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#101 Fred Williams

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Posted 05 February 2008 - 08:47 PM

My_wan touts several lines of evidence for evolution, but like all so-called evidences for evolution they are built upon illusion.

The DNA code itself is universal and was a prediction.


A universal code was never a prediction of evolution. I’ve noticed you’ve made a lot of claims yet you seldom provide actual substance to back them. The fact we found a ‘code’ in the DNA was overwhelming evidence against a naturalistic origin. It was so overwhelming that the co-discoverer (Francis Crick) dropped his belief in neo-Darwinism in favor of the silly panspermia theory (aliens seeded the planet with the information). We know from information science that is impossible for a code to arise naturalistically, it MUST have an intelligent source. Even in the book and subsequent movie Contact, Carl Sagan had enough sense to realize this truth (the movie makes this very claim), but Sagan didn’t apply this truth to origins because his religious atheism got in the way.

Since the existence of a code itself refutes evolution, its universal nature can instead be viewed as solid evidence that there is ONE designer, not multiple designers.

Regarding Cytochrome-C, Deadlock already pointed out the illusion behind it, that you can make all kinds of relationships that evolutionists do not claim are due to recent common decent. I have a much wider chart on Cyto-C that includes more animals, and I would be willing to bet you that if I gave the labels of each animal a code you would not be able to make a coherent sequence of evolution that even remotely matches what evolutionists believe. There are also mosaics in the Cyto C sequence, such as the snake. It would be fun to see where you put the snake in the grand scheme of things.

He uses these bad numbers to say 120 point mutations would require 2,700,000 generations to propagate through the population. Yet this carried even more bad assumptions. He assumed mathematically that each point mutation must first propagate through the population before starting the next mutation. In reality mutations can occur simultaneously throughout the population. When these bad assumptions are removed then even with ridiculously low rate of only 1 mutation every 20 generations you get that 120 point mutations in only 2400 generations. That's barely a month for some microbes and well less than 50,000 years for humans.


Sorry to be so blunt, but this shows remarkable ignorance of genetics. To claim that a mutation can become fixed in a mere 20 generations (and claim this is a “ridiculously low” estimate) is a pipe dream. For one you forgot that microbes are asexual and humans are not (S@xual organisms add an additional 50% hurdle per generation when moving a mutation through a population). You are making your own bad assumptions, and most importantly you are completely ignoring an important mechanism, the cost of substitution. Each mutation must incur its own cost to reach fixation. Haldane believed this[1], and Kimura believed this (in fact the problem with the cost of substitution was a driving force behind why Kimura proposed the neutral theory in the first place). So it turns out that Eden’s assumption that each mutation should be considered serially was actually not a bad assumption at all, and why I suspect he was keenly aware of the substitution problem. One particular cost of substitution (among others) is the cost of harmful mutations, a damning cost indeed that punches a big hole in common decent with a monkey-esque grandaddy. See my article on this:

http://www.youngeart...on_article1.htm

A related debate I had with a biologist:

http://www.evolution...page_debate.htm

What they did do [computer simulations] was demonstrate that the argument that evolution couldn't happen with random mutations doesn't work.


Such programs proved no such thing. Random mutations cannot produce information without an intelligent source present to harness the data. See this pinned thread:

http://www.evolution...p?showtopic=165


The DNA fingerprint of these ERVs are identical. It's like taking a picture on the Bangkok and in Dallas and both pictures being identical. The DNA of these ERVs can also be identified as an individual virus the same way you can be identified from all other people on Earth by your DNA. The damage done to the cell itself was even identical, like two sticks of dynamite creating identical pictures in two parts of a jungle. So we have an individual virus that invaded the exact same cell type in multiple species leaving the exact same damage to the cell and all these cells managed to survive the infection to continue reproducing. Then somehow after all this it follows the same species lineage that we infer from the fossil record. If that's not enough it also agrees with the fossil records timing of when the species split in the past. There is also a lot of other ERVs that did all these same things. So you can say it was put there for an unknown purpose but needing these things does not explain why all these things had to be exactly the same or why it had to match the sequence and timing already inferred from the fossil record.


This is mostly ad hoc story-telling. Evolutionists assume: 1) ancient infection in 2) our alleged simian ancestor, 3) the vast majority of ERVs have no function, 4) the events are random. Since we have already identified some ERVs that are highly conserved and clearly have function, this alone casts doubt on their argument. Another ugly problem for evolution again rears its head, namely convergent evolution. By it’s very definition it is anti-evolutionary, since it describes similar traits in two organisms that cannot be attributed to common ancestry! So the problem is this - we find similar ERVs in organisms no evolutionist would dare claim is a recent common ancestor to humans [2].

[regarding nylon-eating bacteria] You say adaptation not random mutation and/or selection? Why does 9 days speak to anything? Of course it was an adaptation that required a random mutation to produce.


