Thread: That's it, I'm done

Originally Posted by Seismosaur

You said systems, not organs.

Organs are systems.

Complexity isn't based on the physical number of cells, but the number of processes that the cells must be a part of. See what I'm talking about?

Cells are systems.

Cells are comprised of systems.

Which are comprised of systems.

Which are comprised of systems.

Cells can make systems which can make systems which can make systems which can make systems which can make systems. Pick a layer.

Originally Posted by Seismosaur

Cells are systems.

Cells are comprised of systems.

Which are comprised of systems.

Which are comprised of systems.

Cells can make systems which can make systems which can make systems which can make systems which can make systems. Pick a layer.

Sigh, this is ridiculous. You're taking this way to literally.

Originally Posted by bcomp

Sigh, this is ridiculous. You're taking this way to literally.

The point is:

What is the mechanism that prevents speciation or 'Macro-evolution'? What can you put down as the mechanism that prevents something like this from happening:

[Reference from Nature Science Journal]

So far, we have not been presented with anything concrete on the supposed mechanism to prevent speciation, other than assertions. Proof by assertion is not a valid debate tactic, and if you claim there is such a mechanism, you must have something to show for it.

This is also aimed at Ne-yo, but you can answer if you like.

Well I don't think it's so impossible, but Ne-Yo is trying to say that an organism can only work with the genes it has and can't get any more. I do understand his point of view though.

I suppose the evidence would be found in instances of evolution where the change is promoted by mutation or gene destruction rather than the introduction of new, unique genes. Don't know where you'd find that though... but I'm sure it's somewhere. Oh well.

Originally Posted by bcomp

Well I don't think it's so impossible, but Ne-Yo is trying to say that an organism can only work with the genes it has and can't get any more. I do understand his point of view though.

I suppose the evidence would be found in instances of evolution where the change is promoted by mutation or gene destruction rather than the introduction of new, unique genes. Don't know where you'd find that though... but I'm sure it's somewhere. Oh well.

Though we have observed the development of new genes via genetic insertion mutations or even from events such as frame shifts, such as with nylon-digesting bacteria. The 'information' as Ne-yo likes to trumpet, couldn't have existed before the invention of Nylon, as the material is completely synthetic. However, over time, we discovered bacteria that could digest Nylon.

Taking a sample of bacteria that could not digest nylon and put it in a nylon-rich environment, Scientists observed that the bacteria eventually adapted and were able to gain the ability to digest nylon. However, this ability was not as efficient as the precursor protein from which the new protein evolved from, so as it is a new trait, it is understandable that it is not as efficient as it has not been adapted yet for increased efficiency.

The frame shift modified an existing protein to create a completely new one. It was a sudden shift and a completely new trait that would constitute new information as this trait would not have arised and remained in a population had nylon not exist. The fact this protein lent the bacteria an advantage in a nylon-rich environment with a completely new protein would constitute as a good enough example for such 'increases in information'.

References
http://www.ncseweb.org/resources/art...God%27s%20Help
http://www.nmsr.org/nylon.htm

Originally Posted by bluefinger

Though we have observed the development of new genes via genetic insertion mutations or even from events such as frame shifts, such as with nylon-digesting bacteria. The 'information' as Ne-yo likes to trumpet, couldn't have existed before the invention of Nylon, as the material is completely synthetic. However, over time, we discovered bacteria that could digest Nylon.

Taking a sample of bacteria that could not digest nylon and put it in a nylon-rich environment, Scientists observed that the bacteria eventually adapted and were able to gain the ability to digest nylon. However, this ability was not as efficient as the precursor protein from which the new protein evolved from, so as it is a new trait, it is understandable that it is not as efficient as it has not been adapted yet for increased efficiency.

The frame shift modified an existing protein to create a completely new one. It was a sudden shift and a completely new trait that would constitute new information as this trait would not have arised and remained in a population had nylon not exist. The fact this protein lent the bacteria an advantage in a nylon-rich environment with a completely new protein would constitute as a good enough example for such 'increases in information'.

