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Author Topic:   Genetic Equidistance: A Puzzle in Biology?
molbiogirl
Member (Idle past 979 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 31 of 89 (597080)
12-19-2010 1:01 PM


Dr. Shi Huang
I've been reading his blog and some of his papers.
Just want to get some facts on the table.

Shi believes:

1. There are virtually no neutral mutations (only SNPs).
2. Coding DNA is 99.9% of the genome.
3. By "epigenetics" he means "epigenetics".
4. Sequence homology cannot be used to infer genealogical relationships.
5. Micro is the opposite of macro evolution.
6. There is no macroevolution going on right now.
7. There is a "60% maximum because any more mutations will hit the key residues and will abolish gene function and thus affect organism viability" (aka MGD) for all organisms.
8. "The more function a gene performs, the more functional constraints on its mutation, and the less the MGD for this gene."
9. "Humans are the pinnacle of both the tree of life and complexity" and are not apes.
10. Any exception to a "rule" in evolutionary theory negates the theory. Period.
11. MGD has no exceptions. Period.

And here's what Dr. Katz had to say when she reviewed one of his papers for Journal of Experimental Zoology Part B: Molecular and Developmental Evolution:

Dr. Katz writes:

Dear Dr. Huang,

I have now had a chance to read your manuscript and I regret that I am not recommending publication in JEZ-B. While the ideas presented are very intriguing, several key elements lack rigorous definitions and, as written, are inconsistent with observations from across the tree of life. For example, the view of phylogenetic diversity is more consistent with the Scala Natura than current understanding of the tree of life and the nature of biological diversity on Earth. Similarly, the treatment of the term complexity is simplistic at times. For example, limb number is certainly one measure of complexity (e.g. snakes vs. other reptiles) but, if "complex organisms are here defined as those that have complex epigenetic programs" then organisms like ciliates, which rely on epigenetic mechanisms to scan the last generation's somatic genome in forming the next generation's somatic genome, may also be worth considering. As written, the manuscript reads as if humans are the pinnacle of both the tree of life and complexity. Further, the treatment of genetic distance is also simplistic at times, particularly given what we know about patterns and processes driving molecular evolution across genomes.

I do hope that this quick turn around enables you to find a more appropriate journal for your interested manuscript without any unnecessary delay.

Sincerely

Laura Katz

His reply is telling. Some excerpts:

Shi writes:

You did not object to my outrageous statement in the paper that the MGD explains all relevant facts and has yet to meet a factual contradiction. You also did not object to my outrageous claim that the MGD is a better theory than all existing ones based on the best and only criterion that counts, which is to explain all facts and is contradicted by none. ... Therefore, the only realistic way of publishing the MGD is a book. If Darwin changed history by publishing a book, it may well take another book to reset history.

Edited by molbiogirl, : No reason given.

Edited by molbiogirl, : No reason given.


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molbiogirl
Member (Idle past 979 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 32 of 89 (597101)
12-19-2010 5:34 PM
Reply to: Message 29 by crashfrog
12-19-2010 12:28 PM


Re: The Crash Promise
Here are some of LM's thoughts on cytochrome c (from his blog, talkbio.blogspot.com, October 19 post):

Now, the idea that a neutral mutation in yeast is not necessarily neutral in say, humans, is consistent with observations from cytochrome c sequences.
I compared the cytochrome c sequence of two unicellular organisms: Naegleria gruberi and Dictyostelium discoideum.

Next, I aligned the cytochrome c sequence of two organisms as distant as the tuna and humans.

From the dot-matrix alignment and the ClustalX alignment one can see that there is obviously more sequence conservation in human and tuna cytochrome c than in the cytochrome c of the two unicellular organisms. This is what would be expected if a substitution in a unicellular organism was not necessarily neutral for a multicellular organism.

Have a look at the rest here, Crash:

http://talkbio.blogspot.com/search?updated-max=2010-11-04...


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molbiogirl
Member (Idle past 979 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 33 of 89 (597102)
12-19-2010 5:35 PM
Reply to: Message 26 by Livingstone Morford
12-19-2010 12:44 AM


Re: A General Response To Comments Regarding My Character
Is this one of the papers?

I submitted a manuscript to the Journal of the Royal Society Interface. My paper was a critique of a paper by Dryden et al. 2008, "How much of protein sequence space has been explored by life on Earth?"

https://docs.google.com/fileview?id=0B0x8Ne67j7k4NTZiNWY1...