You apparently are missing rbarclay’s point. The mutation happened too quickly and conveniently to be attributed to a random copying error in the DNA. Evolution theory doesn’t accommodate non-random mutations because they clearly imply design.

Fred

1 - JBS Haldane, The Cost of Natural Selection, Journal of Genetics 55, pp 522 (1957)

2- Dupressoir A, Marceau G, Vernochet C, Bénit L, Kanellopoulos C, Sapin V, Heidmann T (2005) Syncytin-A and syncytin-B, two fusogenic placenta-specific murine envelope genes of retroviral origin conserved in Muridae Proc Natl Acad Sci U S A. 102(3):725-730

#102 my_wan

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Posted 07 February 2008 - 03:28 AM

If there is any law in nature from reproducing systems, its that they only produce after their own kinds such that goo-to-you evolution is a violation of  what is observed.

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It would be more useful if you could actually define what "kinds" means. It seems that the term "kinds" gets used to avoid the counterexamples when you use any specific actual definition for species. For instance if we have species A, B, and C. A and B can breed together so they must be the same kind. B and C can breed together so they must be the same kind. Except there is one problem, A and C can not breed together so there not the same kind. What definition of kind would you use to get around examples like these?

It's obvious we haven't been observing for millions of years to see the whole process. We must test for any particular barriers to change on by smaller snapshots from various observations. I don't mind using "kind" in place of species because it is often argued exactly how species should be defined. If you use "kind" though give a definition so we can consider how/where/what this line is that theoretically can't be crossed. I will not argue over any definition, no matter how complex, so long as it can be investigated by observations. You certainly can't call something that's not even defined as a law.

That's not measuring anything...  Its speculating about what may have happened in the past.

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Perhaps you should read my post again. I never said anything about speculating about what happened in the past. Specifically my sentence that said, "Yes the measurements were made directly by comparing the genome of viruses after a set number of generations." When you take identical microbes and reproduce them to see what changes occur after X number of generation it is measuring what happened right there in your petri dish, not some speculation about the past.


Programs have nothing to do with goo-to-you evolution.

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By "goo-to-you evolution" I assume you mean abiogenesis. 3 out of the 4 of my sentences you quoted said that very thing. I have copiously pointed out the limits of what any specific line of empirical evidence can and can't demonstrate. The utility of genetic computer programs is to demonstrate the mechanisms of evolution do in fact work as described regardless of whether we or any animals actually evolved or not. It says nothing about the history of evolution. That is what you accused me of speculating on above when in fact it was a direct observation of and only of what was happening right there in the petri dish. No single piece of evidence will demonstrate every aspect of common descent. I did a whole post just about the pieces of evidence for common descent, separate from the evidence that the mechanisms of evolution actually works that you have simply agreed with me doesn't show common descent.

What he is pointing out is that experimental data supports Yockey's calculations of  the odds of producing the known cytochrome c proteins by trial and error search.

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Reference that you quoted: http://www.arn.org/d.../mb_smu1992.htm

Yes just as I was pointing out the absurd assumption used for the calculation. Yet here you seem to have conflated Yockey's functional protein argument with the cytochrome c argument. Two entirely separate concepts are mixed by bringing Yockey's work into this. Even Behe only mention Yockey's work to concede that the odds aren't as bad as originally thought.

So in the Behe quote you copied he argues that even with this huge reduction in the odds of a given functionality that it was still a vast number against any particular functionality. What he fails to note is the same objection that you quoted from me: "So what does the 1 in 10&% odds of finding a particular function have to do with anything when there is reasonably close to that many useful functions to find?" Quoting that Behe acknowledged that the odds were not as bad as originally thought for a particular function still fails to acknowledge all the possible functions. It's like claiming it's impossible to role 100 dice and get an even number because the odds of getting any particular number is a gazillion to one.

I like the effort Hubert Yockey contributed. Not many people think about the issues at the level Yockey did.

IOW, observable scientific data predicts that will not happen.  Maybe that's comical to you, but I believe a reasonable person will think about it.

Terry

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I read "observable scientific data predicts" and got very confused. Observations and/or data don't/can't predict. Only theory does that. Perhaps I am being technical in the eyes of some but it really is very confusing to me. However, this appears to be your summation of the Behe quote you provided. Based on that I'm assuming the "observable scientific data" is a property of the cytochrome c data. That was the theories prediction, not what made the prediction. Ok maybe now I get what you were trying to say, I hope. However, it still is only a prediction that the odds of a particular function is much better than creationist previously argued and still fails to admit all other possible valid functions. The dice analogy it very pertinent. There are many ways to get the same number with dice too, which only means the concession by Behe works in the dice analogy also.