References
http://www.ncseweb.org/resources/art...God%27s%20Help
http://www.nmsr.org/nylon.htm

Right. Which is why his argument is weak. I suppose though, that he'd say that digesting Nylon wouldn't have been outside the scope of the bacteria's original genes, just as a small dog might not be able to jump over a fence, but after years of natural selection for longer legs it would.

I think it'd be wise to study the bacteria's gene pool to see if there were any genetic combinations that could occur without adding new information that would allow it to digest new substances. I mean, hell, maybe the bacteria's just crazy adaptable and naturally makes randomly generated enzymes until it finds one that works. Who knows.

I think it should definitely be looked into since people obviously have questions about it.

Originally Posted by bcomp

Right. Which is why his argument is weak. I suppose though, that he'd say that digesting Nylon wouldn't have been outside the scope of the bacteria's original genes, just as a small dog might not be able to jump over a fence, but after years of natural selection for longer legs it would.

I think it'd be wise to study the bacteria's gene pool to see if there were any genetic combinations that could occur without adding new information that would allow it to digest new substances. I mean, hell, maybe the bacteria's just crazy adaptable and naturally makes randomly generated enzymes until it finds one that works. Who knows.

I think it should definitely be looked into since people obviously have questions about it.

The problem is the use of the word 'information'. If this trait had arisen before the invention of Nylon, then it would have probably killed off the bacteria with the mutation, or at least disadvantaged the bacteria severely. Therefore it would be seen as noise or a bad mutation. However, when this new trait developed within a population of bacteria present in a nylon-rich environment, the protein that arose was able to form an enzyme capable of digesting Nylon. In this circumstance, it would be seen as new information.

Frame shifts can cause pretty hefty shifts in the genome and do add or delete base-pairs or even whole codons onto or from a gene. So in essence, you have a case of new genetic data being created from rather big shifts in the genome, either through adding onto or deleting bits of the genome.

Originally Posted by bluefinger

The problem is the use of the word 'information'.

Yeah. He's using it wrong. By "new information" he means "traits outside the capabilities of the genome."

Aaaaand with that... I'm tired. Night.

Originally Posted by bcomp

Yeah. He's using it wrong. By "new information" he means "traits outside the capabilities of the genome."

Aaaaand with that... I'm tired. Night.

Yeah, his whole use of the word is flawed.

Anyways, goodnight!

Organs are systems.

whut

Systems are made of organs, for example the digestive system and the circulatory system.

Just so you know.

Xei are you that stuck in a little box that you can't understand how an organ is made up of individual cells that run together as a system? There is different sections of the heart that make the complete organ. Organs aren't just one thing they are made up of cells which is a system that has to make the organ up before it can get to larger systems of the body that contain several organs.

Just so you know.

Originally Posted by Xei

whut

Systems are made of organs, for example the digestive system and the circulatory system.

Just so you know.

Technically only the organism is a system because without all of the components needed for the organism to function like it does it wouldn't function like it does.

Minervas Phoenix are you that stuck in a box that you seriously think you have any idea what the fuck you're on about?

http://en.wikipedia.org/wiki/Biological_system

Systems are collections of organs, end of. That was on page one of my biology textbook I think.

But if all the systems affect each other, and can't run individually, then are they reall systems?

I know what a Biological System is, I'm just pointing this out.

Originally Posted by bluefinger

The problem is the use of the word 'information'. If this trait had arisen before the invention of Nylon, then it would have probably killed off the bacteria with the mutation, or at least disadvantaged the bacteria severely. Therefore it would be seen as noise or a bad mutation. However, when this new trait developed within a population of bacteria present in a nylon-rich environment, the protein that arose was able to form an enzyme capable of digesting Nylon. In this circumstance, it would be seen as new information.

