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

First Author  Rowe GC Year  2013
Journal  Cell Rep Volume  3
Issue  5 Pages  1449-56
PubMed ID  23707060 Mgi Jnum  J:198668
Mgi Id  MGI:5498620 Doi  10.1016/j.celrep.2013.04.023
Citation  Rowe GC, et al. (2013) Disconnecting mitochondrial content from respiratory chain capacity in PGC-1-deficient skeletal muscle. Cell Rep 3(5):1449-56
abstractText  The transcriptional coactivators PGC-1alpha and PGC-1beta 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.
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