#103 my_wan

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Posted 07 February 2008 - 05:27 AM

Fred Williams,
I started my response to you then realized you were the author of the link you posted. Since you did present it here as a reference I'll take more time than I have right now to do it justice.

Good luck.

#104 Teleological

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Posted 14 February 2008 - 11:56 AM

The article also makes another claim that there is a, "clear lack of data to indicate that mutations really accomplish anything new". This makes light of the nylon eating bacteria. This was a mutation that shifted the entire reading frame of of the genes sequence. Not just a single point gene but the whole sequence. It should have been deadly to the poor little bacteria or at least harmful but this one got lucky. It now has a whole new food source, nylon that didn't even exist before 1935. You can claim plasmids are a feature designed to allow bacteria to adapt to new food sources but that mechanisms itself must rely on mutation and often deadly mutations at that. It also requires "designed" in ability to increase its information about its environment via random mutations.

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Hi my_wan

I have not read the whole thread yet, but one thing has caught my attention regarding the nylon bug.
I cannot find the exact PR.C. sequence as cited in the Ohno (1984) paper in any database. Could you perhaps point me to the database and accession number please?

I am skeptical that the protein was indeed formed as the result of a frame-shift mutation. Here is why.
Three enzymes are responsible for the degradation of the nylon oligomers,
NylA (EI): 6-aminohexanoate-cyclic dimer hydrolase
NylB (EII): 6-aminohexanoate-dimer hydrolase
NylC (EIII): endo-type 6-aminohexanoate oligomer hydrolase

EI Has a high homology with amidases present in a lot of strains of bacteria, meaning a pre-existing enzyme was capable of breaking the amide bond of cyclic dimers.
EII (discussed below) is a classical carboxylesterase with B-lactamase folds that has high activity towards carboxylesters with short acyl chains. Proteins with beta-lactam folds with 6-aminohexanoate-dimer hydrolytic activity (non-specific Ald amide hydrolysis) is spread throughout the bacterial and archaeal kingdoms (BLAST it).
EIII High homology with L-aminopeptidase/D-esterases present in many other bacteria.
Use the peptide sequences of the enzymes and the NCBI BLAST site to verify it.

In 2005, Negoro et al. (2005) proposed the following for the EII protein:

Here, we propose that amino acid replacements in the catalytic cleft of a preexisting esterase with the beta-lactamase fold resulted in the evolution of the nylon oligomer hydrolase.

Negoro S, Ohki T, Shibata N, Mizuno N, Wakitani Y et al. X-ray crystallographic analysis of 6-aminohexanoate-dimer hydrolase: molecular basis for the birth of a nylon oligomer-degrading enzyme. J Biol Chem 2005 Nov 25;280(47):39644-52

And Okhi et al. (2006) again emphasizes this.

Based upon the following findings, we propose that the nylon oligomer hydrolase has newly evolved through amino acid substitutions in the catalytic cleft of a pre-existing esterase with the beta-lactamase-fold.

Ohki T, Wakitani Y, Takeo M, Yasuhira K, Shibata N, Higuchi Y, et al. Mutational analysis of 6-aminohexanoate-dimer hydrolase: relationship between nylon oligomer hydrolytic and esterolytic activities. FEBS Lett. 2006 Sep 18;580(21):5054-2058.

Is the pre-existing esterase the result of a frame-shift mutation (PR.C sequence please)? Or was the classic esterase with beta-lactamase folds there from the start?

Another thing that does not make sense is that in the Ohno (1984) paper it was suggested that the coding sequence "originally" specified a 472-residue-long arginine-rich protein. However this "472-residue-long arginine-rich protein" has no significant homology to any known functional protein.

To me, the evidence points to (and seems like the simplest explanation - Occam's razor) that a pre-existing classical carboxylesterase with B-lactamase folds (NylB'/EII') with low activity (0.5% that of EII (nylB)) towards nylon oligomers, gained an increase in activity towards the the oligomers through amino acid substitutions in the catalytic cleft containing the “Ser-X-X-Lys” motive without affecting the activity towards its original substrates. Not a frame shift mutation. For more info how these mutations increased activity: here.

#105 rbarclay

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Posted 14 February 2008 - 03:02 PM

Hi my_wan

I have not read the whole thread yet, but one thing has caught my attention regarding the nylon bug.
I cannot find the exact PR.C. sequence as cited in the Ohno (1984) paper in any database. Could you perhaps point me to the database and accession number please?