Frame shifts can cause pretty hefty shifts in the genome and do add or delete base-pairs or even whole codons onto or from a gene. So in essence, you have a case of new genetic data being created from rather big shifts in the genome, either through adding onto or deleting bits of the genome.

I really hate repeating myself. First of all it is highly unlikely that any of those genes arose through a frame shift mutation, because such mutations forward or reverse would have generated lots of stop codons. So how exactly is it possible that a functional gene arose from a purely random process by accident?

Second: All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes.

Third: Plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism.

Originally Posted by Ne-yo

I really hate repeating myself. First of all it is highly unlikely that any of those genes arose through a frame shift mutation, because such mutations forward or reverse would have generated lots of stop codons. So how exactly is it possible that a functional gene arose from a purely random process by accident?

Second: All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes.

Third: Plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism.

1. Highly unlikely how? It has been shown to be the case though, so what do you have to show that it isn't the case other than an unsubstantiated opinion?
2. Plasmids still are extra-chromosomal genetic data. It is still DNA which can replicate within the bacterial cell without causing the cell itself to divide.
3. 'Designed' how? And what is the designed mechanism by which the new traits arose from? Have anything to substantiate that? Remember, Nylon has only existed for so long so this information could have only arisen within recent times.

Originally Posted by bluefinger

1. Highly unlikely how? It has been shown to be the case though, so what do you have to show that it isn't the case other than an unsubstantiated opinion?

Sorry that's is not an unsubstantiated opion is a fact. I'll break this down more. In 1975, Japanese scientists discovered bacteria that could live on the waste products of nylon manufacture as their only source of carbon and nitrogen. Two species, Flavobacterium sp. K172 and Pseudomonas sp. NK87, were identified that degrade nylon compounds right? Three enzymes are involved in Flavobacterium K172 F-EI, F-EII and F-EIII, and two in Pseudomonas NK87; P-EI and P-EII. None of these have ever been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids; plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas.

Now W.M. Thwaites latched onto these findings as an example of evolution consisting of new information by random mutations and natural selection back in 1985 and another repeat by S.K. Negoro in 1994ref: Talk Origin - http://www.talkorigins.org/indexcc/CB/CB101_2.html

Sub ref; Thwaites work - http://www.ncseweb.org/resources/art..._4_10_2003.asp

Originally Posted by Talk Origin

1. Documentation of mutations producing new features includes the following:
   • the ability of a bacterium to digest nylon (Negoro et al. 1994; Thomas n.d.; Thwaites 1985);

As you can see from the reference links, Thwaites claimed that the new enzyme arose through a frame shift mutation. He based this on a research paper published the previous year where this was suggested. If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to pure chance, however this clearly is not the case. I'll explain why. See there are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress. All five transposable elements are identical, with 764 base pairs each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic degradative genes if they were coding for EI, EII and EIII without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long, so the addition of the transposable elements afterwards cannot be seriously entertained. See my point? This is why Talk Origins information is not to be trusted!

Originally Posted by bluefinger

1. Plasmids still are extra-chromosomal genetic data. It is still DNA which can replicate within the bacterial cell without causing the cell itself to divide.

No you're wrong. This does not look like some random origin of these genes the chance of this happening is low. If the genome of Flavobacterium is about two million base pairs and the pOAD2 plasmid comprises 45,000 base pairs, and if there were say 5 pOAD2 plasmids per cell then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments also resulted in enzyme activity on plasmids then attributing the developement of active enzymes purely to chance mutations become even more impossible.

Originally Posted by bluefinger

1. 'Designed' how? And what is the designed mechanism by which the new traits arose from? Have anything to substantiate that? Remember, Nylon has only existed for so long so this information could have only arisen within recent times.

