Dataset: Expression profiles of C2C12 myotubes in response to PGC-1α (peroxisome proliferator-activated receptor gamma, coactivator 1 alpha) overexpression and/or iron chelation

Mitochondria are centers of metabolism and signaling whose content and function must adapt to changing cellular environments. The biological signals that initiate mitochondrial restructuring and the cellular processes that drive this adaptive response are largely obscure. To better define these systems, we performed matched quantitative genomic and proteomic analyses of mouse muscle cells as they performed mitochondrial biogenesis. We find that proteins involved in cellular iron homeostasis are highly coordinated with this process, and that depletion of cellular iron results in a rapid, dose-dependent decrease of select mitochondrial protein levels and oxidative capacity. We further show that this process is universal across a broad range of cell types and fully reversed when iron is reintroduced. Collectively, our work reveals that cellular iron is a key regulator of mitochondrial biogenesis, and provides quantitative datasets that can be leveraged to explore post-transcriptional and post-translational processes that are essential for mitochondrial adaptation. C2C12 mouse myoblasts were differentiated into myotubes for 3 days, at which point they were infected with adenovirus expressing either green fluorescent protein (GFP) or GFP-tagged PGC-1α (GFP-PGC-1α) ± treatment with the iron chelator deferoxamine (DFO) (for 4 treatments total). The cells were grown for three more days, then RNA was extracted and applied to Affymetrix Mouse 430 2.0 arrays. Gene expression was measured in biological duplicate (4 treatments × 2 replicates = 8 arrays).

Species:

mouse

Samples:

8

Source:

E-GEOD-42299

Updated:

Dec.12, 2014

Registered:

Nov.12, 2014