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Author
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Topic: The IHE
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Mike Gene
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Member # 149
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posted 01. January 2003 12:41
I have argued that the genetic code may have been designed to exploit the mutagenic bias that exists as a consequence of cytosine deamination. In my original analysis, I noted that the genetic code uses cytosine deamination to channel mutations such that they sample from an pool of amino acids that is almost exclusively hydrophobic (IHE or Increasing Hydrophobicity Effect). Furthermore, this pool is biased toward facilitating secondary structure formation. If coupled with carefully chosen initial proteomes, the potential exists that the first major evolutionary steps subsequent to the originally designed state where rigged such that the mutational bias could untap secondary designs that were front-loaded into the original state. For example, this might mean that something like the evolution of multicellularity (and perhaps more) was designed through this biased mutagenic effect.
The first step in testing this hypothesis is to determine whether the IHE plays out in evolution. Since the genetic code is universal, we might expect to see residual traces of this effect even if the sole intention of the design was to guide the first major evolutionary steps. Two extensive analyses have indeed uncovered the IHE in action (although neither paper makes the connection I did in my original analysis).
I'll begin by discussing the first one: Gregory A. C. Singer and Donal A. Hickey. 2000. Nucleotide Bias Causes a Genomewide Bias in the Amino Acid Composition of Proteins. Molecular Biology and Evolution 17:1581-1588
Since evolution through cytosine deamination essentially entails replacing guanine and cytosine (G and C) with adenine and thymine (A and T), it would be interesting to compare the proteomes of GC-rich and AT-rich genomes.
Luckily, this analysis has already been done by Singer and Hickey.
They begin by noting:
quote:
Some organisms, for example, have genomes that are disproportionately rich in guanine and cytosine (G and C), while others have DNA that is rich in adenine and thymine (A and T). Variation in nucleotide composition is usually most pronounced at the synonymous codon positions of genes, and, because of the redundancy in the genetic code, these variations in DNA content may have little effect on the amino acid content of the encoded proteins.
Singer and Hickey then partitioned the genetic code into GC-rich and AT-rich codons. They noted the AT-rich codons would encode phenylalanine, tyrosine, methionine, isoleucine, asparagine, and lysine (FYMINK) while the CG-rich codons would encode glycine, alanine, arginine, and proline (GARP). While the amino acid pools are not the same ones I identified in as the pre- and post-cytosine deamination codons (given the codons they looked at were enriched with AT or GC), there is an overlap, where the AT-rich codons contain mostly hydrophobic residues.
Singer and Hickey then looked at 22 completely sequenced genomes to determine if GC-rich genomes would have proteins that are enriched with GARP amino acids and AT-rich genomes are enriched with FYMINK amino acids. This is exactly what they found.
They took a closer look at Borrelia burgdorferi and Mycobacterium tuberculosis , which have a 25.5% and 65.9% GC content, respectively. These thus represented the two ends of the extreme. They compared 305 genes common to both organisms and measured the synonymous nucleotide frequencies and amino acid contents of each one. They found, "For every gene, the GARP/FYMINK ratio in the M. tuberculosis homolog was higher than that of the corresponding gene in B. burgdorferi".
The authors conclude, Our main finding is not just that protein composition is affected by nucleotide bias, but also that this effect is both very large and very widespread. In fact, they observe:
quote:
When we plotted the relationship between nucleotide bias and amino acid content for the entire set of genomes examined, we were surprised to see that there was no "clumping" of major phylogenetic groups in these graphs and that the archaeal and eubacterial genomes behaved as a single homogenous data set. Moreover, the yeast genome data also fell at the predicted point on these graphs. This suggests that the effects of nucleotide bias on protein composition are operating in all major lineages.
Thus, if nucleotide bias does in large part determine protein composition, and nucleotide bias can be tweaked by cytosine deamination, it becomes clear the Increasing Hydrophobicity Effect I described could very well play out in evolution and thus be a component of the design mechanism.
They end their article with two very interesting observations.