My GOD bluefinger! How could you have missed my entire point? The designed mechanism already existed on the Plasmids. Otherwise you'll have to explain how is can evolution take he point as the mechanism, Because based off Thwaites and Negoro it would look like recombination of codons base pair triplets, not single base pairs, has occurred between the start and stop codons for each sequence. This would probably be about the simplest way that the antisense strand could be protected from stop codon generation. However in this case the mechanism for such a recombination is would definately be unknown.
Stay away from Talk Origins they'll lead you astray and delude your mind with inaccurate information. Do your own research you will not believe how much stuff on that site can be refuted. Good Luck

Damn.

That's intense. Nice researching Ne-Yo.

Here's the published paper on those bacteria.

Originally Posted by Ne-yo

Sorry that's is not an unsubstantiated opion is a fact. I'll break this down more. In 1975, Japanese scientists discovered bacteria that could live on the waste products of nylon manufacture as their only source of carbon and nitrogen. Two species, Flavobacterium sp. K172 and Pseudomonas sp. NK87, were identified that degrade nylon compounds right? Three enzymes are involved in Flavobacterium K172 F-EI, F-EII and F-EIII, and two in Pseudomonas NK87; P-EI and P-EII. None of these have ever been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids; plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas.

Now W.M. Thwaites latched onto these findings as an example of evolution consisting of new information by random mutations and natural selection back in 1985 and another repeat by S.K. Negoro in 1994ref: Talk Origin - http://www.talkorigins.org/indexcc/CB/CB101_2.html

Sub ref; Thwaites work - http://www.ncseweb.org/resources/art..._4_10_2003.asp

As you can see from the reference links, Thwaites claimed that the new enzyme arose through a frame shift mutation. He based this on a research paper published the previous year where this was suggested. If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to pure chance, however this clearly is not the case. I'll explain why. See there are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress. All five transposable elements are identical, with 764 base pairs each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic degradative genes if they were coding for EI, EII and EIII without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long, so the addition of the transposable elements afterwards cannot be seriously entertained. See my point? This is why Talk Origins information is not to be trusted!

From what I read, I don't see what is wrong with TalkOrigins in the first place. So far, the places I use for sources all seem to have something in common... consistency, so again, what is your point?

As for your case against the frame-shift mutation explanation, all I could get from you is that it is somehow impossible. However, looking at this paper in pubmedcentral.nih.gov, it explains in great detail why the conclusion was that a frame shift mutation was reponsible for the new trait in Flavobacterium sp. K172. Now, what you have done is simply said that the conclusion is wrong because it is highly unlikely. Taking into account the differences between PR.C and R-II proteins whilst considering they are not completely alien, as the original sequence is fairly repetitious; there are homologous areas within sequences which can be read in the same reading frame. This however, arises in non-corresponding areas within the sequences, so the functionality of these protein sequences are not expected to be the same.

From this, we see that the former sequence contains no Trp or Asn codons and thus would not have a function as an enzyme of any sort, but the latter sequence does have the two codons present in the sequence, whilst sharing homologous areas between itself and PR.C, all in non-corresponding areas of course. As the change occurred in such a short period of time, and the change observed in the protein sequences shared fundamental differences whilst pointing out multiple areas of similarities thanks to the repetitious nature of the original protein, we can conclude a frame-shift occurred in order to precipitate the development of the new trait. This is supported by the fact that both proteins had nearly completely the same base sequence as each other, except they were processed by different reading frames. All it took was the insertion of a T base after codon 33 in the PR.C protein in order to achieve the result, even causing a new stop codon to emerge between codons 425 and 426 in the PR.C sequence as opposed to 428 being the stop codon, just from a shift in the reading frame. In one fell swoop, one non-functioning protein was activated and changed to represent an enzyme with the ability to degrade Nylon.

More sources

Originally Posted by Ne-yo

No you're wrong. This does not look like some random origin of these genes the chance of this happening is low. If the genome of Flavobacterium is about two million base pairs and the pOAD2 plasmid comprises 45,000 base pairs, and if there were say 5 pOAD2 plasmids per cell then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments also resulted in enzyme activity on plasmids then attributing the developement of active enzymes purely to chance mutations become even more impossible.

