Genetic Equidistance: A Puzzle in Biology?

I’m not sure you get the gist of my argument. For example, an ontogenic amino acid substitution in a human protein must be compatible with every one of the different cell types found in the human organism (every cell, that is, that contains the protein), while an amino acid substitution in say, a yeast protein must be compatible with only one cell type.
An analogy may (in a theoretical sense) be useful here. Say you have protein A. And you have cell type X, Y, and Z. Any substitution mutation in protein A must be compatible with all three cell types. Meanwhile, if you only have cell type X, then protein A needs only to compatible with X (analogy a la Dr. Shi Huang).

Genetic distance is measured primarily on non-coding regions to minimize the effect of selection, so, by definition, your model of equidistance being the result of increased selection against mutations in more complex organisms is false.

What direct effect does cytochrome c have on biological activity outside the mitochondria?

Cytc does not interact with any intracellular proteins outside of the mitochondria.

The only affect the mitochondria has on the cell is the ATP and other cofactors that it produces.

Chances are, a mitochondria that has a broken cytc gene will be processed through autophagy pathways. Dysfunctional mitochondria release specific triggers (a molecular version of a dead man's switch) that start the autophagy pathways. The mutation in that cytc gene will not get passed on to further generations of mitochondria. All of this occurs without the need for cell death.

What would be interesting is to see how specific the binding is between cytc and and the triggers of the apoptotic pathway. Is it possible to switch cytc or the apoptotic proteins that bind to cytc between distantly related organisms? That would be interesting.