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Cell Rep. 2013 May 30;3(5):1449-56. doi: 10.1016/j.celrep.2013.04.023. Epub 2013 May 23.

Disconnecting mitochondrial content from respiratory chain capacity in PGC-1-deficient skeletal muscle.

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1
Cardiovascular Institute, Department of Pathology, Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA 02215, USA.

Abstract

The transcriptional coactivators PGC-1α and PGC-1β are widely thought to be required for mitochondrial biogenesis and fiber typing in skeletal muscle. Here, we show that mice lacking both PGC-1s in myocytes do indeed have profoundly deficient mitochondrial respiration but, surprisingly, have preserved mitochondrial content, isolated muscle contraction capacity, fiber-type composition, in-cage ambulation, and voluntary running capacity. Most of these findings are recapitulated in cell culture and, thus, are cell autonomous. Functional electron microscopy reveals normal cristae density with decreased cytochrome oxidase activity. These data lead to the following surprising conclusions: (1) PGC-1s are in fact dispensable for baseline muscle function, mitochondrial content, and fiber typing, (2) endurance fatigue at low workloads is not limited by muscle mitochondrial capacity, and (3) mitochondrial content and cristae density can be dissociated from respiratory capacity.

PMID:
23707060
PMCID:
PMC3688451
DOI:
10.1016/j.celrep.2013.04.023
[Indexed for MEDLINE]
Free PMC Article
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