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#1 gilbo12345

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Posted 25 April 2010 - 08:31 AM

Hey there. I am sure this has probably been talked about before. But due to my laziness of not wishing to go through pages of info, (and for a more personal talk with people :rolleyes: ), I decided to ask about this here :rolleyes:

I read an article today, saying that bacteria evolved the ability to create nylonase by a random mutation.

Firstly, is this true?

Secondly, if not how did this ability come about?

Thanks in advance for replies :unsure:

#2 jason777

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Posted 25 April 2010 - 10:09 AM

Hey there. I am sure this has probably been talked about before. But due to my laziness of not wishing to go through pages of info, (and for a more personal talk with people :rolleyes: ), I decided to ask about this here :unsure:

I read an article today, saying that bacteria evolved the ability to create nylonase by a random mutation.

Firstly, is this true?

Secondly, if not how did this ability come about?

Thanks in advance for replies ;)

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That was the evo-story before X-ray Crystallographic Analysis. When the mechanism was observed; it turned out to be an adaptation by protein replacement similar to penicillin resistance. If it was a random mutation, then we would have seen a mutation in the genes - but the gene simply produced two different proteins instead, which indicates purposeful adaptation and not something random.

You have to be careful when evolutionists use the word mutation. In their mind, everything came about by accident and chance. :rolleyes:



X-ray Crystallographic Analysis of 6-Aminohexanoate-Dimer Hydrolase
MOLECULAR BASIS FOR THE BIRTH OF A NYLON OLIGOMER-DEGRADING ENZYME*


6-Aminohexanoate-dimer hydrolase (EII), responsible for the degradation of nylon-6 industry by-products, and its analogous enzyme (EII′) that has only ∼0.5% of the specific activity toward the 6-aminohexanoate-linear dimer, are encoded on plasmid pOAD2 of Arthrobacter sp. (formerly Flavobacterium sp.) KI72. Here, we report the three-dimensional structure of Hyb-24 (a hybrid between the EII and EII′ proteins; EII′-level activity) by x-ray crystallography at 1.8 Ã… resolution and refined to an R-factor and R-free of 18.5 and 20.3%, respectively. The fold adopted by the 392-amino acid polypeptide generated a two-domain structure that is similar to the folds of the penicillin-recognizing family of serine-reactive hydrolases, especially to those of d-alanyl-d-alanine-carboxypeptidase from Streptomyces and carboxylesterase from Burkholderia. Enzyme assay using purified enzymes revealed that EII and Hyb-24 possess hydrolytic activity for carboxyl esters with short acyl chains but no detectable activity for d-alanyl-d-alanine. In addition, on the basis of the spatial location and role of amino acid residues constituting the active sites of the nylon oligomer hydrolase, carboxylesterase, d-alanyl-d-alanine-peptidase, and β-lactamases, we conclude that the nylon oligomer hydrolase utilizes nucleophilic Ser112 as a common active site both for nylon oligomer-hydrolytic and esterolytic activities. However, it requires at least two additional amino acid residues (Asp181 and Asn266) specific for nylon oligomer-hydrolytic activity. Here, we propose that amino acid replacements in the catalytic cleft of a preexisting esterase with the β-lactamase fold resulted in the evolution of the nylon oligomer hydrolase.



http://www.jbc.org/c.../39644.abstract




Enjoy.

#3 Isabella

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Posted 25 April 2010 - 10:41 AM

If it was a random mutation, then we would have seen a mutation in the genes - but the gene simply produced two different proteins instead, which indicates purposeful adaptation and not something random.

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Based on that article it sounds like two amino acids have been changed in the protein. Which means that two codons have been changed in the DNA. That sounds like a mutation to me, or did I just misunderstand the article?

#4 Cata

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Posted 25 April 2010 - 11:55 AM

Which means that two codons have been changed in the DNA.

but the gene simply produced two different proteins instead,



#5 AFJ

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Posted 25 April 2010 - 03:20 PM

Based on that article it sounds like two amino acids have been changed in the protein. Which means that two codons have been changed in the DNA. That sounds like a mutation to me, or did I just misunderstand the article?

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[Nylon Eater] 6-Aminohexanoate-dimer hydrolase (EII)...and its analogous enzyme (EII′)... are encoded on plasmid pOAD2


I have not read the entire thing but unless I'm missing something...

