Complementary RNA and protein profiling identifies iron as a key regulator of mitochondrial biogenesis.

Cell Rep
Authors
Keywords
Abstract

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 data sets that can be leveraged to explore posttranscriptional and posttranslational processes that are essential for mitochondrial adaptation.

Year of Publication
2013
Journal
Cell Rep
Volume
3
Issue
1
Pages
237-45
Date Published
2013 Jan 31
ISSN
2211-1247
URL
DOI
10.1016/j.celrep.2012.11.029
PubMed ID
23318259
PubMed Central ID
PMC3812070
Links
Grant list
R01 GM077465 / GM / NIGMS NIH HHS / United States
T32 GM007215 / GM / NIGMS NIH HHS / United States
5T32GM007215-37 / GM / NIGMS NIH HHS / United States
R01GM077465 / GM / NIGMS NIH HHS / United States