Plasmids are still extra-chromosomal DNA, so I don't see what this block of text in particular has anything to do with the point I made beforehand. Also, your use of probabilities is completely pointless.

Originally Posted by Ne-yo

My GOD bluefinger! How could you have missed my entire point? The designed mechanism already existed on the Plasmids. Otherwise you'll have to explain how is can evolution take he point as the mechanism, Because based off Thwaites and Negoro it would look like recombination of codons base pair triplets, not single base pairs, has occurred between the start and stop codons for each sequence. This would probably be about the simplest way that the antisense strand could be protected from stop codon generation. However in this case the mechanism for such a recombination is would definately be unknown.
Stay away from Talk Origins they'll lead you astray and delude your mind with inaccurate information. Do your own research you will not believe how much stuff on that site can be refuted. Good Luck

First of all, frame-shifts can occur with more than one base-pair at a time, but with what I have read on the Nylonase research for Flavobacterium sp. K172, it seems a single base insertion was responsible for the shift. Also, you have not divulged what the design mechanism actually is, only parroted how the frame-shift mutation was impossible. If such a mechanism is 'unknown' why presume it is designed? You are arriving at a conclusion before the evidence is collected and analysed, at least with concern to your 'mechanism'.

Also, what about Talk Origins? Pretty much what is on there is also on other websites like Nature and NewScientist, and they use references for Pub. Med and other journals, so I don't see what the big deal is. Everything is consistent, which is more than that can be said for the proponents of ID.

In the end, flashy presentations only get you so far. You actually have presented little to validate your own argument and only focused on the process that "if A is false, then B must be true!". All you've done here is based your argument on a false dichotomy which does not reflect the reality. Even if it was not a frame-shift mutation, there are still other possibilities to consider other than just 'design'. However, in this case, the evidence points towards a frame-shift mutation considering what frame-mutations are predicted to do and comparing those predictions with what has been observed.

So, are you going to explain what your design mechanism is and what you are basing your conclusion on? That would be good to see.

Originally Posted by bcomp

Damn.

That's intense. Nice researching Ne-Yo.

Thanks, however I was swamped with biology and chemistry growing up. A lot of things just made a kind of permanent imprint on my psyche'

Originally Posted by bluefinger

From what I read, I don't see what is wrong with TalkOrigins in the first place. So far, the places I use for sources all seem to have something in common... consistency, so again, what is your point?

You're right about consistency thats for sure, they all display a sense of consistency in making hostile comments towards creationist views.

Originally Posted by bluefinger

As for your case against the frame-shift mutation explanation, all I could get from you is that it is somehow impossible. However, looking at this paper in pubmedcentral.nih.gov, it explains in great detail why the conclusion was that a frame shift mutation was reponsible for the new trait in Flavobacterium sp. K172. Now, what you have done is simply said that the conclusion is wrong because it is highly unlikely. Taking into account the differences between PR.C and R-II proteins whilst considering they are not completely alien, as the original sequence is fairly repetitious; there are homologous areas within sequences which can be read in the same reading frame. This however, arises in non-corresponding areas within the sequences, so the functionality of these protein sequences are not expected to be the same.

From this, we see that the former sequence contains no Trp or Asn codons and thus would not have a function as an enzyme of any sort, but the latter sequence does have the two codons present in the sequence, whilst sharing homologous areas between itself and PR.C, all in non-corresponding areas of course. As the change occurred in such a short period of time, and the change observed in the protein sequences shared fundamental differences whilst pointing out multiple areas of similarities thanks to the repetitious nature of the original protein, we can conclude a frame-shift occurred in order to precipitate the development of the new trait. This is supported by the fact that both proteins had nearly completely the same base sequence as each other, except they were processed by different reading frames. All it took was the insertion of a T base after codon 33 in the PR.C protein in order to achieve the result, even causing a new stop codon to emerge between codons 425 and 426 in the PR.C sequence as opposed to 428 being the stop codon, just from a shift in the reading frame. In one fell swoop, one non-functioning protein was activated and changed to represent an enzyme with the ability to degrade Nylon.

