This study shows that the mtDNA variant in the individual has a great effect on its interaction with the nuclear DNA. This finding is contrary to what was thought of the effect of mitochondrial replacement.
On 6th July this year, investigators at the National Centre for Cardiovascular Research (CNIC) in Madrid published an article in Nature (read HERE). They showed that mice bred so that their nuclear DNA and mitochondrial DNA (mtDNA) derive from different strains tend to age with better health than mice whose nuclear and mtDNA correspond ancestrally.
Besides knowing that mtDNA is involved in obtaining cell energy, very little is known about the effect that it might have on the characteristics of organisms. This lack of knowledge has been used to claim that mtDNA has no function but this, an argument exploited to support the advance of mitochondrial replacement techniques, despite the ethical concerns that they raise.
This study shows that the mtDNA variant in the individual has a great effect on its interaction with the nuclear DNA. Which in turn affects the synthesis, functionality, and half-life of the mitochondrial proteins, oxidative stress, insulin signaling, obesity and the parameters of aging (including telomere shortening and mitochondrial dysfunction), resulting in profound differences in longevity.
Therefore, it does not seem prudent to continue moving forward in the application of mitochondrial replacement techniques in humans when there is still so much to discover about mtDNA, and more so when the intention is not to treat sick people but to produce new individuals in vitro.