Submit Data |  Help |  Video Tutorials |  News |  Publications |  FTP Download |  REST API |  Citing RGD |  Contact   

Mitochondrial structure, function and dynamics are temporally controlled by c-Myc.

Authors: Graves, JA  Wang, Y  Sims-Lucas, S  Cherok, E  Rothermund, K  Branca, MF  Elster, J  Beer-Stolz, D  Van Houten, B  Vockley, J  Prochownik, EV 
Citation: Graves JA, etal., PLoS One. 2012;7(5):e37699. doi: 10.1371/journal.pone.0037699. Epub 2012 May 21.
Pubmed: (View Article at PubMed) PMID:22629444
DOI: Full-text: DOI:10.1371/journal.pone.0037699

Although the c-Myc (Myc) oncoprotein controls mitochondrial biogenesis and multiple enzymes involved in oxidative phosphorylation (OXPHOS), the coordination of these events and the mechanistic underpinnings of their regulation remain largely unexplored. We show here that re-expression of Myc in myc-/- fibroblasts is accompanied by a gradual accumulation of mitochondrial biomass and by increases in membrane polarization and mitochondrial fusion. A correction of OXPHOS deficiency is also seen, although structural abnormalities in electron transport chain complexes (ETC) are not entirely normalized. Conversely, the down-regulation of Myc leads to a gradual decrease in mitochondrial mass and a more rapid loss of fusion and membrane potential. Increases in the levels of proteins specifically involved in mitochondrial fission and fusion support the idea that Myc affects mitochondrial mass by influencing both of these processes, albeit favoring the latter. The ETC defects that persist following Myc restoration may represent metabolic adaptations, as mitochondrial function is re-directed away from producing ATP to providing a source of metabolic precursors demanded by the transformed cell.

Annotation

Gene Ontology Annotations
Phenotype Annotations
Objects Annotated

Additional Information

 
RGD Object Information
RGD ID: 7240532
Created: 2013-02-14
Species: All species
Last Modified: 2013-02-14
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.