Genetic Equidistance: A Puzzle in Biology?

Mr. Morford,I was trying to think of a way to test your ideas. I was thinking of comparing sponges, mammals, and fungi to see if they were genetically equidistant. Sponges do have a limited set of genes that control development, but they are primitive compared to the gene regulation and development pathways found in mammals. Does this sound like a good test?Edited by Taq, : No reason given.

However, if there is constraint on the sequences due to a more complex gene regulation network in the human clade then humans should be closer to fungi than sponges are. This is due to harsher selection (therefore fewer substitutions) in the mammalian clade compared to the simpler sponge. Wouldn't you agree?

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.We also have the fact that cytc from one species can be used in another distantly related species.

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In fact, the cytochrome c genes from tuna (fish), pigeon (bird), horse (mammal), Drosophila fly (insect), and rat (mammal) all function in yeast that lack their own native yeast cytochrome c (Clements et al. 1989; Hickey et al. 1991; Koshy et al. 1992; Scarpulla and Nye 1986).
29+ Evidences for Macroevolution: Part 4

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Mr. Morford needs to include this in his model as well. Why is it that cytc from a rat can replace the cytc in a yeast cell without any problems occuring.Edited by Taq, : No reason given.

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. The mitochondria can be seen as the battery of the cell. As long as it is putting out the correct amperage and voltage the cell doesn't care how it is designed on the inside. The only interaction the cell has with the mitochondria is the energy it pumps out.

Fair enough, but this is a pathway for cell death, not cell function or epigenetic function as Mr. Morford has stressed. The only constraint is the ability of proteins in the apoptosis pathway to recognize specific mitochondrial proteins. I was focused more on cell function, not cell dysfunction followed by cell death (or destruction of dysfunctional mitochondria). The argument put forward by Mr. Morford is that proteins are constrained due to DNA regulatory pathways which are more complex in the vertebrate clades. Cytc has nothing to do with embryonic development. Even the apoptotic pathways used in embryonic development (e.g. destruction of the postanal tail) do not involve cytc (as far as I know).

It appears I need to study up on the mit genome. Thanks for the correction.

I agree. However, every cell with mitochondria expresses cytc. Therefore, cytc can not be used to differentiate tissues or initiate specific developmental apoptotic pathways. Is it possible that cytc is involved further down in the pathway beyond initiation? Very possible. However, it is the initiation of the pathway during development that is important.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.