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The most parsimonious explanation of the observed patterns of amino acid composition in these genomes is an underlying mutational bias that varies between lineages. The resulting amino acid sequence changes are nonrandom, since the mutational bias is strongly directional, and yet they are not caused by natural selection acting directly on protein function. Consequently, their evolutionary dynamics cannot be described in terms of either Darwinian selection or random genetic drift. They may, however, result in secondary selective changes in the protein sequence. For example, amino acid bias could result in a change of the charge distribution within a protein, as well as an alteration of the protein's secondary and tertiary structures. Such proteins may then undergo positive selection at other sites to counter the potentially deleterious effects of these nucleotide bias–induced changes. The long-term result might be a cascade of compensatory changes to reduce the impact of amino acid bias on protein structure and function. The problem of distinguishing between functional constraint in protein sequences and mutation-driven biases in the composition of these same sequences will provide a future challenge for molecular evolutionists.
This line of reasoning nicely complements the mechanism I describe and outline in Figure 7 of Evolution's Design :
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Figure 7. The C-to-T transitions can be likened to a stream, constantly pushing amino acid content toward a more hydrophobic state. Given the context provided by the originally designed state (continually reflected by evolution's tendency to borrow from pre-existing states), buried secondary designs may be unmasked on a somewhat regular basis. If the act of unmasking occurs in an appropriate environment, selection will lock the secondary design into the biosphere.
Going back to Singer and Hickey, they note:
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In conclusion, we recognize that other factors, such as selective constraint, adaptive change, and genetic drift, all play important roles in protein sequence evolution. The results presented here, however, demonstrate that mutational pressure on DNA composition can also be a very powerful and pervasive force in long-term protein evolution.
Such mutational pressure could very well help to unlock buried designs in front-loaded states.
Another implication of all this concerns convergent evolution, which is well situated in the hypothesis of front-loaded evolution. The authors offer their own take:
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This result has implications for many studies that are based on the interpretation of amino acid sequence data. For instance, it has already been shown that nucleotide bias can affect the functional properties of proteins and that convergent amino acid composition can affect the construction of phylogenetic trees based on protein. For instance, Foster and Hickey showed that unrelated taxa were grouped together in a phylogenetic tree due to convergent amino acid sequences. Although this problem in phylogenetic reconstruction has been identified, a satisfactory method of dealing with the problem has not yet been found. Because of the relationship between primary amino acid sequence and secondary protein structure, nucleotide bias may also affect the evolution of protein structure .
This raises the fascinating question of whether any examples of convergent molecular evolution involved CT transitions at key points.
[ 01. January 2003, 12:43: Message edited by: Mike Gene ]
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Frances
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posted 01. January 2003 21:58
An interesting posting to which I will respond later (using the 24 hour rule proposed by Mike) but I would like to provide the following reference
R. Knight et al "A simple model based on mutation and selection explains trends in codon and amino-acid usage and GC composition within and across genomes" Genome Biology 2001, 2(4)
and I would like to encourage Mike to explain to us how his ideas of front loading can be distinguished from natural processes?
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Mike Gene
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posted 02. January 2003 12:00
Frances,
Thanks for the reference, as several of their points nicely complement what I am saying.
As for distinguishing front loading from "natural processes," I think that is the wrong question to pose. Front-loading, by definition, is using natural processes to carry out an objective. In a sense, it is not opposed to "natural processes," but does stand against the Gouldian view that places primary emphasis on contingency. I offer some preliminary thoughts here.
Knight et al. write:
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Our model suggests that GC content drives codon usage (rather than the converse). It unifies a large body of empirical evidence concerning relationships between GC content and amino-acid or codon usage in disparate systems. The relationship between GC content and codon and amino-acid usage is ahistorical; it is replicated independently in the three domains of living organisms, reinforcing the idea that genes and genomes at mutation/selection equilibrium reproduce a unique relationship between nucleic acid and protein composition.
These type of findings add to the growing plausibility of the ability to design evolution. That is, the initially designed states, coupled with such designed mechanisms of evolution, could have a significant reach that doesn't have to be strongly deterministic.
