I hope it is that simple, but prudence tells me that I cannot assume that, I must see it verified in experiment.If this question means something like if 50 subunits are needed, how do we assure one mito does not get 75 subunits, while another one gets only 25, then the answer is simple. We don't. For statistical reasons, distributions close to the average are just much more likely than distributions that are far away. This is ultimately due to the same forces that drive the universe towards ever increasing entropy, but I would recommend to google a little bit for introductory thermodynamics, which can be quite revealing about this kind of phenomena.
There are a great many reasons I can think of why mitochondria will not require relatively similar amounts of various proteins at various times.
First, and simplest, is that I don't know if protein turnover is a continuous, stochastic process, or if it comes and goes. In other words, does a mitochondrion occassionally do "spring cleaning", replacing worn out protein parts? If so, is this activity synchronized among all the mitochondria in a cell, or do some actually have higher demands for replacement proteins from time to time?
Second, rebuilding, repair, division. When a mitochondrion divides, I'm assuming that the two new daughter organelles will require a higher influx of proteins parts for the next few hours.
Third, usage. For all I know, mitochondria that happen to be close to power hungry systems (the nucleus maybe, or ribosomes, or lysosomes, or...) might have a higher workload, and hence a higher protein turnover rate.
Fourth, size. As little as a 7% increase in linear dimensions can add more than 20% to a mitochondrion's volume, and hence it's protein needs, relative to another mitochondrion.
Fifth, density of mitochondria distribution within a cell. If a certain region has a higher density of mitochondria (for function reasons, since statistically the distribution should be fairly uniform, albeit lumpy at the local level), and if the distribution of proteins is fairly uniform, then mitochondria in low density regions will get more proteins.
The list could go on and on. Some of the items on the list may not be concerns. Others definitely will be.
So I can't rely on statistical distribution to fix the problem. We need to know that there is a system that not only ensures proper transport into a mitochondrion upon arriving at one (which de Grey covered), but that we get the proteins to the mitochondria in the first place.
Now, if nature doesn't already have machinery to do this, but relies instead on statistical uniformity to get the job done, then there's no work on our part. BUT, if there IS an existing machinery to cause a non-uniform distribution of proteins, then we must ensure that the 13 new allotropic genes take advantage of that same machinery.
Again, I'm not talking about a practical hurdle, just a scientific difficulty (more work), so don't mistake this for the type of criticism that I've given to WILT. I happen to agree with allotropic expression of mtDNA genes. I'm merely trying to ensure that we have all the basic science out of the way. If not, we may be underestimating the difficulty of allotropic expression versus another method.
If these ideas have already been covered by the SENS participants, I apologize. I am beginning to download the presentations, and I will try to get myself caught up on the science in the coming weeks. So while I have many more criticisms, I will save them until after I've made sure that I'm not rehashing old issues.
But, I had to address this one issue, since the issue was already in discussion.