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Thursday, 30 June 2011
Mitochondria are bacteria that wandered into each of our cells about two billion years ago and set about making themselves indispensable.
They still reproduce separately from the rest of us, though. All your mitochondria came from your mother via her egg. They exist in sperm, too, and those sperm mitochondria enter an egg when it's fertilised, but then they are assassinated.
The mechanism of that assassination is superficially understood: ubiquitin is tacked onto the sperm's mitochondria in the egg, which marks their proteins for destruction. But as far as I have been able to find out, no one knows what it is in the egg that does the ubiquitin attachment.
I'd lay a hefty (well, a few quid...) bet that it is the egg's mitochondria that do the dirty deed. Look at things from the evolutionary perspective: the egg's mitochondria are in a secure comfortable environment with plenty of resources (a whole big egg) when along come some unrelated interlopers that will compete with them for lebensraum. But those interlopers are exhausted after powering a very long swim in a midget submarine, and their defences are low. Best exterminate them now before they recover.
And suppose some sperm mitochondria mutated to put energy into developing defences. Of course, their sperm would come last in the race as a consequence, so the forearmed mitochondria would never reach the egg in the first place.
The main nuclear genetic material in both the egg and the sperm have no dog in this fight - they don't care where they get their mitochondria from. So they look on dispassionately and don't take sides.
The trouble with this arrangement (from our perspective) is that mutations can accumulate in our mitochondria because there is no sexual combination going on to allow such mutations to be shelved as recessive and all the other shuffling advantages that sex confers. The results are many different types of mitochondrial disease such as early-age diabetes with deafness, various neuromuscular conditions (some fatal), certain epilepsies and - well; the list goes on.
What can we do? We can't attempt to give the sperm's mitochondria an effective defence against ubiquitination so that we all end up with two types of mitochondria from egg plus sperm, at least half of which ought to work. Any defence that we cook up will be at an evolutionary disadvantage for the reasons outlined above. It will not be evolutionarily stable.
Instead let's confiscate all the mitochondrias' DNA and save it as extra genes in our cell neuclei. Those genes would still build the protiens that would make mitochondria in our cells. But those mitochondria would have no genetic material of their own. They would just be a useful cell structure like many others.
Now, of course, those extra genes could have alleles, and could be equally inherited from both parents. This would allow much more variation and recombination than is possible with the - essentially bacterial - way that mitochondria reproduce at the moment, which in turn would make things far more robust and less prone to inherited disease.