And perhaps, in the end, when much of this is figured out and better characterized, we might be able to use something like Dembski's approach to argue not about a sequence here or there, but about this thing we call 'evolution.'
[ 02. January 2003, 12:00: Message edited by: Mike Gene ]
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Frances
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posted 02. January 2003 12:10
Hi Mike,
Thanks for your answer. It seems that you are saying that front loading is nothing different from natural processes did it other than that one takes a different view on how the initial condition happened. But since there seems to be no evidence that the initial condition required intelligent design, the design you may see in biology could very well be totally naturally including the initial conditions.
You seem to find Knight et al's claim to be in support of design but natural processes seem to have been totally responsible for these similarities as far as we can tell and no evidence has been provided to support your thesis. In fact I would argue that your hypothesis may very well be indistinguishable from natural processes since we can always move back the time of the front loading to perhaps the Planck time.
How do you intend to use 'Dembsksi's approach' I wonder? In fact I would argue, like Murray, that Dembski's approach cannot distinguish between front loading (or stacking the deck as Murray calls it) and intervention either.
So where is the evidence that these initial states were 'designed'? Unless by designed you include natural design
quote:
Let me merely say that we have just begun to understand evolution and I think we will one day find that the processes of evolution are far too sophisticated to fit comfortably in the Modern Synthesis. Darwin helped us to understand things like finch beaks and the spread of antibiotic resistance. His concept has been extrapolated to all other origin events merely because we don't understand evolution very well and have no better explanation. Those days are changing.
Perhaps Mike could explain to us why these days are changing and how they are changing? I would argue that 'front loading' is not different from what we have right now.
[ 02. January 2003, 12:44: Message edited by: Frances ]
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nobody
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posted 02. January 2003 13:26
quote:
Such mutational pressure could very well help to unlock buried designs in front-loaded states.
Mike,
Is your term "front-loaded" roughly equivalent to what I call the programming of life?
You are saying that information was front-loaded, aren't you? That sounds like extremely skillful programming.
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Mike Gene
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posted 02. January 2003 14:55
Frances,
You continue to work under the impression that design must be a supernatural process and we thus invoke it only when it is "required," that is, when someone can prove it is impossible that natural processes could produce something. But there are many other ways to think about design and front-loading is one of them. Front-loading entails a simple question - how could you design the future through the present? My focus is on this question and determining how plausible this is. Recall, that this forum is designed to explore positive expressions of teleological thinking and my focus is on an investigation. Thus, when you say:
quote:
But since there seems to be no evidence that the initial condition required intelligent design, the design you may see in biology could very well be totally naturally including the initial conditions.
...this is nothing more than a caveat that I recognize. Of course I could be mistaken, but that is no reason to abandon an investigation. No, I cannot prove that design is required for the initial conditions. But that is irrelevant, at least at this point in the investigation.
Could the original cells have been designed such that they were front-loaded to render the evolution of metazoan life forms more likely? Certain types of metazoan life forms more likely? Etc. These are the questions to ask in my investigation, not questions about establishing that ID is "required." Front-loading, by definition, is using natural processes to carry out an objective, so it makes no sense to complain that I have only invoked natural processes. In a sense, it is not opposed to "natural processes," but does stand against the Gouldian view that places primary emphasis on contingency.
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You seem to find Knight et al's claim to be in support of design
Not quite. I noted that this was yet one more data set that illustrates the plausibility of designing through evolution and designing evolution itself.
quote:
So where is the evidence that these initial states were 'designed'?
To be clear, and as explained many times before, the hypothesis is that the earth was seeded with cells that were the products of bioengineering at the hands of some form of advanced human-like intelligence. The "initial conditions" were the originally designed state of these stem cells.
I have also shown, in several places, that there is much more to the "where is the evidence?" question than meets the eye. For example, I could likewise ask, where is the evidence that the initial states were indeed spawned by the Earth? I could ask what type of data you would accept as evidence. Etc. But I'd rather not get into generic questions in this thread. I'd rather stick to the topic of the original posting - the effects of cytosine deamination, as channeled by the genetic code, do seem to play out in evolution.