You’re excluding a major point to this topic, you keep stating that the frame shift mutation was responsible for the new trait in Flavobacterium however based off Susumu Ohno’s paper you’ve presented clearly states that the analysis of the published based sequence resides in the pOAD2 plasmid of Flavobacterium sp. K172. Okay so here’s the kicker bluefinger, The number of bases repeated is not a multiple of 3 however in this case, 10 bases are probably the repeating unit. See, 10 bases were translated in all three possible reading frames the second repeat was one base offset for translation relative to the first repeat, and the next was offset one more base, etc. Also, none of those reading frames gave rise to stop codons. See this is important considering the 10-base repeat was translatable in any reading frame without causing any stop codons, the sequence was able to undergo an insertion which could alter the reading frame without prematurely terminating the protein.

Now I do understand that the mutation did cause a stop codon, but the stop codon was not because of frame shift but to the sequence introduced by the inserted nucleotide. Simultaneously, the mutation introduced a start codon in a different reading frame, which now encoded an entirely new sequence of amino acids. This is the key aspect of the sequence. It had this special property that it could tolerate any frame shift due to the repetitive nature of the original DNA sequence. Now as I’m sure you’re well-aware that in biology, a frame shift causes a stop codon and either truncation of the protein normally due to the premature stop codon or destruction of the abberant mRNA by the nonsense-mediated decay pathway. I don’t recall seeing stop-codons arising in PR.C, I’m not sure where you got that from. Nonetheless, the nylonase enzyme, once it arose, had no stop-codons so it was able to make a novel, functional protein.

Originally Posted by bluefinger

Plasmids are still extra-chromosomal DNA, so I don't see what this block of text in particular has anything to do with the point I made beforehand. Also, your use of probabilities is completely pointless.


First of all, frame-shifts can occur with more than one base-pair at a time, but with what I have read on the Nylonase research for Flavobacterium sp. K172, it seems a single base insertion was responsible for the shift. Also, you have not divulged what the design mechanism actually is, only parroted how the frame-shift mutation was impossible. If such a mechanism is 'unknown' why presume it is designed? You are arriving at a conclusion before the evidence is collected and analysed, at least with concern to your 'mechanism'.

Why are my probabilities irreleavant but the moment someone talks about impossibilities of abiogenesis and non-living matter giving rise to living matter, then the first thing someone does is hit all the probabilities of this happening. And somehow it’s always determined that the probabilites are on the side of evolution. So I guess probabilites can be presented in one case but not in all huh?

Originally Posted by bluefinger

Also, what about Talk Origins? Pretty much what is on there is also on other websites like Nature and NewScientist, and they use references for Pub. Med and other journals, so I don't see what the big deal is. Everything is consistent, which is more than that can be said for the proponents of ID.

In the end, flashy presentations only get you so far. You actually have presented little to validate your own argument and only focused on the process that "if A is false, then B must be true!". All you've done here is based your argument on a false dichotomy which does not reflect the reality. Even if it was not a frame-shift mutation, there are still other possibilities to consider other than just 'design'. However, in this case, the evidence points towards a frame-shift mutation considering what frame-mutations are predicted to do and comparing those predictions with what has been observed.

So, are you going to explain what your design mechanism is and what you are basing your conclusion on? That would be good to see.

I know that, however, if only 6 of these 47 mutations were essential for the evolution, the probability of achieving it in 30 years is about 3 x 10^35. but if I’m not mistaken this occurred in only 9 days! So, if the evolution could not be random, then it would have to be nonrandom, which means they would be triggered by the environment. That is, the capability is built into the bacterium and the environment triggers the mutations. Now in regards to what I mean by design, I am making this statement in the sense that the original DNA sequence was preadapted for frame-shift mutations to occur without destroying the protein-coding potential of the original gene. Indeed, this protein sequence seems ‘designed’ to be specifically adaptable to novel functions would you not agree?

