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Author Topic:   Impossible evolution of new beneficial proteins
GreenBlue
Inactive Member


Message 1 of 75 (84160)
02-07-2004 7:18 AM


Hi I am a Creationist and I have a question that will trouble you evolutionists.
I will accept Gene Duplication as a mechanism for increasing the number of genes, but changing the duplicates into *new* genes with *new* *beneficial* function via mutation seems statistically impossible.
In a gene of 250 amino acids there are 20^250 different combinations of amino acid sequences. The specific sequence determines the final 3D structure that makes up the protein. The 3D structure is critical to how the produced protein can interact in the body. Slight changes to a proteins 3D structure via one amino acid being changed can cause diseases.
The point is a change to the 250 amino acid sequence which results in a new 3D structure of the protein will produce a very different 3D structure.
At any stage, one point mutation in a 250 amino acid sequence can only change the sequence into a few hundred of the 20^250 possible sequences. What is the chance that any of these hundred sequences will fit snuggly in the organism and be beneficial and useful? Next to none. Instead we have to rely on point mutation after point mutation, without any selective driving force, eventually stumbling across a new beneficial protein sequence. That is statisically impossible and is a nightmare for evolution.

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crashfrog
Member (Idle past 1467 days)
Posts: 19762
From: Silver Spring, MD
Joined: 03-20-2003


Message 2 of 75 (84161)
02-07-2004 7:56 AM
Reply to: Message 1 by GreenBlue
02-07-2004 7:18 AM


What is the chance that any of these hundred sequences will fit snuggly in the organism and be beneficial and useful? Next to none.
How are you calculating these odds? What do you mean when you say "useful and beneficial"? Beneficial with respect to what?
This sounds like you don't want it to be probable, so you're unwilling to believe that it is probable. I don't understand why I should credit your personal opinion any more than anybody else's.

This message is a reply to:
 Message 1 by GreenBlue, posted 02-07-2004 7:18 AM GreenBlue has replied

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Stephen ben Yeshua
Inactive Member


Message 3 of 75 (84167)
02-07-2004 8:37 AM
Reply to: Message 2 by crashfrog
02-07-2004 7:56 AM


Big numbers
Crash,
The question here is a good one, though. I keep hoping someone will make an effort to actually do the numbers, to see if we are in a ball-park or reason. Because of what we know of genetic engineering, we can suppose that new genes could be introduced from viruses or bacteria. Lot of those around for random mutations to happen to, over a very long time, and they reproduce so quickly, so we have lots of room for natural selection. But is it enough? As Greenblue notes, to get a new and useful protein requires an incredibly large number of steps, all of which have to be adaptive for a while, anyway.
And what are you hoping for, Crash, and willing or unwilling to believe? What do you do with your subjectivity?
Stephen

This message is a reply to:
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GreenBlue
Inactive Member


Message 4 of 75 (84169)
02-07-2004 8:46 AM
Reply to: Message 2 by crashfrog
02-07-2004 7:56 AM


How are you calculating these odds? What do you mean when you say "useful and beneficial"? Beneficial with respect to what?
First of all I must admit I am not calculating odds. This is more of a "what is the mechanism?" question where I am simply posing a potential problem for evolution.
I am thinking of the genes which humans have and simple bacteria don't. To explain the origin of these genes often gene duplication is put forward as a favoured mechanism.
But how possible is it to take an existing sequence and convert it into a new sequence via random mutation?
Surely the sequences of these genes are very different from one another, so it would take many many point mutations to go from one to the other. Surely such a hurdle is beyond chance when you consider that each intermediatery stage will have no benefit and cannot be sustained by natural selection.
Without natural selection the process becomes nothing more than trial and error, not a very convincing mechanism for design when you don't have infinite time.
In fact being neutral means there is no reason why one of these point mutations couldn't end up trashing the gene by overwriting its end codon before a useful configuration was reached

This message is a reply to:
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 Message 5 by Loudmouth, posted 02-07-2004 4:30 PM GreenBlue has replied

  
Loudmouth
Inactive Member


Message 5 of 75 (84314)
02-07-2004 4:30 PM
Reply to: Message 4 by GreenBlue
02-07-2004 8:46 AM