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Mike Gene
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posted 02. January 2003 15:02
Nobody,
Yes, I'd say that front-loading is roughly equivalent to the programming of life. However, at this stage, I entertain only the most modest form of front-loading - something that is not strongly deterministic. Consider the fact that casinos in Las Vegas generate gobs of profits. Is this a coincidence?
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Frances
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posted 03. January 2003 00:18
Hi Mike,
There seems to be some confusion about what I said. You seem to be under the impression that my statements reflect the idea that design needs to be supernatural. On the contrary, I am asking how you suggest to differentiate between front loading design and natural processes. Since the topic is intelligent design and front loading seems to have become a more popular interpretation of intelligent design I was wondering if there was any way to distinguish between ID and natural processes. If not, I would like to understand what the assumption of front loading via ID adds to our understanding as opposed to lets say front loading through natural processes.
As I have argued, if front loading cannot be distinguished from natural processes then for all practical purposes ID does not seem to add much to the scientific inquiry. If the argument is that ID adds to the discussion then one would presume that ID makes predictions that would allow one to distinguish between front loading via ID and front loading via natural processes. Otherwise we are merely talking about initial conditions.
While it surely is interesting in speculating about natural processes and how they could have led to the initial states, I am still confused as to what the ID hypothesis is and how such an assumption can contribute to our knowledge if it cannot be distinguished from natural processes?
And since ID does not even seem to make any predictions about when the initial states were initialized we may as well move them back to the Big Bang Planck time limit which would truely place it outside our realm of scientific inquiry.
Murray states it quite eloquently when he says
quote:
So perhaps disciplinary territorialism should not rule out Intelligent Design as a genuinely
scientific explanation. But we are not out of the woods yet. For even though countenancing design
as an explanation might in principle count as genuine science, it cannot if the design hypothesis is not empirically distinguishable from explanations which appeal only to the natural powers of natural substances. If such empirical distinguishability is not possible, then there is no scientifically respectable way, by IDT’s own lights, to defend intelligent design as an explanation distinct from law and chance.
I would also like to explore further how your ideas can be reconciled with the ideas of William Dembski, whose work would seem to suggest that front loading would require all the CSI to be present in the original 'genome' of our ancestor(s).
As far as the ideas about hydrophobicity, cytosine deamination and GC excess, I have been doing literature research online which suggests that the idea has existed for quite a while see for instance this finding prompted an analysis of the correlation between (GC3) and the amino acid frequencies in the encoded proteins, which has shown that positive correlations exist between (GC3) values of coding sequences and the hydropathy of the corresponding proteins. These correlations are due to the fact that hydrophobic and amphypathic amino acids increase, whereas hydrophilic amino acids decrease with increasing (GC3) values.. But there seem to be some interesting issues to deal with such as
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... as the genomic GC content increases, both strongly hydrophobic and strongly hydrophilic amino acids tend to change to ambivalent amino acids, suggesting that the majority of these amino acid substitutions are not caused by positive Darwinian selection.
or
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The following is an example of a selective model for bias in amino acid usage: the global hydrophobicity of proteins is the main factor
for variation in amino acid content of proteins in E. coli (Lobry and Gautier, 1994). This is due to a selective pressure to increase the content of hydrophobic amino acids (e.g. Phe, Ile, Leu, Met, Val, Trp, Tyr) for integral membrane proteins. Because of the nature of the genetic
code, the result will be an asymmetric selective pressure between coding and non-coding strand with an excess of T over A in the second position. However, this group only makes up about 10% of the total amount of proteins (Lobry and Gautier, 1994), and is probably too small to have any impact on global composition patterns.
other questions to be resolved include
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Generally, hydrophobic amino acids are more abundant in proteins coded by the proximal region of the chromosome, whereas hydrophilic amino acids are more abundant in proteins coded by regions close to the terminus of chromosome replication.
and
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Selection to maintain hydrophobic amino acids in integral membrane proteins is a primary factor driving protein evolution in E. coli but is a secondary factor in Buchnera. In E. coli, gene expression is a secondary force driving amino acid usage, and a correlation with tRNA abundance suggests that translational selection contributes to this effect. Although this and previous studies demonstrate that AT mutational bias and genetic drift influence amino acid usage in Buchnera, this genome-wide analysis argues that selection is sufficient to affect the amino acid content of proteins with different expression and hydropathy levels.
fascinating work indeed.