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molbiogirl
Member (Idle past 979 days)
Posts: 1909
From: MO
Joined: 06-06-2007


Message 34 of 89 (597103)
12-19-2010 5:36 PM


Livingstone Morford's blog
For those who might be interested:

http://talkbio.blogspot.com/


Replies to this message:
 Message 36 by Dr Adequate, posted 12-19-2010 6:22 PM molbiogirl has not yet responded

  
Dr Adequate
Member
Posts: 16107
Joined: 07-20-2006
Member Rating: 8.3


Message 35 of 89 (597105)
12-19-2010 6:13 PM
Reply to: Message 30 by crashfrog
12-19-2010 12:32 PM


I don't think a priori you can make such a statement, since there's too many confounding factors. Most proteins in the cell have no idea whether they're in a liver cell, or a brain cell, or a pancreatic cell.

Well, all of them have "no idea", poor little things. But all that is necessary is that some mutation which is neutral with respect to one cellular environment should be harmful in another (in which it is also expressed, otherwise examples, while commonplace, would also be irrelevant).

For example, here's an account of the research of one Kevin Talbot:

The commonest and most debilitating of these diseases is amyotrophic lateral sclerosis, which is relentlessly progressive and fatal on average 3 years after onset. The key question for our research is why mutations in genes which are expressed in every cell in the body result in specific and selective degeneration of motor neurons. Using primary neuronal cell culture systems his group has explored the effect of mutant small heat shock protein on axonal function. Mutations in the gene for glycyl tRNA synthetase lead to another form of lower motor neuron degeneration. He is using a combination of structural, biochemical and cellular studies to understand why mutations in a ‘house-keeping’ gene expressed in all cells lead to specific neuronal degeneration.

It would seem, then, that the mutations he's studying would be neutral in an organism too primitive to have motor neurons.

Obviously cell environment has an effect on which mutations prove to be deleterious, because some of that effect is the result of changes in a protein's interactions with other components of the cell environment. But to predict the effect of diversity of cell environment on a mutated protein (and vice-versa) you need a finer-grained study than "liver cell; muscle cell."

Yes ... but we don't need to be able to predict the effects of a mutation to support the thesis that number of cell types correlates inversely with neutrality of mutations.

Well, it's a standard practice in constructing phylogenies to use proteins with identical function across the compared clades. That would seem to rule out any effect of diversity of cell environment.

The site quoted above specifically mentions glycyl-tRNA synthetase. This, as the name suggests, attaches glycine to transfer RNA with glycine antocodons. Hence glycyl-tRNA synthetase performs a very basic (and ancient) function --- which is the same function performed by glycyl-tRNA synthetase in prokaryotes. And yet there are mutations to it which apparently in humans only produce problems with motor neuron cells.

---

The questions remain: what is the magnitude of this proposed effect? And how on Earth are IDiots weaving this hypothesis into their tissue of nonsense? I don't see how this would help them any.


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Dr Adequate
Member
Posts: 16107
Joined: 07-20-2006
Member Rating: 8.3


Message 36 of 89 (597108)
12-19-2010 6:22 PM
Reply to: Message 34 by molbiogirl
12-19-2010 5:36 PM


Re: Livingstone Morford's blog
For those who might be interested:

http://talkbio.blogspot.com/

I notice that his subtitle is "The biological ramblings of a dwarf struggling to stand on the shoulders of giants."

"Stand on the shoulders"? Shouldn't that be "kick at the ankles"?


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Livingstone Morford
Junior Member (Idle past 3111 days)
Posts: 28
From: New Mexico
Joined: 12-13-2010


Message 37 of 89 (597109)
12-19-2010 6:27 PM
Reply to: Message 29 by crashfrog
12-19-2010 12:28 PM


Re: The Crash Promise
Due to the large volume of responses to my posts, I will respond to those posts which I think are the most pertinent and most important to this topic. If someone feels like their post deserves a response, please inform me.

That said,

quote:

Cytochrome c isn't in the environment of the cell, it's buried deep in the intermembranous space of the mitochondria, and from that perspective all cells are basically the same.

