Short-Lived Species Might Not Be Much Use in Deciphering the Role of Mitochondrial DNA Damage in Aging
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Mitochondria are the power plants of the cell, responsible for producing the energy store molecule ATP that powers cellular operations. Hundreds of these organelles can be found in every cell, the distant descendants of symbiotic bacteria long ago integrated into core cellular mechanisms. They contain their own small remnant genome, and when worn or damaged, they are broken down and recycled by cellular maintenance mechanisms. Mitochondria reproduce by fission like bacteria, but also fuse together at times, and promiscuously swap component parts among one another. Cells can also transfer mitochondria between them. This makes it something of a challenge to track the consequences of mitochondrial damage in aging.

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Mitochondrial DNA is more vulnerable and less capable of repair than the nuclear genome deeper inside cells. Some forms of random damage can knock out mitochondrial genes necessary for the most efficient form of energy production. Mitochondria with this particular problem are inefficient, but also somehow more likely to replicate than their peers: they either evade maintenance processes, or perhaps replicate more rapidly. A cell can be quickly taken over by broken mitochondria running inefficient, harmful forms of energy production. The cell becomes dysfunctional and exports damaging, oxidative molecules into the surrounding tissue.

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