Reactive oxygen species (ROS) are traditionally viewed as the toxic by-product of cellular respiration. A new study suggests a homeostatic role for ROS in maintaining stable respiratory phenotypes across genetic variants of the mitochondrial genome.
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Baughman, J., Mootha, V. Buffering mitochondrial DNA variation. Nat Genet 38, 1232–1233 (2006). https://doi.org/10.1038/ng1106-1232
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DOI: https://doi.org/10.1038/ng1106-1232
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