Genetic Equidistance: A Puzzle in Biology?

My Message 19 which refutes your estimate of the expected overlap in the locations in differences between human and alligator and human and frog cytochrome c (from your Message 11). Except that I now believe that I can do better.A mutation in the lineage from the most recent common ancestor with the alligator should be expected to show as a difference with both other lineages. The chance that it will be "masked" by one of the other lineages mutating to have the same residue at that location is relatively small, and offset by other ways in which an overlap could be found. Thus the size of the overlap should be close to the number of mutations in the human lineage since the last common ancestor wit the alligator.If genetic equidistance is explained by mutations accumulating at the same rate in each lineage we would therefore expect half of the 13 differences between human and alligator to be shared with the frog. Which is 6-7, in close agreement with the actual figure of 7. Obviously this data poses no problem for the mainstream view at all - it is completely unsurprising..We should also note that since the size of the overlap is dominated by the number of changes in the human lineage, and that number is on the high side of the expected value, any hypothesis that predicts that the human lineage should show fewer changes than the other two DOES have a problem with this data.Edited by PaulK, : Restoring the parts that mysteriously vanished

It's involved in apoptosis*, when released from the mitochondria it complexes with Apaf-1 and a few other bits to form the apoptosome.* - a form of cell death that is directed by the cells own processes, aka programmed cell death. See HERE Technologies | The world's #1 location platform for a pretty video.Edited by Mr Jack, : Subtitle

1. Do you agree with Dr. Huang that there are .1% neutral mutations in the genome? If so, how do you explain your response in Message 12?2. Do you agree with Dr. Huang that humans and orangs are "of different biological complexity"? If so, why?3. Do you agree with Dr. Huang that sequence homology cannot be used to infer genealogical relationships? If so, why?4. Do you agree with Dr. Huang that any exception to a biological "rule" negates that rule?Edited by molbiogirl, : No reason given.

What effect? And please support your assertion with cites. It's a far cry from "There is some constraint" to "All mutations are deleterious in all cases".Please provide cites that support your contention that all mutations are deleterious in all tissues in all cases.

The idea that different proteins evolve at different rate is not new. The modern molecular clock | Nature Reviews GeneticsPlease explain to me how slow genes are a problem for the molecular clock.Please provide cites.And no, a cite that suggests the mere existence of slow genes is not enough.

Is that in fact his contention? If so, I missed it.

What I meant to say is "Please provide cites that support your contention that all deleterious mutations are deleterious in all tissues in all cases."My bad.And, as he is parroting Dr. Huang's assertions, I can only assume he agrees with Dr. Huang that SNPs are the only neutral mutations.Dr. Huang is quite adamant that there are virtually no neutral mutations. .1% in fact.Which means that 99.9% of all mutations are either beneficial or deleterious. I'd like him to provide support for that assertion too.

It smells like the "only reduction in info since The Fall" arguments, dontcha think?ABE: Well, maybe not. But the whole "there's a limit to how much mutation can happen" argument does go hand in hand with it.Edited by Catholic Scientist, : No reason given.

The paper LM is relying on, Huang, S. (2009) Inverse relationship between genetic diversity and epigenetic complexity, has not been peer reviewed.Nature Precedings Nature PrecedingsABE: Whoa. Just found this in the conclusion of the "paper". Does not need independent validation!!!I knew it. The guy has no data. No support.And Shi got banned on another site because he refused to support his assertions: Science and Religion Forum - InformationEmphasis added.Edited by molbiogirl, : No reason given.Edited by molbiogirl, : 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.

As I pointed out, upthread, this is incorrect. Cytochrome c is involved in apoptosis. It binds to Apaf-1, and forms the apoptosome. Um, no, not so. edit: (btw: if you think about it you knew this already, how could a mitochondrion trigger the autophagic pathways you mentioned in another post without interacting with other cellular elements?)Edited by Mr Jack, : Added aside

Cytochrome c is encoded by nuclear DNA* and imported into the mitochondria, rather than encoded by the mitochondria DNA itself. While what you describe here would be true for the four transport proteins themselves, it is not true for cytochrome c.* Specifically, in humans, by the CYCS gene located on chromosome 7.

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).