A plasmid is responsible--that's not a random mutation. Plasmids from outside the bacteria incorporate their DNA into the bacterium's DNA, and many times change the phenotype. It is a system, not a random process. The plasmid DNA is not considered foreign to the bacteria or it would be destroyed by restrictive enzymes. The plasmid DNA has specific insertion sequences on the ends that insert at specific sites on the bacterium's chromosome. In this case, the protein enzyme (EII) and it's analogous enzyme (EII′) are created by the plasmid DNA insertion.

This shows pre existing information that works within an already existing system --not creation of new information by a random process.

Most importantly, a new enzyme is not a new 'kind' of organism. Time is not important here--but the right DNA. This DNA was pre-existant. If evolution into a new kind is possible, and this the mechanism for bacteria, there should be more plasmids out there which will change the bacteria into another 'kind.'

#6 gilbo12345

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Posted 25 April 2010 - 03:26 PM

Ah ha thanks.

So if it is actually wrong? Why do people still think it is acase for evolution?

Just that next semester, we will be doing "Evolutionary Biology", so I guess I'll be bombarded with all these "proofs"..

I just want to be prepare myself :rolleyes: (If you guys don't mind me asking lots of questions :rolleyes: )

#7 AFJ

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Posted 25 April 2010 - 03:50 PM

Ah ha thanks.

So if it is actually wrong? Why do people still think it is  acase for evolution?

Just that next semester, we will be doing "Evolutionary Biology", so I guess I'll be bombarded with all these "proofs"..

I just want to be prepare myself :rolleyes: (If you guys don't mind me asking lots of questions :rolleyes: )

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I would get me a basic microbiology book. It will give you the fundamentals of what's going on inside our cells. Alot of changing is happening, but it's not random at all. You are not going to change the curriculum, but you have a right to do your own research!

There are actually smart credible experienced creationists you could read. You don't have to accept everything every one says on either side. But will it hurt to read another interpretation of evidence? Yes there are unqualified ignorant creationists too. But that goes for evos also. The only difference is their worldview. They see the same science--just interpret it differently when it comes to the origin of life. Everything else is the same.

#8 gilbo12345

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Posted 25 April 2010 - 04:14 PM

Thanks AFJ

May I ask, is there some journal articles refuting evolution... (I doubt it)...

Just that people turn to that when they have nothing else...

"Oh your evidence isn't peer reviewed, mine is better than yours"....lol

Thanks

#9 gilbo12345

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Posted 25 April 2010 - 04:34 PM

Sorry I sound like an evolutionist...

I am not sure of there being journal articles as, in the end, they are a business... (almost like a magazine)...

They won't publish stuff that undeniably goes against the grain of the "scientific community" as they would lose face...

#10 Isabella

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Posted 25 April 2010 - 05:03 PM

A plasmid is responsible--that's not a random mutation. Plasmids from outside the bacteria incorporate their DNA into the bacterium's DNA, and many times change the phenotype. It is a system, not a random process. The plasmid DNA is not considered foreign to the bacteria or it would be destroyed by restrictive enzymes. The plasmid DNA has specific insertion sequences on the ends that insert at specific sites on the bacterium's chromosome. In this case, the protein enzyme (EII) and it's analogous enzyme (EII′) are created by the plasmid DNA insertion.

This shows pre existing information that works within an already existing system --not creation of new information by a random process.

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Plasmids are just small rings of DNA. They don’t really come from an outside source as you seem to imply. They are either kept within the bacteria as part of their normal genome, or transferred from one bacterium to another.

The enzyme which changed was coded for on the plasmid. The plasmid DNA must have mutated at some point to code for a different sequence of amino acids. I don’t know why you claim that a mutation didn’t happen.

#11 AFJ

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Posted 25 April 2010 - 06:50 PM

Plasmids are just small rings of DNA. They don’t really come from an outside source as you seem to imply. They are either kept within the bacteria as part of their normal genome, or transferred from one bacterium to another.

The enzyme which changed was coded for on the plasmid. The plasmid DNA must have mutated at some point to code for a different sequence of amino acids. I don’t know why you claim that a mutation didn’t happen.

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Yes, I know that plasmids are kept in bacteria. They are passed through conjugation. They are not just small rings of DNA but some of them have entire genes.

I correct myself--phages are outside, and plasmids can not not live outside the host. But the facts I gave about the insertion sequences and specific sites on the bacterium's DNA are true. As well as the fact that the bacteria accept the DNA without destoying it (plasmids are passed), unlike much phage DNA. You can check this if you'd like.