Although the cytochrome-c is located in the mitochondria, this does not imply that it does not have an affect on biological activity outside the mitochondria.

quote:

I think the most fruitful line of attack is the way in which you characterize a deleterious substitution mutation as an "incompatibility with cell type." I think this is a unclarifying way to look at mutations. A deleterious amino acid substitution in cytochrome c, for instance, is going to be lethal to the cell regardless of cell type because electron chain activity is critical for meeting the cell's energy budget… Some number of mutations are going to be deleterious because they change the way the protein interacts with other components of the cell, or they may introduce a new interaction with the cell, but actual cell type isn't going to have much to do with that. Interaction-based deleteriousness happens at a finer grain of cellular environment than "this is a liver cell; this is a muscle cell."

You suggest that there is no such thing as a substitution that would be incompatible with the cell type. Or more precisely, that the harmful affects of a substitution (or other type of mutation, so long as it is not synonymous) are not exclusive to only certain tissues. However, observations from biology tell a different story. Can your position be reconciled with say, the observation that brain specific genes evolve slower than immune specific genes, or that members of the nAChR family are more constrained when they are in the central nerve system than those in the peripheral nerve system? With respect, I beg to differ on the grounds that your position will have difficulty in explaining away the data presented by Miyata et al. (1994), where we see that:
“A molecular phylogenetic analysis of tissue specific isoforms that are identical to one another in function but differ only in tissue distribution revealed frequent gene duplications and rapid accumulations of amino acid substitutions during the early evolution of chordates where rapid evolution at the tissue or organ levels is thought to have occurred.”

And,
“Members that are virtually identical to each other in function, but differ only in tissue distribution often form a single cluster (subgroup) on the phylogenetic tree.”
And,
“As we showed above, molecules are constrained more or less from tissues or organs (i.e., global constraint) and liberation of functional constraints at the tissue level result in the rapid accumulation of genetic variations as demonstrated by the blind mole rat crysallin [Hendrik et al., 1987]. Thus the relaxed constraint at the phenotypic level in the early evolution of chordates may permit many isoform duplications as well as rapid accumulation of amino acid substitutions.”

Also, you might want to explain away the observations made by Zhang and Li (2004),
“Do housekeeping genes, which are turned on most of the time in almost every tissue, evolve more slowly than genes that are turned on only at specific developmental times or tissues? Recent large-scale gene expression studies enable us to have a better definition of housekeeping genes and to address the above question in detail. In this study, we examined 1,581 human-mouse orthologous gene pairs for their patterns of sequence evolution, contrasting housekeeping genes with tissue-specific genes. Our results show that, in comparison to tissue-specific genes, housekeeping genes on average evolve more slowly and are under stronger selective constraints as reflected by significantly smaller values of Ka/Ks.”

According to Kuma et al., 1995:
“…we compared evolutionary rates of kinase domains between members of the Ig family and showed evolutionary properties characteristic of family members: a wide difference of evolutionary rates among members, a correlation of evolutionary rates between different domains in a molecule, and the tissue dependence of evolutionary rate. These evolutionary properties could not be understood by local constraint along, but rathery they suggest the presence of a global constraint derived from higher levels like tissues or organs, because the structure and function of the kinase domain and those of the Ig domain are similar between different members. Thus the evolutionary rates are expected to be similar between members, if the global constraint is less important.”

Also,
"Evidence suggests the presence of an alternative constraint derived from higher levels: cells and tissues consist of many molecules, interacting directly or indirectly with each other. Functional alternations of molecular would influence more or less the functions of higher levels like cells or tissues where the molecules are involved…We report here evidence suggesting that the global constraint derived from higher levels like tissues or organs actually exist and that the evolutionary rates of family members are strongly influenced by tissues where they are expressed specifically.”

And,
“To maintain normal physiological functions, different tissues may have different developmental constraints on expressed genes. Consequently, the evolutionary tolerance for genomic evolution varies among tissues. Here, we formulate this argument as a "tissue-driven hypothesis" based on the stabilizing selection model. Moreover, several predicted genomic correlations are tested by the human-mouse microarray data…for genes with the same expression broadness, we found that genes expressed in more stringent tissues (e.g., neurorelated) generally tend to evolve more slowly than those in more relaxed tissues (e.g., hormone-related). We conclude that tissue factors should be considered as an important component in shaping the pattern of genomic evolution and correlations.” (Gu and Su, 2007)

Until these observations can be explained away, I believe that I am compelled to hold to the position that a neutral substitution in a simple organism is not necessarily neutral when that protein is present in more cell types.

In passing, I might add that Newgard et al. (1986) report that mammalian genes present in muscle tissue have a higher G+C content than those genes expressed in the liver.