Also websites like Nature, National Geographic, New Scientist and the ‘most’ of the others that Talk Origins use are notorious for their hostility toward the creationist. And their promotions of evolutionary frauds and myths. Now in the end it’s not all about flashy presentations because I honestly don’t have anything to prove, I look at both angles and unlike you I don’t take things at face value, just because Talk Origins says this is true and they snowball you with tons of information so that you do not check the validity of the sources which they makes claims of reliability, doesn’t always seem to be the case. However we are all different and in the “real end” that’s exactly how it should be.

[Citation Needed]

Also: Creationism has NO SUBSTANCE. There's nothing there. It's just a void that says "Modern Science is wrong".

I know that, however, if only 6 of these 47 mutations were essential for the evolution, the probability of achieving it in 30 years is about 3 x 10^35. but if I’m not mistaken this occurred in only 9 days! So, if the evolution could not be random, then it would have to be nonrandom, which means they would be triggered by the environment. That is, the capability is built into the bacterium and the environment triggers the mutations. Now in regards to what I mean by design, I am making this statement in the sense that the original DNA sequence was preadapted for frame-shift mutations to occur without destroying the protein-coding potential of the original gene. Indeed, this protein sequence seems ‘designed’ to be specifically adaptable to novel functions would you not agree?

Do you not know anything about evolution?

Probabilities are irrelevant because it HAPPENED. Of course the environment had to do with; don't you know what natural selection is??

Also:

- Argument from ignorance
- Argument from personal incredulity

Originally Posted by Ne-yo

Thanks, however I was swamped with biology and chemistry growing up. A lot of things just made a kind of permanent imprint on my psyche'

Like religion for example. Especially all that hell-fire and brimstone stuff...

Originally Posted by Ne-yo

You're right about consistency thats for sure, they all display a sense of consistency in making hostile comments towards creationist views.

O RLY? Because they tear apart your creationist views with scientific evidence makes them not worthy of use? Let me guess, Answers In Genesis is your source for all your claims?

Originally Posted by Ne-yo

You’re excluding a major point to this topic, you keep stating that the frame shift mutation was responsible for the new trait in Flavobacterium however based off Susumu Ohno’s paper you’ve presented clearly states that the analysis of the published based sequence resides in the pOAD2 plasmid of Flavobacterium sp. K172. Okay so here’s the kicker bluefinger, The number of bases repeated is not a multiple of 3 however in this case, 10 bases are probably the repeating unit. See, 10 bases were translated in all three possible reading frames the second repeat was one base offset for translation relative to the first repeat, and the next was offset one more base, etc. Also, none of those reading frames gave rise to stop codons. See this is important considering the 10-base repeat was translatable in any reading frame without causing any stop codons, the sequence was able to undergo an insertion which could alter the reading frame without prematurely terminating the protein.

Now I do understand that the mutation did cause a stop codon, but the stop codon was not because of frame shift but to the sequence introduced by the inserted nucleotide. Simultaneously, the mutation introduced a start codon in a different reading frame, which now encoded an entirely new sequence of amino acids. This is the key aspect of the sequence. It had this special property that it could tolerate any frame shift due to the repetitive nature of the original DNA sequence. Now as I’m sure you’re well-aware that in biology, a frame shift causes a stop codon and either truncation of the protein normally due to the premature stop codon or destruction of the abberant mRNA by the nonsense-mediated decay pathway. I don’t recall seeing stop-codons arising in PR.C, I’m not sure where you got that from. Nonetheless, the nylonase enzyme, once it arose, had no stop-codons so it was able to make a novel, functional protein.

