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Question For E. Coli Long-Term Evolution Experiment


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#101 NewPath

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Posted 27 June 2012 - 02:49 AM

There's nothing particularly unbelievable about that. There are 4 possible base pairs, the human genome contains 3 billion base pairs, 98% of it noncoding (and noncoding doesn't mean non-functional, but 98% of the genome isn't regulatory either). Every single 3-base pair combination codes for an amino acid, an initiation site or a stopping site. The odds that there exist short strings of codons in there that correspond to a functional protein and are just lacking an ORF isn't low at all. If those had been very long genes it would be another story but in fact they're very very short.

I really don't see how we can go further with this, can't we go back to the other points we were talking about before discussing this article took over the whole conversation ?

(although I would still like to find out more about those gibbons with chronic lymphocytic leukemia, I still haven't been able to find anything on that, maybe you could give me google search terms with which to find out more if nothing else ?)


I'm sorry, if you cannot at least admit to the possibility of those four apes independently having that disabler, then I see you are far too stubborn to be able to discuss issues with. Why discuss issues if there are going to be no conclusions?

You are referring to 4 possible base pairs , I am referring to entire genes in humans involving thousands of base-pairs each. You say this gene was never coding, and humans evolved, and this became a coding region. I don't think you quite get the lack of randomness in genes. Its like a computer code, a precise set of information that produces precise functions in the human body through the production of proteins. You seem to brush over the statistical impossibility of this spontaneously occurring across a unique combination of thousands of unique base-pairs. Our previous discussion involved the possibility of duplicating and changing a gene, now we are talking about novel functional genes in a non-coding format waiting to be activated. Maybe your wording implies that this is all natural and possible, but only a complete idiot would think that an entire non-coding region could suddenly become coding and contribute non-damaging proteins in a functional manner (eg producing specific antibodies) . Production of proteins has to be done in a very precise balanced manner, it cannot occur across a few novel unique genes spontaneously and in full functional form.

#102 gilbo12345

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Posted 27 June 2012 - 03:41 AM

I'm sorry, if you cannot at least admit to the possibility of those four apes independently having that disabler, then I see you are far too stubborn to be able to discuss issues with. Why discuss issues if there are going to be no conclusions?

You are referring to 4 possible base pairs , I am referring to entire genes in humans involving thousands of base-pairs each. You say this gene was never coding, and humans evolved, and this became a coding region. I don't think you quite get the lack of randomness in genes. Its like a computer code, a precise set of information that produces precise functions in the human body through the production of proteins. You seem to brush over the statistical impossibility of this spontaneously occurring across a unique combination of thousands of unique base-pairs. Our previous discussion involved the possibility of duplicating and changing a gene, now we are talking about novel functional genes in a non-coding format waiting to be activated. Maybe your wording implies that this is all natural and possible, but only a complete idiot would think that an entire non-coding region could suddenly become coding and contribute non-damaging proteins in a functional manner (eg producing specific antibodies) . Production of proteins has to be done in a very precise balanced manner, it cannot occur across a few novel unique genes spontaneously and in full functional form.


Good work NP may I add a bit more

Compounding the issue of complexity of non-functional to functional keep in mind that a coding gene requires a signal system to turn on / off the gene products.. (A cell will not code for the production of something if it isn't required), this also has to "evolve" somehow whilst the gene is either functional or non-functional... Its almost like a chicken and the egg dilemma since if a gene becomes coding but cannot be expressed via the signal system to turn on gene expression then nothing happens, yet if the signal system "evolve" first and the gene doesn't code for anything then it is wasted.

#103 aelyn

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Posted 27 June 2012 - 03:50 AM

We aren't talking about thousand of base-pairs here, we're talking about a few hundred at most (it looks like a lot less on the figures, but the authors say the proteins coded for are 121 to 163 amino-acids long; either way they clearly call those short). Everything else you say would be more convincing if you knew more about genetics than the geneticists who actually work in the field. But I guess I'm too stubborn to take your word for it.

I'm sorry, if you cannot at least admit to the possibility of those four apes independently having that disabler, then I see you are far too stubborn to be able to discuss issues with. Why discuss issues if there are going to be no conclusions?

Well gosh, to learn new things ? To learn about other people's point of views ? To learn to improve one's own arguments ? To work through a thought process with someone else to bounce off of ? What kind of magical land do you live in where every conversation ends in agreement ?

But never mind that. I was really hoping to get some answers to the many questions I've asked you before you made the whole conversation about this side-issue but I guess that's not going to happen, so I'll leave the conversation now. It was enjoyable for most of it, thank you for that at least.

