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The Primary Axiom or Evolution is just a lie and should be replaced by Intelligent Design

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posted on Apr, 13 2016 @ 09:50 PM
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originally posted by: neoholographic
a reply to: Noinden

Again, you didn't provide any evidence. You couldn't articulate a response so you posted 3 links and said go fish.

Just imagine if every thread on ATS consisted of just links with no commentary or context LOL.

YOU CAN'T BE SERIOUS!

If you can't articulate a response then you should find a forum where people just post links without commentary or context.


They won't answer the paradox because they can't. Any logically deducing observer has gotten what they can out of the presentation of the various impossibilities of evolution already - repeating ourselves may be erroneous at this point. Ironically, I don't think any of the super zealous evolutionists even understand the logical dilemma that has been presented to them.




posted on Apr, 13 2016 @ 09:54 PM
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a reply to: neoholographic

Now we enter the logical fallacy realm of ....Playing on Emotion coupled with suggesting the other side is unhinged. Again that is a capitulation on your part.

Ok big boy.

What link (they are papers neighbour) had nothing to do with the thread? Go on. It will be in your browser history, easy to find. Go on. DO IT


I return to the fact, evidence has been provided. You can't talk to it. Thus you are trying to ignore of discredit it, sans actually speaking about it. This makes your argument one which is intellectually dishonest.



posted on Apr, 13 2016 @ 09:55 PM
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a reply to: cooperton

We have answered it. Just because you refuse to acknowledge it, it does not mean it was not answered.



posted on Apr, 13 2016 @ 09:56 PM
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a reply to: neoholographic

It? Are plurals its now? Them, you read them, or you read none of them. I cited several papers. I read them all. You have read none.



posted on Apr, 13 2016 @ 09:57 PM
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a reply to: peter vlar

I have to ask again, do you read what you post. You quoted this:


Thus, the mutation, which interferes with expression of the normal TRIM5α protein, instead contributes to expression of a novel protein.


Where was any new function created that regulates gene expression.

I have asked you several times to list the sequences that regulat the expression of TRIM5, CypA and TRIM5-CypA. Do you even know them?

Here's a hint:

IT INTERFERES WITH THE EXPRESSION IT DOESN'T CHANGE HOW THE EXPRESSION IS REGULATED.

A random mutattion can't give meaning or function to a sequence that regulates gene expression. You haven't presented anything that says this can occur.

This whole post, I have been talking about gene regulation, transcription, translation, error correction and more. Nothing you said answers this question:

Where's the evidence that random mutations and natural selection can give a DNA sequence meaning and function that regulates gene expression?



posted on Apr, 13 2016 @ 10:08 PM
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a reply to: neoholographic

You need to provide citations to prove your assertions here neighbor. Otherwise you are stating opinion. Ignoring a paper, or misrepresenting one (as you are doing in so many places) is an argument from willful ignorance. That is a capitulation.

SO to recap. Several sources of evidence that mutation produces new function have been provided. But here is some more, just to show how ridiculous your argument is.

Nature Genetics 27, 103 - 107 (2001)
Nature Genetics 36, 377 - 381 (2004)

Also consider Bacterial resistance to antibiotics (it occurred IN OUR TIME)



posted on Apr, 13 2016 @ 10:08 PM
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originally posted by: cooperton

originally posted by: neoholographic
a reply to: Noinden

Again, you didn't provide any evidence. You couldn't articulate a response so you posted 3 links and said go fish.

Just imagine if every thread on ATS consisted of just links with no commentary or context LOL.

YOU CAN'T BE SERIOUS!

If you can't articulate a response then you should find a forum where people just post links without commentary or context.


They won't answer the paradox because they can't. Any logically deducing observer has gotten what they can out of the presentation of the various impossibilities of evolution already - repeating ourselves may be erroneous at this point. Ironically, I don't think any of the super zealous evolutionists even understand the logical dilemma that has been presented to them.


EXACTLY!!

Who post links and then they don't provide any context or commentary to the links they're posting.

It's asinine.

I'll say it again, if ATS forums were filled with nothing but links without context or commentary there would be no forum.

I'm wondering if he's serious or just trolling. Just look at the forums. How many people answer questions with just links. It was just like the other Poster who answered questions by posting links to PDF's LOL. If the person can't articulate an argument as it relates to the topic being discussed that's not my fault.



posted on Apr, 13 2016 @ 10:12 PM
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a reply to: neoholographic

There we have it folks. He has capitulated. He can not prove evolution is a big lie, and will not read counter evidence.



posted on Apr, 13 2016 @ 10:16 PM
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a reply to: Noinden

Please stop trolling. People here are trying to debate the issue. If you can't articulate a coherent argument that's not my fault.



posted on Apr, 13 2016 @ 10:18 PM
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a reply to: neoholographic

Why is it you refuse to read the papers? I am very serious in this question. You are avoiding evidence. WHy is that?



posted on Apr, 13 2016 @ 10:19 PM
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a reply to: neoholographic



Did you read what you quoted?