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Mike Gene
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posted 03. January 2003 03:01
Frances,
You want ways to distinguish between front loading design and natural processes. Yet it's way too early in the investigation to provide such a definitive answer. At this stage in the game, FLE represents an alternative perspective. That is, if the two perspectives cannot be distinguished, there is no reason for me to ignore the FLE perspective and focus entirely on natural processes to the exclusion of their possible teleological use. Now, after the FLE perspective has been thoroughly fleshed out, to answer several of the questions I have posed, we can then return to your question. That is, let's first see what falls out from a more focused FLE perspective, okay?
FLE does not need some clear-cut way of teasing itself apart from the non-teleological perspective in order for it to offer practical additions to scientific inquiry. The Murray argument you cite are only words that are trumped by my experience. You seem to forget how this particular interest of mine got started. It began when scientists, focused only on "natural processes" proclaimed, in the peer-reviewed scientific literature, that no engineer would have included cytosine in the DNA. This was the conclusion delivered by the "natural processes only" perspective. Yet because of my prior interest in front-loading, I was able to make a connection . Y'see, the differences between the teleological and non-teleological perspective are often subtle. Much of the time, they only involve different points of emphasis that connect things is slightly different ways. Murray's quest for the "magic bullet test" is too clumsy to be meaningful at this point. What is needed is a highly sensitive state responsive to subtle clues.
As for moving the front-loaded state back to Big Bang Planck time limit, I'm quite open to that. But in this instance, we're talking about some fairly specific states: 1) Life that uses the following amino acids - LSPTYHEQRAFIMCWV; 2) Genetic material that uses cytosine; 3) A genetic code that exploits cytosine deamination to extract all the hydrophobic residues from that pool. If you want to make the case that these states were front-loaded at the Big Bang, go for it. Which would mean you should probably begin with the questions I posed here
quote:
So perhaps it is my turn to ask a couple of questions.
1. According to Robert Shapiro, cytosine has not been reported in analyses of meteorites nor is it among the products of electric spark discharge experiments. And because of its predisposition to deaminate, under mild conditions, it was a half life of only about 340 years. Put simply, there is not a convincing case that cytosine would have been among the major players of the prebiotic soup. Furthermore, cytidine is not needed for ribozyme function. Recently, Joyce was able to synthesize a functional ribozyme containing only A,G, and U.
So here's the question for the non-teleologists - why does RNA have cytosine?
2. How does the non-teleologist explain the relationship I discovered between the most common form of DNA mutation and its functional consequence as mediated by the genetic code? Is this yet another example of something that "just happened?"
In the meantime, the hypothesis that the earth was seeded with cells that were the products of bioengineering at the hands of some form of advanced human-like intelligence is worth talking about. Don't you agree?
Finally, you provide some very interesting quotes. Could you provide the sources? Thanks.
[ 03. January 2003, 03:03: Message edited by: Mike Gene ]
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Frances
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posted 03. January 2003 12:12
A quick posting to address the 'couple of questions'
Origin of cytosine
There are a variety of options
1. the initial PNA, a possible precursor to RNA, did not have cytosine
Here
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Numerous problems exist with the current thinking of RNA as the first genetic material. No plausible prebiotic processes have yet been demonstrated to produce the nucleosides or nucleotides or for efficient two-way nonenzymatic replication. Peptide nucleic acid (PNA) is a promising precursor to RNA, consisting of N-(2-
aminoethyl)glycine (AEG) and the adenine, uracil, guanine, and cytosine-N-acetic acids. However, PNA has not yet been demonstrated to be prebiotic. We show here that AEG is produced directly in electric discharge reactions from CH4, N2, NH3, and H2O. Electric discharges also produce ethylenediamine, as do NH4CN polymerizations. AEG is produced from the robust Strecker synthesis with ethylenediamine. The NH4CN polymerization in the presence of glycine leads to the adenine and guanine-N9-acetic acids, and the cytosine and uracil-N1-acetic acids are produced in high yield from the reaction of cyanoacetaldehyde with hydantoic acid, rather than
urea. Preliminary experiments suggest that AEG may polymerize rapidly at 100°C to give the polypeptide backbone of PNA. The ease of synthesis of the components of PNA and possibility of polymerization of AEG reinforce the possibility that PNA may have been the
first genetic material.