#104 gilbo12345

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Posted 27 June 2012 - 05:24 AM

We aren't talking about thousand of base-pairs here, we're talking about a few hundred at most (it looks like a lot less on the figures, but the authors say the proteins coded for are 121 to 163 amino-acids long; either way they clearly call those short). Everything else you say would be more convincing if you knew more about genetics than the geneticists who actually work in the field. But I guess I'm too stubborn to take your word for it.


Well gosh, to learn new things ? To learn about other people's point of views ? To learn to improve one's own arguments ? To work through a thought process with someone else to bounce off of ? What kind of magical land do you live in where every conversation ends in agreement ?

But never mind that. I was really hoping to get some answers to the many questions I've asked you before you made the whole conversation about this side-issue but I guess that's not going to happen, so I'll leave the conversation now. It was enjoyable for most of it, thank you for that at least.


If 120-150 amino acids are a short protein then the minimum amount of bases you are talking about will be between 360 to 450 bases, apparently the average length of a human protein is 480 bases meaning that the average base pair length you guys are discussing will be around 1400 bases... Yes its not in the thousands, (as in multiples of thousands, though the larger ones will be), however it is much more than just "a few hundred at most"...

#105 aelyn

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Posted 27 June 2012 - 06:23 AM

If 120-150 amino acids are a short protein then the minimum amount of bases you are talking about will be between 360 to 450 bases, apparently the average length of a human protein is 480 bases meaning that the average base pair length you guys are discussing will be around 1400 bases... Yes its not in the thousands, (as in multiples of thousands, though the larger ones will be), however it is much more than just "a few hundred at most"...

We aren't talking about average proteins, we're talking about the proteins in that paper. In fact they make a point in said paper of those proteins being particularly short, which is what one would expect from proteins that arose de novo from a noncoding sequence.

#106 gilbo12345

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Posted 27 June 2012 - 06:29 AM

We aren't talking about average proteins, we're talking about the proteins in that paper. In fact they make a point in said paper of those proteins being particularly short, which is what one would expect from proteins that arose de novo from a noncoding sequence.


No probs :) I thought you guys were also talking about in general since there are larger proteins that what is stated in that paper, therefore considerations for larger base sizes will also need to be made.

#107 aelyn

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Posted 27 June 2012 - 06:38 AM

No probs Posted Image I thought you guys were also talking about in general since there are larger proteins that what is stated in that paper, therefore considerations for larger base sizes will also need to be made.

To be fair NewPath might have switched what he was talking about at some point and I didn't notice, but as far as I can tell the conversation has been about the article ever since we stopped talking about the other stuff and that's what I've been talking about.

#108 NewPath

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Posted 27 June 2012 - 11:28 PM

(although I would still like to find out more about those gibbons with chronic lymphocytic leukemia, I still haven't been able to find anything on that, maybe you could give me google search terms with which to find out more if nothing else ?)


http://vir.sgmjourna...8/1901.full.pdf

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#109 NewPath

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Posted 28 June 2012 - 12:16 AM

We aren't talking about thousand of base-pairs here, we're talking about a few hundred at most (it looks like a lot less on the figures, but the authors say the proteins coded for are 121 to 163 amino-acids long; either way they clearly call those short). Everything else you say would be more convincing if you knew more about genetics than the geneticists who actually work in the field. But I guess I'm too stubborn to take your word for it.

The same logic applies to "a few hundred" as to thousands. I'm glad you admitted that we not just talking about 4 base pairs here as you said earlier. They cannot spontaneously evolve into a uniquely recognisable functional gene with a non-damaging protein expression whilst staying inactive. I hope you have the open-mindedness to acknowledge this point, but normally pride gets in the way in these discussions.

Well I don't really see the point in discussing issues with me, if my views are unimportant because I'm less qualified? Seems like this conversation was a bit of a time-waster when you only emphasize my lack of qualification at this stage of the discussion after I have been expressing myself for many posts.

Well gosh, to learn new things ? To learn about other people's point of views ? To learn to improve one's own arguments ? To work through a thought process with someone else to bounce off of ? What kind of magical land do you live in where every conversation ends in agreement ?

But never mind that. I was really hoping to get some answers to the many questions I've asked you before you made the whole conversation about this side-issue but I guess that's not going to happen, so I'll leave the conversation now. It was enjoyable for most of it, thank you for that at least.