References:

Miyata T, Kuma K, Iwabe N, Nikoh N. A possible link between molecular evolution and tissue evolution demonstrated by tissue specific genes. Jpn J Genet., 69(5):473-80 (1994).

Hendriks W., et al. The lens protein alpha A-crystallin of the blind mole rat, Spalax ehrenbergi: evolutionary change and functional constraints. PNAS, 84(15): 5320–5324 (1987).

Zhang Liqing, Wen-Hsiung Li. Mammalian Housekeeping Genes Evolve More Slowly than Tissue-Specific Genes. Molecular Biology and Evolution, 21(2): 236-239 (2004).

Kuma K, Iwabe N, Miyata T. Functional constraints against variations on molecules from the tissue level: slowly evolving brain-specific genes demonstrated by protein kinase and immunoglobulin supergene families. Mol Biol Evol., 12(1):123-30 (1995).

Gu X, Su Z. Tissue-driven hypothesis of genomic evolution and sequence-expression correlations. PNAS, 104(8):2779-84 (2007).

Newgard C.B., et al. Sequence Analysis of the cDNA encoding human liver glycogen phosphorylase reveals tissue-specific codon usage. PNAS, 83(8): 8132 – 8136 (1986).

Edited by Livingstone Morford, : No reason given.

Edited by Livingstone Morford, : No reason given.


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crashfrog
Inactive Member


Message 38 of 89 (597110)
12-19-2010 6:33 PM
Reply to: Message 37 by Livingstone Morford
12-19-2010 6:27 PM


Re: The Crash Promise
Although the cytochrome-c is located in the mitochondria, this does not imply that it does not have an affect on biological activity outside the mitochondria.

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

You suggest that there is no such thing as a substitution that would be incompatible with the cell type.

No, I don't suggest that. I suggested the exact opposite - that there were many mutations whose degree of deleteriousness depends entirely on the interactions of the protein with other cellular components. In fact you quoted me saying precisely that. So why pretend that I'm saying something that I'm not?

And you were starting out so well.

Until these observations can be explained away

This is a great deal of observation marshaled against a position I don't hold. You'd do a lot better trying to find evidence for your own position.


This message is a reply to:
 Message 37 by Livingstone Morford, posted 12-19-2010 6:27 PM Livingstone Morford has responded

Replies to this message:
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Livingstone Morford
Junior Member (Idle past 3111 days)
Posts: 28
From: New Mexico
Joined: 12-13-2010


Message 39 of 89 (597111)
12-19-2010 6:39 PM
Reply to: Message 38 by crashfrog
12-19-2010 6:33 PM


Re: The Crash Promise
quote:

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

At the fundamental level, everything in the cell is connected. That does not mean that there is a direct effect on biological activity outside the mitochondria.

quote:

No, I don't suggest that. I suggested the exact opposite - that there were many mutations whose degree of deleteriousness depends entirely on the interactions of the protein with other cellular components.

So do you, or do you not, agree that a substitution in a protein in one cell type can have a different effect if that same substitution occurred in the same protein but in a different cell type?


This message is a reply to:
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Replies to this message:
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crashfrog
Inactive Member


Message 40 of 89 (597115)
12-19-2010 6:47 PM
Reply to: Message 39 by Livingstone Morford
12-19-2010 6:39 PM


Re: The Crash Promise
At the fundamental level, everything in the cell is connected.

In many cases, the cell can only function because things are not connected. A cell with no ability to sequester some molecules from others is a cell that rapidly enters chemical equilibrium with its environment - i.e., dies.

That does not mean that there is a direct effect on biological activity outside the mitochondria.

Well, ok, but a minute ago you seemed to be reasoning from the assumption that there was.

So do you, or do you not, agree that a substitution in a protein in one cell type can have a different effect if that same substitution occurred in the same protein but in a different cell type?

This is certainly something that happens. There's not any reason to think that it happens in enough cases to substantially throw off our confidence in molecular phylogenies.


This message is a reply to:
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Replies to this message:
 Message 42 by Livingstone Morford, posted 12-19-2010 7:09 PM crashfrog has responded

  
Dr Adequate
Member
Posts: 16107
Joined: 07-20-2006
Member Rating: 8.3


Message 41 of 89 (597118)
12-19-2010 6:59 PM
Reply to: Message 37 by Livingstone Morford
12-19-2010 6:27 PM


I still don't see what this has to do with cdesign proponentism. Perhaps you could explain. So far as I can see, you are proposing that an eminently Darwinian mechanism would plausibly account for certain observations. There is nothing in such a suggestion to keep a biologist awake at night or give consolation to a crank.