The point is that this is not some random happening--it is a system. There is no way insertion sequences just happened to mutate into the proper sequence and just happen to insert into DNA in a place that just happens to match. It all fits together, which is quite indicative of a designed system. Moreover enzymes are required for all of this, and they must be coded for also. Why would unguided mutation happen to code for enzymes that work with the system and of which the system is dependent? Which came first the enzyme or the system? You have to have both simultaneously in many cases. Just like you have to have all the parts of an engine or it won't work.

I didn't say a mutation didn't happen--I said a random mutation didn't happen. It is a designed change for adaptation, and you will not see a change in kind. Are you under the impression that creationists don't believe in adaptation within kinds. It would seem to be quite empirical. However to take this example and say that the organism will evolve into another organism is not empirical. And scientists obviously can't imagine any selective pressure that would do so or they would have done it in the lab.

Also most mutations are not so beneficial as this change. There are potential or serious problems when inversions, frame shifts, insertions, and deletions take place. The odds are not in favor of beneficial mutation at all.

#12 jason777

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Posted 25 April 2010 - 08:13 PM

The enzyme which changed was coded for on the plasmid. The plasmid DNA must have mutated at some point to code for a different sequence of amino acids. I don’t know why you claim that a mutation didn’t happen.


The gene already has the ability produce numerous different proteins. It is'nt proven if the entire protein was replaced by a new one or if two amino acids were added to a pre-existing protein. We only observed the before and after - not the actual process.

Although, no mutation was observed anywhere else as you claim must have happened. So, it is more likely that the entire protein was replaced by a different one. Genetic engineers are finding it hard to engineer genes that can change proteins at will at any given time. The record holder is a gene in fruit flies that can code for more than 30,000 different proteins and a gene in humans is known to code for 64 proteins.



Thanks.

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Posted 26 April 2010 - 07:41 AM

The gene already has the ability produce numerous different proteins. It is'nt proven if the entire protein was replaced by a new one or if two amino acids were added to a pre-existing protein. We only observed the before and after - not the actual process.

Although, no mutation was observed anywhere else as you claim must have happened. So, it is more likely that the entire protein was replaced by a different one. Genetic engineers are finding it hard to engineer genes that can change proteins at will at any given time. The record holder is a gene in fruit flies that can code for more than 30,000 different proteins and a gene in humans is known to code for 64 proteins.
Thanks.

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This one has always been entertaining. I'm still puzzled that most science will never asked the important common sense question. When you consider the micro-biological world, "What is the basic purpose and function of such organisms?" :)

Okay, right, that would be way off the materialist radar because such reasonable LOGICAL (debatable as to it's definition = shell game) questions don't address that evolution is after all pointless, without intent, and never has a goal in mind because there is no motivational intelligence directing anything. ;)

First you have to consider all their flavourite examples. Besides the notoriously wonderful randomly Nylonase, we have the randomly mutated Swine Flu, randomly mutated AIDS virus, randomly mutated Spanish Influenza , etc, etc. The connection never made or considered is that in every one of these tragic incidences, there was a human fingerprint because of greed , selfishness, stupidty, arrogance, ignorance, etc. The Nylonase bacteria was activated by the stupidy of human error of something science created in the first place but as usual gave no consieration to a responsible environmental waste disposal. It must be noted that entire ecosystems have an engineered checks and balances programmed into them. This discussion really goes back to the engineering algorithm genes with the redundancy error correction mechanisms. The purpose of most all micro-organisms is recycling our planet. What happens above the ground in the ecosystems we all see is a direct result of the balanced invisible machinery we don't see.

Here's a link to a more responsible explanation of how the non-random machinery actually works with purpose and intent. The elements or material substrate of Nylon comes from the Earth. It didn't come from Krypton, Vulcan, Romulus , etc. It's earthly and the programming for tackling any new situation has always been right there for dealing with earthly situations. Again it's a carbon copy illustration of what our own immune system does from the time we are born and tackling whatever foreign invader comes after it, that is if taken care of properly.

Nylon Bug - Arthur S Lodge

Nylon Bug 3 - Arthur S Lodge


AND . . . . .


"Are mutations truly random?"

The Scientist - January 13th 2010

Are Mutations Truly Random ?