Certainly we do, at least three times we have tried to explain this simple sentence to you. You refuse to make even the slightest attempt to understand it. I'll try one more time though...

The gene, called TRIM5-CypA,

This is a NEW gene, a completely NEW gene.

well characterized elsewhere (AIDS, 2007; PNAS, 2008),

This NEW gene has been described in the quoted papers.

is a hybrid of two existing cellular genes

A mutation occurred that combined two pre-existing genes - TRIM5 and CypA. This resulted in a completely NEW gene called TRIM5-CypA. They could have called it Xyqr14, but chose to call it TRIM5-CypA for convenience and to remind that it was a hybrid.

Whatever it is called it is a NEW gene. It is NOT TRIM5 and it is NOT CypA. It is TRIM5-CypA.



This is not new information or a new function


It most certainly is. It is a NEW gene, a gene that produces a NEW protein. A protein that provides important NEW benefits for the populations that carry it.



but it's the convergence of two gene sequences that already exist


You continue to attempt to use the 'ambiguity' of language to hide your refusal to understand this. The gene sequences did not 'converge'; they 'combined'.



which is a rare event according to the source you quoted.


Please get the following points clear in your mind:

1] The word 'convergence' used in the article had nothing to do with the mutation of the gene sequences.
2] The article was totally silent on the how rarely or how frequently a mutation that combines genes occurs.
3] The phrase 'convergent evolution' used in the article refers to the fact that similar mutations occurred and produced a similar NEW gene and similar NEW function in two completely different populations on opposite sides of the world.
4] It is the occurrence of the similar mutations in different populations that is 'rare'.
5] Another examples of convergent evolution is that of the wing in birds and in bats. This example doesn't involve just one mutation of course, but hundreds or thousands or more. But the end result is a similar 'solution' to a common 'problem'.

Please, don't confuse my use of the words 'solution' and 'problem' in point 5 above with an intention to imply 'direction'. There is no direction in evolution and mutations don't happen 'on purpose'. There is only change that sometimes works and sometimes doesn't.

edit on 13/4/2016 by rnaa because: (no reason given)



posted on Apr, 13 2016 @ 10:31 PM
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originally posted by: rnaa

The gene, called TRIM5-CypA,

This is a NEW gene, a completely NEW gene.



No its not. Its the result of "Alternative splicing giving rise to chimeric transcripts encoding the TRIM motif fused to a C-terminal CypA domain (TRIM5-CypA). " Alternative splicing is a form of gene regulation, and has an epigenetic aspect to it. In other words, the pieces are there, and it is gene regulation that determines if it gets expressed or not through alternative splicing. It is not a completely new gene.

You guys are clowns. Rot in ignorance all you want, but stop leading others astray.



posted on Apr, 13 2016 @ 10:31 PM
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OK so you want discussion with information, because you appear to be too lazy to read them yourself?
Here


"Many of the bacterial pathogens associated with epidemics of human disease have evolved into multidrug-resistant (MDR) forms subsequent to antibiotic use."

Look evolved.

Thus, bacteria, evolved resistance to antibiotics.



posted on Apr, 13 2016 @ 10:38 PM
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originally posted by: cooperton

originally posted by: rnaa

The gene, called TRIM5-CypA,

This is a NEW gene, a completely NEW gene.



No its not. Its the result of "Alternative splicing giving rise to chimeric transcripts encoding the TRIM motif fused to a C-terminal CypA domain (TRIM5-CypA). " Alternative splicing is a form of gene regulation, and has an epigenetic aspect to it. In other words, the pieces are there, and it is gene regulation that determines if it gets expressed or not through alternative splicing. It is not a completely new gene.

You guys are clowns. Rot in ignorance all you want, but stop leading others astray.


EXCELLENT POST!

This is the point and this is why they keep dodging the questions because they have no answer.



posted on Apr, 13 2016 @ 10:46 PM
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a reply to: neoholographic

Except, alternative splicing is a type of mutation aka a splice site mutation. Thus it is a mutation. THUS it casued new function. QED this is evidence of mutation causing new function.



posted on Apr, 13 2016 @ 10:51 PM
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Continuing on.

Lac tosetollerance has been shown to be a mutation, allowing adult humanity in certain areas to tolerate dairy (lactose containing things for those needing it clarified (mmm butter)). This presented in populations associated with herding cows. Thus this is a NEW function. It can be date using genetic clocks to coincide with the apparent adoption of cattle herding.