The paper I presented said the frame-shift was a single T base injection after codon 33 on the PR.C protein sequence, resulting in a single frame shift that later induced a stop codon in between codons 425 and 426, even though there were several close calls along the same sequence, but because of the reading frame, were not processed to be stop codons. It is even highlighted quite clearly with the diagram of the sequence in the paper (all the back marks between the two sequences highlighting stop codons. Unless you know the DNA codes for stop codons, you'd probably miss it, but it is all there. Just look for those black marks and compare them to the two reading frames for PR.C & R-II).

However, with frame shift mutations, the sequence can extend beyond the original sequence if no stop codons are induced within the sequence and the resulting shift causes the primary stop codon to be misread. Then it is a case of the next sequence that causes a stop codon within the reading frame. There is nothing saying it has to be shorter than the original sequence. Most of the time, frame-shifts are pretty destructive, and result in abnormally long or short proteins, and can cause an affected gene to contain all the wrong codons and generally wreak havoc upon the genome. However, occasionally, it does allow for the development of completely new and novel traits such as Nylonase, not to mention add more bases to the genome.

Originally Posted by Ne-yo

Why are my probabilities irreleavant but the moment someone talks about impossibilities of abiogenesis and non-living matter giving rise to living matter, then the first thing someone does is hit all the probabilities of this happening. And somehow it’s always determined that the probabilites are on the side of evolution. So I guess probabilites can be presented in one case but not in all huh?

Using probabilities for past events will always bring up huge odds stacked against them from even happening, and yet, the events happened as normal. Probabilities are used for predicting future events, not for speculating on past ones. For past events, we deal with evidence of whether they occurred or not.

Originally Posted by Ne-yo

I know that, however, if only 6 of these 47 mutations were essential for the evolution, the probability of achieving it in 30 years is about 3 x 10^35. but if I’m not mistaken this occurred in only 9 days! So, if the evolution could not be random, then it would have to be nonrandom, which means they would be triggered by the environment. That is, the capability is built into the bacterium and the environment triggers the mutations. Now in regards to what I mean by design, I am making this statement in the sense that the original DNA sequence was preadapted for frame-shift mutations to occur without destroying the protein-coding potential of the original gene. Indeed, this protein sequence seems ‘designed’ to be specifically adaptable to novel functions would you not agree?

Random mutations are random by nature. The insertion point for that extra base in codon 34 in PR.C could have happened at any point along the sequence. If it had, a different protein would have arisen, and it could have been a lot shorter or longer, not to mention the codons that would arise would have been quite different. There is no pre-adaptation as there is no conscious motive for such shifts. The only reason such a trait became prevalent was because the resulting protein was able to degrade a synthetic molecule. Had such a molecule not been present in the environment, such a frame-shift would have caused an unnecessary trait and wouldn't give the bacteria with the mutations any advantage.

There is nothing to suggest a design, only circumstance. In this circumstance, the mutation proved to be beneficial. In any other case, it would have been selected against.

Originally Posted by Ne-yo

Also websites like Nature, National Geographic, New Scientist and the ‘most’ of the others that Talk Origins use are notorious for their hostility toward the creationist. And their promotions of evolutionary frauds and myths. Now in the end it’s not all about flashy presentations because I honestly don’t have anything to prove, I look at both angles and unlike you I don’t take things at face value, just because Talk Origins says this is true and they snowball you with tons of information so that you do not check the validity of the sources which they makes claims of reliability, doesn’t always seem to be the case. However we are all different and in the “real end” that’s exactly how it should be.

There is a good reason why they don't support creationism, because there is nothing to show for it. At least with Evolution, I have a peer-review literature of about 200,000 papers to go through. There is plenty to show for Evolution, all of which comes from about 150 years of research on the field. And what sources do you use perhaps? Answers in Genesis?

I did my research, and it was pretty clear what the evidence was pointing to in this case. Whether it is Pub Med Central, Nature, TalkOrigins, or whatever, the case presented on all the sources was consistent and supported by evidence.