs cycle meets the cell cycle: mitochondria and the G1-S transition

Toren Finkel et al. Proc Natl Acad Sci U S A. .
No abstract available

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Conflict of interest statement

The authors declare no conflict of interest.

Figures

Fig. 1.
Fig. 1.
A putative model for the role of mitochondria in the G1–S transition. Throughout most of the cell cycle, mitochondria appear as a combination of either tubular or fragmented morphologies. Surprisingly, at the G1–S transition, the mitochondria coalesce into a giant, single tubular network. This network is electrically coupled and exhibits a hyperpolarized mitochondrial membrane potential (ψm). Because ψm is the ionic gradient used to generate ATP, it is not surprising that this unique morphological and bioenergetic mitochondrial network appears to allow for increased ATP generation. Based on ref. , and previous studies in mammalian cells and lower organisms, the absence of this energetic boost may trigger a G1–S checkpoint that involves the sequential activation of AMPK and p53 and ultimately the down-regulation of cyclin E levels. In addition, ref. suggests that increased mitochondrial activity can positively regulate cyclin E levels and trigger S-phase progression. Note, in this putative model, p53 regulates events in several different contexts, including the transcriptional induction of p21, the cell cycle regulator, and SCO2, a factor that has been demonstrated to regulate mitochondrial oxygen consumption.
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