Understandable that each person has their own agenda, I discuss issues to reach conclusions. Hoping that both parties throw around ideas in an open-minded fashion until its acknowledged what is conclusive and what isn't conclusive based on the available evidence. I believe this is a win-win approach because it focuses on the evidence itself, an honest search for unbiased truth, but you are right its not a realistic appoach. I have come across one evolutionist able to discuss like this, and he openly admitted that evolution had insufficient observable support for these gene adding processes. This human-ape issue wasn't a side issue, this particular discussion was the main issue, it was alleged that evolutionists actually had some proof for evolutionary processes being observed at a molecular level. All the other issues were distractions from the main issue of trying to gather if there is any proof for theoretical evolutionary processes. This is why I joined this particular thread.

But thanks for the discussion.

#110 aelyn

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Posted 29 June 2012 - 09:41 AM

The same logic applies to "a few hundred" as to thousands. I'm glad you admitted that we not just talking about 4 base pairs here as you said earlier.

o_O the 4 possible bases are A, T, G and C. Which is relevant to the number of combinations they can form. If you're thinking I was referring to 4-bp genes that would certainly explain your confusion, but I wasn't.

Well I don't really see the point in discussing issues with me, if my views are unimportant because I'm less qualified?

Nonsense, I never said that. I really appreciate you sharing your views with me, and your qualifications don't make your views less important. What I don't appreciate is you requiring that I agree with your views as a precondition for continuing to talk with you... and even that isn't so much something that I don't appreciate as something I can't do - I change my views based on what convinces me, not on what someone requires of me. I never asked that you agree that the articles' authors' arguments were conclusive - in fact I repeatedly said I didn't expect you to agree on any such thing, and acknowledged all the alternate possibilities to their arguments. You're the one who insisted that I agree their arguments were inconclusive, i.e. that your ad-hoc, evidence-free (or with circumstantial evidence at best) possibilities were not only possible, but as or more likely than the authors' inferences. When you do that, yes, your relative competence in the field of study in question does become relevant.

#111 NewPath

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Posted 30 June 2012 - 04:09 AM

o_O the 4 possible bases are A, T, G and C. Which is relevant to the number of combinations they can form. If you're thinking I was referring to 4-bp genes that would certainly explain your confusion, but I wasn't.


Aelyn, the reason I thought you were referring to 4 base pairs is because you said 4 base pairs, you didn't say 4 bases, so I thought you were referring to a disabling sequence within the gene. I assume now that was just a typing error, no problem, but even your reference to 3 billion base pairs seems to indicate you were in fact referring to base pairs in the original context of the last post on page 5:
"There are 4 possible base pairs, the human genome contains 3 billion base pairs"

Nonsense, I never said that. I really appreciate you sharing your views with me, and your qualifications don't make your views less important. What I don't appreciate is you requiring that I agree with your views as a precondition for continuing to talk with you... and even that isn't so much something that I don't appreciate as something I can't do - I change my views based on what convinces me, not on what someone requires of me. I never asked that you agree that the articles' authors' arguments were conclusive - in fact I repeatedly said I didn't expect you to agree on any such thing, and acknowledged all the alternate possibilities to their arguments. You're the one who insisted that I agree their arguments were inconclusive, i.e. that your ad-hoc, evidence-free (or with circumstantial evidence at best) possibilities were not only possible, but as or more likely than the authors' inferences. When you do that, yes, your relative competence in the field of study in question does become relevant.


I was just wanting you to acknowledge the possibility, I was not requiring you to believe my view is more likely. If you do not believe its possible that the same gene can disable independently then there is no point in continuing this discussion. I believe matching independent mutations are common, just due to the fact that organisms have populations in the millions, and yet coding genes only occur in the thousands if that, and mutations are regularly observed. Disabling mutations of one gene at a time occur regularly throughout the genome. If there is any selection pressure (a widespread disease that affects many species) its only logical that a disabled gene can become widely selected across independent populations. This is both a logical theoretical process, and observed. To project this logic across 4 populations when already observed in some form across 2 populations is a possibility, even if unlikely in your eyes and likely in my eyes, it remains a possibility. If you cannot at least acknowledge this as a possibility I see you as illogical and therefore cannot discuss any further issues with you, because frankly I would be wasting my time.

Additionally I would like you acknowledge the unlikelihood of an entire gene (100s of base pairs) with a unique function having evolved whilst remaining non-coding. Then this gene is enabled and the proteins it produces are so perfectly balanced that it does no damage to the organism, and yet creates a benefit to the organism. I would say this particular process is impossible, but I'm happy if you just acknowledge it appears an unlikely process. These are not illogical points I have brought up, despite my lack of qualification, but you are not acknowledging the logic.
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