2. Here
quote:
We report on a plausible prebiotic synthesis of naturally occurring purine and pyrimidine derivatives from formamide under catalytic conditions. In the presence of catalysts formamide leads to the formation of purine, adenine, cytosine, and 4(3H)-pyrimidinone. The role of catalysts is also relevant in providing a high selectivity in the products distribution. A circular reaction involving synthesis and degradation of purines and pyrimidines based on Formamide chemistry has been identified, making plausible an important role of formamide in prebiotic bio-oriented chemistry. The role of a specific catalyst in the selectivity of pre-biotic reactions is demonstrated by the sequence-selective degradation of oligonucleotides. This finding links the formamide-based cyclic synthetic-degradative reactions with the onset of Darwinian molecular evolution, potentially leading to self-replicating structures. All the compounds involved are present in extraterrestrial environments.
or
Here
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The prebiotic synthesis of cytosine from urea and cyanoacetaldehyde (Robertson and Miller, 1995) has recently been criticized (Shapiro, 1999) because of the possible side reactions of the reactants and inapplicability of prebiotic syntheses under concentrating conditions. The prebiotic synthesis of diaminopyrimidine, cytosine, isocytosine, and uracil have been previously demonstrated from dry down experiments using guanidine and cyanoacetaldehyde (Robertson, et al., 1996). We show that cytosine and uracil are produced under dry down conditions from urea and cyanoacetaldehyde. Although dimerization has been claimed to interfere with this reaction, the prebiotic synthesis of these pyrimidines from urea and cyanoacetaldehyde dimer at 100 °C is an efficient reaction. At low temperatures cytosine and uracil are also produced from urea and cyanoacetaldehyde or the dimer. Concentration by evaporation is considered one of the most useful mechanisms to achieve the high concentrations necessary for prebiotic synthesis on the primitive earth (Miller and Orgel, 1974). We discuss the efficiency of concentrating solutions of organics from concentrations as low as 10-6 M and show that dilute solutions concentrate approximately according to theory. These results demonstrate the validity of prebiotic syntheses under dry beach conditions and concentration by evaporation. Prebiotic syntheses on drying beaches may have served as a source of cytosine and other pyrimidines for the RNA and pre-RNA world.
As to how to explain the DNA mutation and its functional consequence, what's wrong with 'we don't know'? How does that compare to your explanation? After all one can easily find 'patterns' that need not be explained by any form of teleology where basic chemistry would suffice.
quote:
In the meantime, the hypothesis that the earth was seeded with cells that were the products of bioengineering at the hands of some form of advanced human-like intelligence is worth talking about. Don't you agree?
Sure, it makes for an interesting concept especially with the recent Raelian news. I am looking forward to the supporting evidence. Perhaps we could also consider that the earth was seeded with cells that were the product of natural processes?
These questions are very interesting but in the end they need to be reconciled with Dembski's claim that CSI cannot arise naturally. Thus either all CSI was present in the initial cell or we have 1) CSI was inserted by intelligence during its evolution 2) Dembski's claim is erroneous.
As far as an 'alternative perspective' one need to show why the perspective requires the addition of intelligence, how such a difference can be detected. In absence of such why the need for these extraneous additions?
