As the mysterious Mitochondria are considered the ‘powerhouses’ of many (including human) cells, would it be possible to increase longevity/health in humans by either genetic tinkering, or, ahem, ‘simply’ transplanting a superfit mitochondrian into a mother’s egg cell?
Like most visions of genetically engineering “super-humans,” the proposition is much more difficult than fixing genetic diseases with a known single-gene cause.
Evolution has already had many millions of years to work with mitochondria and ourselves to “optimize” their efficiency. Now, perhaps these mitochondria are optimized to the wrong focus. For example, our immediate ancestors had to cope with long periods of doubt and starvation, and presumably a slightly different organism will evolve to adapt to a period of constant food and water, but science certainly isn’t at the point now where we really know where to go.
So let’s look at mitochondria’s main job right now: the citric acid (Krebs) cycle.
http://web.indstate.edu/thcme/mwking/tca-cycle.html
So let’s pick a random enzyme, how about isocitrate dehydrogenase. I don’t know, but those people identify that as the enzyme that’s responsible for the rate limiting step in the TCA cycle, so this might be our, “weak link,” for our mitochondria. We know a fair bit about it, we know it’s structure:
http://www.pdb.org/pdb/cgi/explore.cgi?pdbId=1t0l
Pop quiz, hot shot, now what? Should you substitute residue 312 for a lysine to make the enzyme more efficient? What? Again, lots of trial and error (evolution) will be required and at this point scientists wouldn’t know what to do.
errrrrr…yes, let’s give that a whirl…
Your link appears to be mind-bogglingly complex, but I take it your point is that the processes within mitochondria, and between them and the host cell, are not understood to the point where one can tinker.
Does this also mean that high-functioning mitochondria cannot be identified and then cloned and implanted into egg cells? Or does the long-standing symbiosis mean that the resultant person would be a hybrid of the egg donor and the mitochondrian donor?
Without bothering to look it up, I’d make the reasoned guess that the subunits containing the active site of that enzyme are coded for by nuclear DNA, rather than the mitochondrial genome. Most mitochondrial proteins are coded in nuclear DNA.
That fact severely limits the utility of swapping out crummy old regular mitochondria for ‘supermitos’.
If I recall correctly, it is the case that some populations of humans have greater numbers of mitochondria per cell. If I further recall correctly, this is one of the adaptations to high altitude found in either the native population of the Andes or the Himalayas. But the mitochondria they have are more or less the same as everyone else’s.
Well, I learn something new every day.
This Wikipedia article was pretty informative:
“Mitochondrial DNA (mtDNA) is present in mitochondria as a circular molecule and in most species codes for 13 or 14 proteins involved in the electron transfer chain,…In total, the mitochondrion hosts about 3000 proteins, but only about 37 of them are coded on the mitochondrial DNA.”
According to this map [warning, PDF]
http://www.mitomap.org/mitomapgenome.pdf
the genes actually on the mtDNA include:
-NADH dehydrogenase
-Cytochrome C oxidase
-Cytochrome C oxoreductase
-ATP synthase
So, certainly some big and important ones that almost anyone that’s taken a survey biochemistry course will recognize, but apparently not our little friend isocitrate dehydrogenase.
So, long story short, Squink is right. If one were to try to optimize the performance of a mitochondrion, most of your gene targets would actually be upon chromosomal DNA rather than mitochondrial DNA.
But that’s not to say that maternal inheritance of “bad” mitochondria can’t screw things up.
So when any of these things go wrong, they can really screw things up but it doesn’t seem as if there’s much chance that genetically engineering “super-mitochondria” or selecting for high-performing mitochondria would do much good, again, because the enzymes that actually limit the upper end of mitochondrial performance are likely encoded on the chromosome.
The best analogy I can think of would be the parts of a car. The mtDNA might encode for the key and the shift-knob (which you’re screwed without) but it isn’t what dictate if your car is a Ferrrari or a Taurus, the chromosomal DNA does that.
More interestingly, some have greater numbers of midichlorians. 
There are several problems in your scenario. It may be that superfit mitochondria would be deleterious to health. After all the body should be in balance, and if one system works too fast that may not be good (e.g. think cancer). As others have said, it is not even clear how to engineer such a thing at the moment.
However, the mitochondria are the target of several experimental drugs to relieve oxidative stress (e.g. after surgery) and will be increasingly looked at in future in biomedicine.