#14 gilbo12345

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Posted 27 April 2010 - 08:53 AM

Thanks for the links!! ;) :)

Also thanks for the responses guys... When I first read the article about it, I was getting really worried.. You guys have reassured me :)

#15 AFJ

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Posted 27 April 2010 - 07:43 PM

Thanks for the links!! :) :)

Also thanks for the responses guys... When I first read the article about it, I was getting really worried.. You guys have reassured me :)

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Here's some more by Perdom and Anderson

The mutational changes of EII (6-aminohexanoatedimer hydrolase) have been characterized in detail. This analysis suggests that point mutations in a carboxyesterase gene lead to amino acid substitutions in the enzyme’s catalytic cleft. This altered the enzyme’s substrate specificity sufficiently that it could also hydrolyze linear nylon oligomers.74, 75 Yet, the EII enzyme still possesses the esterase function of the parent esterase. Thus, the mutational alteration results in a reduction of the parent enzyme’s specificity (Figure 4). This enables it to hydrolyze a wider range of oligomers that include nylon oligomers.76

Nonetheless, reduced specificity of a pre-existing enzyme is biochemically degenerative to the enzyme,77, 78 even if it provides a presumed phenotypic benefit. The “beneficial” phenotype of nylon degradation requires the a priori existence of the enzyme and its specificity. Its degeneration is not a mechanism that accounts for the origin of either the enzyme or its specificity.

Also on pOAD2 is a DNA region with a high homology to opp genes.79 These genes are involved in oligopeptide transport. Nylon oligomers have many chemical similarities to oligopeptides, thus genes on this region of the plasmid may be involved in nylon transport into the cell. No analysis of how these genes may have been altered by mutations has yet been preformed. However, it is reasonable to speculate that a pre-existing opp gene or set of genes has been altered sufficiently by mutations so that the transport proteins now have an affinity for nylon in addition to naturally occurring oligopeptides. As with enzymes, reduction of transport protein specificity is biochemically degenerative.

The enzyme and putative transport genes on pOAD2 appear to form a nylon degrading operon.79 As a plasmid based operon, it can be transferred to various bacterial species. Thus, this gives it the potential for widespread distribution in the bacterial world. What is more, the increasing amount of microbial degradation of synthetic material11 may likely involve a similar mutational strategy as found with nylon degradation. This is a testament to the versatility of bacterial adaptation. However, these mutations do not account for the origin of the enzyme or transport protein specificity, merely their degeneration. Thus, this adaptive versatility has imposed limits as well, and this fits well within the types of mutational changes predicted by a creation model.
Horizontal Gene Transfer

Horizontal gene transfer (HGT) is cell-to-cell transfer of genetic material, usually plasmids or transposons. Plasmids are autonomous extrachromosomal segments of DNA. They may posses a variety of genes, including genes for mobilization and antibiotic resistance.

HGT of plasmids merely transfers genetic material from one cell to another. Introduction of specific genes, such as antibiotic resistance genes, via a plasmid can be beneficial for bacterial survival. However, HGT of plasmids does not directly account for the origin of the gene(s) being transferred, merely their movement within the microbial world. The genes’ existence is a priori. This is consistent with a creation model where genes, regulatory sites, and other genetic activity were formed at the initial creation event, and are not solely the result of mutational or recombination events. The transfer of pre-existing genes and other genetic activity does not account for the origin of the transferred activity. Also, unless the plasmid incorporates into the host chromosome, it does not result in a mutation. Therefore, the contribution of plasmid HGT to bacterial adaptation is a separate topic outside the scope of this paper.

A transposon is a segment of DNA that can be transferred from cell-to-cell via HGT. The transposon can be maintained on a plasmid, but typically exists autonomous of plasmids, and merely moves from chromosome to chromosome. Most cellular “transformation” by transposons involves (a) incorporation of new genes into the cell from the transposon, (:( activation of “silent” genes, and/or © insertional disruption of genes and regulatory sites on the host’s chromosome. The introduction of new genes into a cell (such as the antibiotic resistant genes typically found on commonly studied transposons) may provide new genetic capability to the transformed cell. However, as with plasmids discussed above, this does not account for the origin of these genes. Their existence is a priori in the biological world.

By analogy, this is like transferring money from the left to the right pocket. The right pocket now has money that it did not posses before, but you are no richer. This type of mechanism cannot account for the origin of the money, merely its transfer among the population. As applied to the biological world, HGT of genes fails to explain their origin, thus it fails to fulfill the genetic requirements for common descent. However, HGT does fit within the creation model where the transfer of existing genes would be predicted as an adaptive design feature.






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