[ 03. January 2003, 12:15: Message edited by: Frances ]
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Janitor@MIT
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posted 03. January 2003 14:35
I’m sorry, but isn’t “selection” the explanation of any difference that makes a difference? In so far as that goes, how is that an “explanation”?
Since Francis is so insistent, please explain to us what a “natural” explanation or process is exactly. I, for one would appreciate it and have asked for it several times before. (Sorry, I'm getting cranky.)
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Art
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posted 03. January 2003 16:35
Another quote that may be relevant: (from Maki, Ann.l Rev. Genet. 36, 279-303, 2002):
quote:
“The nature of native replication errors caused solely by action of the replicative apparatus has been extensively characterized, whereas less is known about spontaneous DNA lesion that potentially induces spontaneous mutations (24). Active oxygen species are produced in aerobically growing cells and attack DNA to produce a wide range of lesions. An estimated 3000–5000 oxidative DNA lesions/cell/generation are produced in cells of E. coli under normal aerobic growth conditions (78). Free nucleotides are attacked more efficiently by oxygen radicals than DNA, and in a number of different species, oxidized nucleotides are produced in the cellular nucleotide pool. Among them, 8-oxodGTP (58) and 2-OHdATP (37) possess extraordinarily strong mutagenicity. Considering their high production rate, these mutagenic compounds are potentially the most powerful source of spontaneous mutations. Methylation and hydrolytic decomposition of DNA such as depurination and cytosine deamination cause a variety of endogenous DNA lesions (24). However, the spontaneous frequency of these events is estimated to be much lower than that for the oxidation of DNA.”
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Mike Gene
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posted 03. January 2003 17:13
Frances,
I think you misunderstood the first question. I was not asking if it was possible for cytosine to exist on the prebiotic earth. I was asking why this base is part of RNA considering the factors that I raised. The quotes you provide are interesting, but not really relevant to the question I asked.
As for the second question, you ask, "As to how to explain the DNA mutation and its functional consequence, what's wrong with 'we don't know'? How does that compare to your explanation?"
Nothing is inherently wrong with pointing out that we don't know if this pattern is traced back to purely non-teleological causes. Thus, clearly a teleological possibility deserves a place at the table. As for the comparison you want, my explanation provides subsidiary testable hypotheses that can guide research. An "I don't know" exclamation is itself rather useless (Joy had some good things to say about this on ARN). I will also show, in the next few weeks, that other connections can be made. Since my approach adds nothing novel to scientific inquiry (according to you), you should have no problem anticipating where I will go. So where am I going?
Nevertheless, as I explained above, these two questions are part of the context for your attempt to situate the front-loading at the Big Bang. Remember the three states I mentioned above and explain the Big Bang conditions that rigged Nature to unfold these states.
As for supporting evidence of my thesis, I plan on sharing some of this here over the next few months.
Yes, "in the end," we might attempt to apply Dembski's claims to my front-loading claims. But there is no need to think in binary terms here. It may be a question of high CSI vs. low CSI and whether intelligent intervention is the best explanation to the origin of some particular form of CSI.
But there is no reason to be impatient. I have the patience to wait many years as I further develop this lines of thought. When you are dealing with an investigation sensitive to subtle clues (and thus at high risk of building on false positives), impatience is poison.
Finally, as for this claim:
quote:
As far as an 'alternative perspective' one need to show why the perspective requires the addition of intelligence, how such a difference can be detected. In absence of such why the need for these extraneous additions?
I don't agree at all. I am under no burden to explain why I need to demonstrate that intelligence is required . You are free to ignore the "extraneous additions." I personally find them to be quite helpful for generating novel testable hypotheses. They also serve as a good check against the intellectual inertia that leads many to stop at the level of "just happened." And the fact that science ignores an alternative perspective is sufficient reason alone to explore it.
Sorry, but I have no obligation, whatsoever, to first demonstrate that I need ID before I can use it. Utility is not always tied up in necessity.
[ 03. January 2003, 17:15: Message edited by: Mike Gene ]
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warren_bergerson
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posted 04. January 2003 09:07
Mike,
Quote from Singer and Hickey: Consequently, their evolutionary dynamics cannot be described in terms of either Darwinian selection or random genetic drift.
