and COIII), whereas the remaining polypeptides are encoded by nuclear genes. Only in complex II are all the necessary enzymatic subunits (four in this case) encoded by just one genome (the nuclear). Nuclear genes are also intimately involved in other basic mitochondrial functions. Indeed, mtDNA does not encode any of the proteins that are directly involved in its own replication, transcription, translation, surveillance, or repair. In short, mtDNA is just a tiny snippet of DNA that by itself would be absolutely helpless to itself and to the organism in which it is housed. None of this makes any biological sense, except in the light of evolutionary science (which has discovered that modern mitochondria are remnants of a microbe that invaded or was engulfed by a protoeukaryotic cell in an endosymbiotic merger that took place billions of years ago).
Like the other genetic systems we have considered thus far, the mitochondrial genome is plagued by mutations that often compromise molecular operations. Indeed, on a per-nucleotide basis, mtDNA experiences about 5–10 more mutations per unit time than do typical protein-coding nuclear genes (Brown et al., 1979). Many mtDNA mutations are of little or no consequence to a person’s health, but many others have negative effects ranging from mildly debilitating to deadly. Clinical disabilities from mtDNA mutations disproportionately involve high-energy tissues and organs (Wallace, 2005; McFarland et al., 2007): brain, eye and other components of the peripheral nervous system, heart, skeletal muscle, kidney, and the endocrine system. Mutations in mtDNA have also been implicated in a spectrum of cancers (Copeland et al., 2002). In short, an emerging paradigm is that many of the degenerative diseases of aging have their etiologies in mitochondria, either as deleterious mutations in the mtDNA molecules themselves or as operational flaws in nuclear-mitochondrial interactions.
The serious health problems that arise from mtDNA mutations immediately challenge any claim for omnipotent perfection in mitochondrial design. Perhaps these mutational aberrations can be viewed as unfortunate but inevitable byproducts of molecular complexity. However, the intellectual challenges for ID go much deeper. Considering the critical role of cellular energy production in human health and metabolic operations, why would an intelligent designer entrust so much of the production process to a mitochondrion, given the outrageous molecular features this organelle possesses? Why would a wise designer have imbued mtDNA with some but not all of the genes necessary to carry out its metabolic role (and then put the remaining genes in the nucleus instead)? Why would a wise engineer have put any crucial genes in a caustic cytoplasmic environment in which they are exposed routinely to high concentrations of mutagenic oxygen radicals? Why would he have dictated that the mitochondrial genetic code must differ from the nuclear genetic code,