Mitochondrial DNA in the Nucleus and Species Life Span Differences
A large merged double edition of the journal Rejuvenation Research is now online, bringing with it a lot of papers to look through. I thought I'd direct your attention to one of those many papers, as it presents an interesting evolutionary background to the SENS approach to the mitochondrial DNA damage that accumulates with age.
Our mitochondria are biological power plants within our cells, the evolved descendants of symbiotic bacterial species. They convert food into ATP, the chemical used as fuel by cells. Mitochondria have their own DNA, a relic left over from when they were some form of free-living species. Over time, portions of that mitochondrial DNA have become incorporated into our own nuclear DNA at the heart of the cell. By evolutionary considerations, these changes must have prospered and spread because they provided some form of advantage. One thing to consider in this respect is that nuclear DNA is far better protected from damage than mitochondrial DNA. Indeed, one root cause of aging is that our mitochondrial DNA is battered over the years by side-effects of the chemical reactions that produce ATP. This is not a problem suffered by nuclear DNA to anywhere near the same degree.
So what is the result of more mitochondrial DNA showing up in the armored cell nucleus? As it turns out, there is a good argument that the result is a longer life. The researchers here find a strong correlation between more mitochondrial DNA in the nucleus and longer life span for a species:
NUMT ("New Mighty") Hypothesis of Longevity
Maximum life span (MLS) and abundance of mitochondrial DNA (mtDNA) insertions in the nuclear DNA (NUMTs) were analyzed in 17 animal species with completely sequenced mitochondrial and nuclear genomes. Highly significant positive correlations were found between MLS and NUMT number, total size, or density (both in mammals and all animal species).
This is most interesting when you consider that the SENS approach to removing the contribution of mitochondrial DNA damage to aging is exactly this: copy the remaining vital mitochondrial genes into our nuclear DNA. If the necessary proteins encoded by these genes are still being produced by the cell and delivered to the mitochondria even after the mitochondrial gene is somehow damaged, then that damage will have no effect.
Muradian, K., Lehmann, G., & Fraifeld, V. (2010). NUMT (“New Mighty”) Hypothesis of Longevity Rejuvenation Research, 13 (2-3), 152-155 DOI: 10.1089/rej.2009.0974