I think the attempt to demonstrate the existence of front loading in genetic processes is admirable. My comments relate not to the ‘fact’ of front loading but to the interpretation.
To begin, front loading can be defined as a non random search for an adaptive solution. In mathematical terms, assume that a particular adaptive solution has complexity or improbability of 1 in 10^10,000. If a system can find the solution to this adaptive problem in say 100 generations, then we could say the solution was front loaded or in my terminology, the system found the adaptive or teleological solution using a non-random search.
Given the existence of an occurrence of front loading, we have three questions to address:
1. How much front loading or non-random processing is required to explain the identified change?
2. How can you model, explain, or develop a testable predictive theory to explain the observed front loading?
3. When was the front loading generated?
4. How was the front loading generated?
MAGNITUDE OF FRONT LOADING
In dealing with simple genetic processes the magnitude of front loading or non-random search may be small, but when we look at macro evolution, level of front loading which reduce evolutionary change times from 10^10,000 generations to 100 generations are easily identified.
MODELING FRONT LOADING
It appears to be impossible to model front loading using only random variation and whole organism or natural selection. If you use non-random variation and selection other than ‘natural or whole organism selection’ it is relatively easy to model or simulate any level of front loading.
It appears to be impossible to develop a testable, predictive theory of front loading based on permanent and universal causal relationships. It appears to be relatively easy to develop testable, predictive theories of front loading based on dynamic and teleological causal relationships.
WHEN WAS FRONT LOADING GENERATED
If we require explanations in terms of permanent and universal causal relationships, then front loading processes we require front loading to have been ‘created’ at the beginning of time. If we accept scientific explanations based on dynamic and teleological causal relationships or ‘laws of nature’, then front loading processes could have developed, been created or evolved at any point in time.
HOW WAS FRONT LOADING GENERATED
Again if we limit the creation of front loading to permanent and universal causal relationships or laws, front loading either existed from the beginning of time or was introduced subsequently by an external designer. Including dynamic and teleological causal relationships in scientific explanations, means there are relatively simple explanations for front loading.
SUMMARY
IMO, while demonstrating the existence of front loading (or non-random adaptive change) in genetic systems is an important topic for research, a far more interesting aspect of front loading is the question of how do you develop predictive scientific models and theories.
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Art
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posted 04. January 2003 10:55
Perhaps another relevant study:
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J Bacteriol 2002 Dec;184(24):6866-72
Transcription-dependent increase in multiple classes of base substitution mutations in Escherichia coli.
Klapacz J, Bhagwat AS.
Department of Chemistry, Wayne State University, Detroit, Michigan 48202, USA.
We showed previously that transcription in Escherichia coli promotes C. G-to-T. A transitions due to increased deamination of cytosines to uracils in the nontranscribed but not the transcribed strand (A. Beletskii and A. S. Bhagwat, Proc. Natl. Acad. Sci. USA 93:13919-13924, 1996). To study mutations other than that of C to T, we developed a new genetic assay that selects only base substitution mutations and additionally excludes C. G to T. A transitions. This novel genetic reversion system is based on mutations in a termination codon and involves positive selection for resistance to bleomycin or kanamycin. Using this genetic system, we show here that transcription from a strong promoter increases the level of non-C-to-T as well as C-to-T mutations. We find that high-level transcription increases the level of non-C-to-T mutations in DNA repair-proficient cells in three different sequence contexts in two genes and that the rate of mutation is higher by a factor of 2 to 4 under these conditions. These increases are not caused by a growth advantage for the revertants and are restricted to genes that are induced for transcription. In particular, high levels of transcription do not create a general mutator phenotype in E. coli. Sequence analysis of the revertants revealed that the frequency of several different base substitutions increased upon transcription of the bleomycin resistance gene and that G. C-to-T. A transversions dominated the spectrum in cells transcribing the gene. These results suggest that high levels of transcription promote many different spontaneous base substitutions in E. coli.
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