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A Seemingly Definitive Refutation of the "No new information" canard
Taken largely intact from a clever IIDB member.
The claim: No genetic mutation may increase information.
1. Point mutations are reversible.
2. Suppose a point mutation in gene G at nucleotide N changes a T to an A. Per the claim, this represents a decrease in information.
3. Suppose a point mutation at N changes the A back to a T. Per the claim, this also represents a decrease in information.
4. It follows from premises 3 & 4 that two chemically identical configurations of G have distinct information contents.
It seems almost too neat.
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Originally Posted by TeddyKGB
Taken largely intact from a clever IIDB member.
The claim: No genetic mutation may increase information.
1. Point mutations are reversible.
2. Suppose a point mutation in gene G at nucleotide N changes a T to an A. Per the claim, this represents a decrease in information.
3. Suppose a point mutation at N changes the A back to a T. Per the claim, this also represents a decrease in information.
4. It follows from premises 3 & 4 that two chemically identical configurations of G have distinct information contents.
The claim: No genetic mutation may increase information.
1. Point mutations are reversible.
2. Suppose a point mutation in gene G at nucleotide N changes a T to an A. Per the claim, this represents a decrease in information.
3. Suppose a point mutation at N changes the A back to a T. Per the claim, this also represents a decrease in information.
4. It follows from premises 3 & 4 that two chemically identical configurations of G have distinct information contents.
It seems almost too neat.
To end the proof you should state that this is a contradiction. - Which it is. I have used this argument in the past, but creationists don't seem to get it.
Nonetheless it is sound - the premises are correct, the conclusion states that I(G) > I(G) where I is some information counting function, but the output of that function can only be a number, and for any number, "a > a" is false.
Thus the argument is valid and sound, providing a reductio ad absurdum disproof of the claim, "mutations can never increase information."
Isn't information always in reference to something else though?
The beauty of this example is that it doesn't rely on any particular definition of information. It holds as long as there is some measure for the information content of a genome.
Let G be a genome and I(G) the information content of that genome.
Let G' be a genome produced from G via a single nucleotide substitution.
Evolution deniers assert that I(G) >= I(G'), for all G, G' in the real world.
Unfortunately for them, the same mutation that made G' out of G is known to occur in reverse, making G out of G'.
Since this latter is also a mutation, evolution deniers claim then that I(G') >= I(G), for all G, G'.
The only way this can be true is if I(G) = I(G'), for all G,G', which by extension means there is never any difference in information content for genomes of the same length, something so ridiculous they could never sell it even to their scientifically and mathematically illiterate support base.
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Isn't information always in reference to something else though? Anti-biotic resistance qualifies as new information right?
Sure its through sort of directed hypermutation, but the mutations themselves were still random.
I think co-dependent information would be a better argument. I absolutely cannot comprehend why anyone would say "no new information".
well the thing is there's two factors in evolution:
First you have random mutations, which are just that, random.
Then you have Natural selection, which is a non-random process that determines which organisms are fit based on their environment. This process determines which of the above random mutations are "fit" and which arn't.
So which mutations are selected is non-random dependent on the environment.
But which mutations happen in the first place is random. So no, new information is not always in reference to something else. But the mutations that survive the filter of natural selection often are.
You can get around this by changing "mutations always decrease information content" to "mutations don't increase information content" (you essentially change I(G) > I(G') to I(G) >= I(G') ), but that will logically imply that "all genomes have the SAME information content", which makes talking about information content meaningless.
This looks pretty airtight, I wonder what huggybear and his ilk will have to say to this (if they bother responding...)
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The claim: No genetic mutation may increase information.
1. Point mutations are reversible.
2. Suppose a point mutation in gene G at nucleotide N changes a T to an A. Per the claim, this represents a decrease in information.
3. Suppose a point mutation at N changes the A back to a T. Per the claim, this also represents a decrease in information.
4. It follows from premises 3 & 4 that two chemically identical configurations of G have distinct information contents.
It seems almost too neat.
There is a hole. You did not explain where the original information in G came from.
Lee Spetner (if memory serves) conceded that back mutations produce new information, but he also stated that there was no net gain of information if one includes the original gene in the equation.
There is a much better example that covers most of the bases. IDers have argued that genetic information is front loaded into the genome. Therefore, if a new function emerges they will claim that mutations are only unlocking the information that was already there. They can also claim that these are just back mutations so no net information was gained.
To get around this one can start with a purely random sequence produced in the lab and insert it into a genome. If this purely random sequence produces function then all of their arguments are out the window. This experiment has been done.
Can an arbitrary sequence evolve towards acquiring a biological function?
Hayashi Y, Sakata H, Makino Y, Urabe I, Yomo T.
Department of Biotechnology, Graduate School of Engineering, Osaka University, 2-1 Yamada-oka, 565-0871, Suita City, Osaka, Japan.
To explore the possibility that an arbitrary sequence can evolve towards acquiring functional role when fused with other pre-existing protein modules, we replaced the D2 domain of the fd-tet phage genome with the soluble random polypeptide RP3-42. The replacement yielded an fd-RP defective phage that is six-order magnitude lower infectivity than the wild-type fd-tet phage. The evolvability of RP3-42 was investigated through iterative mutation and selection. Each generation consists of a maximum of ten arbitrarily chosen clones, whereby the clone with highest infectivity was selected to be the parent clone of the generation that followed. The experimental evolution attested that, from an initial single random sequence, there will be selectable variation in a property of interest and that the property in question was able to improve over several generations. fd-7, the clone with highest infectivity at the end of the experimental evolution, showed a 240-fold increase in infectivity as compared to its origin, fd-RP. Analysis by phage ELISA using anti-M13 antibody and anti-T7 antibody revealed that about 37-fold increase in the infectivity of fd-7 was attributed to the changes in the molecular property of the single polypeptide that replaced the D2 domain of the g3p protein. This study therefore exemplifies the process of a random polypeptide generating a functional role in rejuvenating the infectivity of a defective bacteriophage when fused to some preexisting protein modules, indicating that an arbitrary sequence can evolve toward acquiring a functional role. Overall, this study could herald the conception of new perspective regarding primordial polypeptides in the field of molecular evolution.
In this study the random sequence mutated and resulted in a virus that was more infectious than the wild type virus. Not only that, but the mutations in the random sequence were vital for the increased infectivity which is a great example of evolution producing an irreducibly complex system.
__________________ "Since YAC [Young-Age Creation] epistemology accepts Biblical claims over physical evidence and human reason, logical or evidential arguments for evolution and/or against YAC are likely to be ineffective in converting most YACists."--Kurt Wise
To get around this one can start with a purely random sequence produced in the lab and insert it into a genome. If this purely random sequence produces function then all of their arguments are out the window. This experiment has been done.
In this study the random sequence mutated and resulted in a virus that was more infectious than the wild type virus. Not only that, but the mutations in the random sequence were vital for the increased infectivity which is a great example of evolution producing an irreducibly complex system.
Total wowz.
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