Yet again, a mutation causing new function.



posted on Apr, 13 2016 @ 10:55 PM
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Then there are all the "abnormal" mutations in hemoglobin. Again mutations (very simple ones usually) which alter function. Some of which have proven to be beneficial in circumstances.

Then there are the mutations which cause low melanin in Europeans. Important in low daylight areas, dangerous for those of us under the ozone hole



posted on Apr, 13 2016 @ 10:58 PM
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a reply to: neoholographic

I hope someone at least appreciates the humor of the DS9 video without doing other things with that comment (not quite sure how to describe it).

I'm not talking about you, except when I used "I hope someone...". Not sure what my purpose for this comment is, perhaps I'm hoping some other people notice something I just noticed and I want to stress looking into what certain persons don't want others to be looking into. Including an honest description of how the word "evolution" is used and has been used since Darwin's time. Which I tried to point at by quoting you when you quoted Dr. Sanford, he's also considering the whole show (or story involved with both so-called "chemical evolution" as well as so-called "biological evolution").

Should I mention something about "information overload" again? This thread suddenly filled up quick after a lull in proceedings.
edit on 13-4-2016 by whereislogic because: addition



posted on Apr, 13 2016 @ 11:00 PM
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a reply to: cooperton




No its not. Its the result of "Alternative splicing giving rise to chimeric transcripts encoding the TRIM motif fused to a C-terminal CypA domain (TRIM5-CypA).


And that is a new gene. And it produces a new protein. It is a mutation that provides new benefit to the population that bears it.



" Alternative splicing is a form of gene regulation, and has an epigenetic aspect to it.


Epigenetics has nothing to do with this mutation, by any definition of the word 'epigenetics'. Epigenetics is specifically defined as 'heritable changes in gene function that cannot be explained by changes in DNA sequence'. Yet this mutation is clearly explained by changes in DNA sequence.

From Peter Vlar's post at the bottom of page 24: (go there for the link to the source)


We have previously reported that the TRIM5 coding sequence of old world monkeys is highly polymorphic [7]. In the course of genotyping the TRIM5 locus in a colony of captive bred rhesus macaques, we identified a single-nucleotide polymorphism in the terminal nucleotide of intron 6 (Figure 1). The SNP is the result of a G-to-T substitution that alters the canonical 3′ splice acceptor site (AG to AU) immediately upstream of exon 7. Initial sequence data revealed the presence of this mutation in 2 of 8 animals, including one homozygote (T/T) and one heterozygote (G/T). The cis-acting AG element at the end of introns is a highly conserved feature of 3′ splice sites, and the presence of such a mutation is predicted to interfere with mRNA splicing.


I repeat there is nothing 'epigenetic' about this mutation. It is specifically identified as a coding change mutation in a specific DNA sequence location.



In other words, the pieces are there, and it is gene regulation that determines if it gets expressed or not through alternative splicing. It is not a completely new gene.


You are completely 100% wrong on this.

You have asked for 'proof' and refused to read or even discuss the papers that were cited to provide that proof.

You have demanded that instead of being pointed to the paper that provides that proof, that you be spoon fed the exact part of the paper that discusses, in context, the proof you demand.

Well Peter Vlar bowed to your demand.

Now read it, understand it, and stop pretending that you know more about genetic biology than genetic biologists.
edit on 13/4/2016 by rnaa because: (no reason given)



posted on Apr, 13 2016 @ 11:07 PM
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a reply to: rnaa

You said:


The article was totally silent on the how rarely or how frequently a mutation that combines genes occurs.


Apparently, you didn't read the article:

Moreover, the kinds of molecular events required to construct the two TRIM5-CypA genes are thought to be rare.

Look, nothing you said answers the question. Random mutation and natural selection don't create any new function. They don't bestow meaning and function on a sequence of letters that regulate expression.

This is why you guys will not list the regulatory sequences that express TRIM5-CypA. Eventually I will but it's fun watching you guys either dodge the question or maybe you don't know.

The point is, random mutations can interfere with expression but they can't give meaning to a sequence that regulates expression.

Let me give you a practical example.

Let's say I construct an automated system that makes a can of pop. Intelligence constructed the automated process through a sequence of letters and numbers that regulate the expression or the can of pop.

During this automation, the process may get mixed up and then a different flavor of pop is produced.

As the owner of this brand, I may like the flavor even though it's a mistake. Now the mistake didn't create any new sequences that regulate the process of making a can of pop. There's no new function or information in the sequences that regulate the expression of a can of pop.

This is what was quoted earlier.

Thus, the mutation, which interferes with expression of the normal TRIM5α protein, instead contributes to expression of a novel protein.

Mutation can interfere with the expression which in most cases are harmful or neutral. They don't give meaning or function to DNA sequences that regulate expression.

THAT'S A FANTASY!
edit on 13-4-2016 by neoholographic because: (no reason given)




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