Am I missing something?


This message is a reply to:
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Livingstone Morford
Junior Member (Idle past 3111 days)
Posts: 28
From: New Mexico
Joined: 12-13-2010


Message 42 of 89 (597120)
12-19-2010 7:09 PM
Reply to: Message 40 by crashfrog
12-19-2010 6:47 PM


quote:

In many cases, the cell can only function because things are not connected.

And..? There are still many biological networks involved in the cell.

quote:

Well, ok, but a minute ago you seemed to be reasoning from the assumption that there was.

There is a difference between a direct effect and a mere effect, however discernible.

quote:

This is certainly something that happens. There's not any reason to think that it happens in enough cases to substantially throw off our confidence in molecular phylogenies.

Okay, so finally we agree on one thing: and that is that a neutral substitution in a protein in one cell type is not necessarily neutral in another. It happens enough to be detected in phylogenetic analysis [e.g., Miyata et al., 1994]. I cited six papers to the effect that tissues do constrain the substitutions in proteins – in some cases tissues constrain a protein one hundred times more than other tissues [Kuma et al., 1995].

References:

Miyata T, Kuma K, Iwabe N, Nikoh N. A possible link between molecular evolution and tissue evolution demonstrated by tissue specific genes. Jpn J Genet., 69(5):473-80 (1994).

Kuma K, Iwabe N, Miyata T. Functional constraints against variations on molecules from the tissue level: slowly evolving brain-specific genes demonstrated by protein kinase and immunoglobulin supergene families. Mol Biol Evol., 12(1):123-30 (1995).


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Replies to this message:
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Livingstone Morford
Junior Member (Idle past 3111 days)
Posts: 28
From: New Mexico
Joined: 12-13-2010


Message 43 of 89 (597121)
12-19-2010 7:12 PM
Reply to: Message 41 by Dr Adequate
12-19-2010 6:59 PM


“I still don't see what this has to do with cdesign proponentism.”

So I guess because I happen to disagree with the orthodox view that the phenomenon of genetic equidistance is best explained by the time lapsed since divergence, and since I am proposing another model, that all of a sudden means that I am using this as evidence for intelligent design?

“Am I missing something?”

Yes.


This message is a reply to:
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crashfrog
Inactive Member


Message 44 of 89 (597126)
12-19-2010 7:48 PM
Reply to: Message 42 by Livingstone Morford
12-19-2010 7:09 PM


There are still many biological networks involved in the cell.

Yes, there are. The cell is such a complex place that you really can't say, except in the specific, whether or not mutations are related to cell type diversity.

Okay, so finally we agree on one thing: and that is that a neutral substitution in a protein in one cell type is not necessarily neutral in another

I don't believe that you can make that characterization. There are definitely proteins for which that is apparently true, like tRNA-glycine amino-acyl transferase in humans. There are proteins for which that doesn't seem to be true, like cytochrome c or ribosomal subunit 16S. The only reason to expect that a putative molecular phylogeny is going to be confounded by cell diversity effects is if the phylogeny is constructed on the basis of proteins that have that kind of relationship with their cellular environment.

Are they?

It happens enough to be detected in phylogenetic analysis

When you look at tissue-specific genes. That's not in dispute. What's in dispute is that all genes on which phylogenies are constructed are tissue-specific. They are, in fact, not.


This message is a reply to:
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Dr Adequate
Member
Posts: 16107
Joined: 07-20-2006
Member Rating: 8.3


Message 45 of 89 (597129)
12-19-2010 8:09 PM
Reply to: Message 43 by Livingstone Morford
12-19-2010 7:12 PM


So I guess because I happen to disagree with the orthodox view that the phenomenon of genetic equidistance is best explained by the time lapsed since divergence, and since I am proposing another model ...

It's not clear that that's what you are doing. Thus far, clarity has not been your strongest suit.

... that all of a sudden means that I am using this as evidence for intelligent design?

No, but your blog where you say that you're an "staunch proponent of intelligent design" and the fact that you seem to have drawn your idea from an IDiot suggest that there may be some relationship between ID and whatever idea it is that you're currently advocating.

If you will clearly and distinctly say that none of this is evidence for ID then I shall not ask you any further questions about their possible connection.


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