I am skeptical that the protein was indeed formed as the result of a frame-shift mutation. Here is why.
Three enzymes are responsible for the degradation of the nylon oligomers,
NylA (EI): 6-aminohexanoate-cyclic dimer hydrolase
NylB (EII): 6-aminohexanoate-dimer hydrolase 
NylC (EIII): endo-type 6-aminohexanoate oligomer hydrolase

EI  Has a high homology with amidases present in a lot of strains of bacteria, meaning a pre-existing enzyme was capable of breaking the amide bond of cyclic dimers.
EII (discussed below) is a classical carboxylesterase with B-lactamase folds that has high activity towards carboxylesters with short acyl chains. Proteins with beta-lactam folds with 6-aminohexanoate-dimer hydrolytic activity (non-specific Ald amide hydrolysis) is spread throughout the bacterial and archaeal kingdoms (BLAST it).
EIII High homology with L-aminopeptidase/D-esterases present in many other bacteria.
Use the peptide sequences of the enzymes and the NCBI BLAST site to verify it.

In 2005, Negoro et al. (2005) proposed the following for the EII protein:

Negoro S, Ohki T, Shibata N, Mizuno N, Wakitani Y et al. X-ray crystallographic analysis of 6-aminohexanoate-dimer hydrolase: molecular basis for the birth of a nylon oligomer-degrading enzyme. J Biol Chem 2005 Nov 25;280(47):39644-52

And Okhi et al. (2006) again emphasizes this.

Ohki T, Wakitani Y, Takeo M, Yasuhira K, Shibata N, Higuchi Y, et al. Mutational analysis of 6-aminohexanoate-dimer hydrolase: relationship between nylon oligomer hydrolytic and esterolytic activities. FEBS Lett.  2006 Sep 18;580(21):5054-2058.

Is the pre-existing esterase the result of a frame-shift mutation (PR.C sequence please)? Or was the classic esterase with beta-lactamase folds there from the start?

Another thing that does not make sense is that in the Ohno (1984) paper it was suggested that the coding sequence "originally" specified a 472-residue-long arginine-rich protein. However this "472-residue-long arginine-rich protein" has no significant homology to any known functional protein.

To me, the evidence points to (and seems like the simplest explanation - Occam's razor) that a pre-existing classical carboxylesterase with B-lactamase folds (NylB'/EII') with low activity (0.5% that of EII (nylB)) towards nylon oligomers, gained an increase in activity towards the the oligomers through amino acid substitutions in the catalytic cleft containing the “Ser-X-X-Lys” motive without affecting the activity towards its original substrates. Not a frame shift mutation. For more info how these mutations increased activity: here.

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Teleological

I have come across an by Dr. Brad Harrub "Are Viruses 'Evolving'?" http://www.creationd...llyEvolving.htm. and he makes a reference to a study done by Monica Sala and Simon Wain-Hobson "Are RNA Viruses Adapting or Merely Changing?" published in July 2000 issue of the Journal of Molecular Evolution. The study apparently concludes that viruses change as a result of genetic drift not as a response to drugs. Also that the drift appears to occur at constant rate whether they are exposed to drugs or not. I have not been able to obtain a copy of this study so if you have any anything to add on this subject I would appreciate it.

Bob Barclay

#106 Hippocampus

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Posted 14 July 2008 - 09:28 AM

Also what dilema were some of our most brilliant minds and scientists like Sir Isaac Newton struggling with when observing and studying our world from his supernatural view? Nothing. When we allow science to speak for itself it glorifies God and men like Albert Einstein are in awe of such discoveries.

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But there are no supernatural elements in Newton's theories. And though Einstein may have been "in awe" of them, it didn't stop him correcting them, again, with no recourse to the supernatural.

#107 Hippocampus

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Posted 15 July 2008 - 09:33 AM

I know that most people on this site, including me, do not believe in evolution.  But my question is:

What do you think is their strongest case for evolution?  [U][SIZE=7]

If you believe in evolution, feel free to put your best foot forward.

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The OP asked for evidence of evolution, but it seems we've done nothing but fossils so far. How about these other forms of evidence?

1. Every lifeform is similar to its parents, but different. These differences, over time, add up. Over many generations, great differences in form, structure and behaviour can develop.

2. Some creatures show anomalies of design that can best be explained by evolution. The air-breathing mammals that live in the sea. The snakes, with their curious remnants of leg bones. The seal, with an appendage at the back that is halfway between a tail and a pair of feet. The mole with furred-over eyes.

3. Sheer complexity. Millions of species of beetles, all doing the same job, living in almost the same way. What designer would be so profligate? The much-discussed blood-clotting process in humans – only evolution would produce such a needlessly complicated system. Evolution isn’t intelligent, isn’t elegant, and cares only about whether the system works.

4. The curious similarities between creatures with wildly different life styles. Compare the skeletons of mice and polar bears, the designs of crabs and woodlice.

5. The geographical distribution of lifeforms shows regularities which suggest evolution, not design. Why do the rainforests of South America, Africa, Madagascar and Asia have different creatures? Why are there so many species of finches on the Galapagos Islands? Why are there no mammals native to New Zealand?

I'll expand on this a bit when I have more time.




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