Few roads in the life sciences are straight and broad, and the way forward to prove and quantify the contribution of mitochondrial DNA damage to aging is turning out to be particularly winding. The open access paper noted below is the latest in a series of attempts to engineer mice that generate specific forms of mitochondrial mutation at an accelerated rate. The hope here is that this sort of study will, even if carried out for other reasons, help to clarify contradictory results obtained from prior lineages of mitochondrial mutator mice, but I’m not sure that any such goal has been achieved in this case. When compared with the theory of what is expected to happen as the result of a greater number of mitochondrial mutations, the results here are more of an additional puzzle than an answer to outstanding questions.
There is a herd of mitochondria in every cell, replicating like bacteria, and each carrying their own small circular genome – mitochondrial DNA. One important view of mitochondrial DNA mutation in aging is summarized in the SENS research proposals. In short, deletion mutations eliminate important mitochondrial genes, and an affected mitochondrion malfunctions