If you are saying that beneficial mutations don't exist, then you are completely wrong. In this abstract, hemoglobin C confers resistance to malaria (hemoglobin C is mutatated hemoglobin A).;
-------------------
Hemoglobin C is associated with reduced Plasmodium falciparum parasitemia and low risk of mild malaria attack.
Rihet P, Flori L, Tall F, Traore AS, Fumoux F.
Universite de la Mediterranee, IFR48, Faculte de Pharmacie, 27 Bd Jean Moulin, 13385 Marseille Cedex 5, France. rihet@luminy.univ-mrs.fr
Genetic predisposition to malaria has been shown by epidemiological, case-control and linkage studies. In particular, case-control studies have recently shown association between hemoglobin C and resistance to severe malaria in Mali and to clinical malaria in Burkina Faso. In a longitudinal study of families living in an endemic area, we investigated whether hemoglobin C is associated with reduced Plasmodium falciparum parasitemia and low risk of mild malaria attack. We surveyed 256 individuals (71 parents and 185 sibs) from 53 families during 2 years. Hemoglobin C carriers had less frequent malaria attacks than AA individuals within the same age group (P=0.01). Since age correlated with malaria attack and parasitemia (P<0.0001), we took age into account in association analyses. We performed combined linkage and association analyses, which avoid biases due to population structure. Using multi-allelic tests, we evidenced association between hemoglobin genotype and phenotypes related to malarial infection and disease (P<0.001). We further analyzed individual hemoglobin alleles and detected negative association between hemoglobin C and malaria attack (P=0.00013). Analyses that took into account confounding factors confirmed the negative association of hemoglobin C with malaria attack (P=0.0074) and evidenced a negative correlation between hemoglobin C and parasitemia (P=0.0009). These associations indicate that hemoglobin C reduces parasitemia and confers protection against mild malaria attack.
-------------------
If you are saying that amino acid sequence can not be rearranged or truncated without losing function then you are incorrect as well. My own work (being sent to press as of this moment) deals with proteolytic cleavage of a bacterial enzyme. The enzyme does not decrease in activity, specificty, or rate of reaction even though 40% of its amino acids are cleaved off. As soon as it is accepted for print I will post the abstract. However, there are numerous examples of just this phenomena in the literature which can be found at http://www.pubmed.com
Secondly, amino acid sequences are not statistically signifigant (ie, they appear to be random), as can be seen in this abstract:
------------------
Information content of protein sequences.
Weiss O, Jimenez-Montano MA, Herzel H.
Institute for Theoretical Biology, Humboldt University Berlin, Invalidenstr. 43, Berlin, D-10115, Germany.
The complexity of large sets of non-redundant protein sequences is measured. This is done by estimating the Shannon entropy as well as applying compression algorithms to estimate the algorithmic complexity. The estimators are also applied to randomly generated surrogates of the protein data. Our results show that proteins are fairly close to random sequences. The entropy reduction due to correlations is only about 1%. However, precise estimations of the entropy of the source are not possible due to finite sample effects. Compression algorithms also indicate that the redundancy is in the order of 1%. These results confirm the idea that protein sequences can be regarded as slightly edited random strings. We discuss secondary structure and low-complexity regions as causes of the redundancy observed. The findings are related to numerical and biochemical experiments with random polypeptides. Copyright 2000 Academic Press.
------------------------
Random, arbitrary sequences of amino acids can also change via random mutation and selection to take on better function. In one case, a random sequence was inserted into a viral genome. Just a small tidbit from the abstract:
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.
" 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."
The change in sequence was in the D2 domain of the g3p protein. Through mutation and selection there was a 240-fold and a 37-fold increase after the sequence was mutated and clones were selected.
To conclude, I have shown that through information theory protein sequences are slightly altered random strings. I have also shown that mutation can increase fitness.
My question to you is this, what is stopping the process of random mutation and natural selection from changing amino acid sequences in a way that confers increased fitness? If this process were to continue for long periods of time, by what criteria could you identify genes that were duplicated and left to random mutation over very long time periods (lets say 100 million years)?
I am sorry if you feel overwhelmed, but this is the actual state of science. The evidence for the mechanism of improved fitness via random mutation and selection is quite staggering. The above is just the very tip of the iceberg.

This message is a reply to:
 Message 4 by GreenBlue, posted 02-07-2004 8:46 AM GreenBlue has replied

Replies to this message:
 Message 6 by GreenBlue, posted 02-07-2004 7:46 PM Loudmouth has replied
 Message 69 by Stephen ben Yeshua, posted 02-17-2004 6:42 PM Loudmouth has replied

  
GreenBlue
Inactive Member


Message 6 of 75 (84343)
02-07-2004 7:46 PM
Reply to: Message 5 by Loudmouth
02-07-2004 4:30 PM


No I don't deny beneficial mutations.
If you are saying that amino acid sequence can not be rearranged or truncated without losing function
Yes
then you are incorrect as well
Ah
That's interesting, so you can effectively cut a lot of amino acids from an enzyme and it will still function correctly? thats pretty cool
My question to you is this, what is stopping the process of random mutation and natural selection from changing amino acid sequences in a way that confers increased fitness?
Well I don't think natural selection is going to come into play until a useful sequence is reached. Until then you have to rely on random mutation just coming across a useful sequence by chance.
While obviously I have nothing to base the numbers on I can make a rough calculation to show you what my point is:
A 300 amino acid sequence has 20^300 different combinations. My understanding is that a large number of those sequences will not code for a protein useful to the organism.
Lets say there are 20^100 useful sequences (and I think that is a conservative figure) for the organism within the search space, then it appears that for every useful protein sequence there are 20^200 useless protein sequences. So I would expect all the useful sequences to be reasonably far apart, seperated by useless sequences.
My point is that if these sequences are far apart, seperated by useless intermediatery sequences, then natural selection cannot "guide" mutations to a new sequence.
Natural selection is perfectly able to improve a protein sequence, or preserve a protein sequence, but it is unable to guide a protein sequence for one function to a protein sequence for an entirely different function.
Then again it could happen by chance via lots of mutations building up and chancing upon a new sequence (but if that was the case wouldn't it be more probable that the gene was damaged eventually?). I just wonder if anyone has done the maths on this or if we simply don't have the numbers to do the maths yet
[This message has been edited by GreenBlue, 02-07-2004]

This message is a reply to:
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Loudmouth
Inactive Member


Message 7 of 75 (84352)
02-07-2004 8:40 PM
Reply to: Message 6 by GreenBlue
02-07-2004 7:46 PM


Preface: If you are not that familiar with science or science terminology, just read the last couple sentences of each abstract. They usually contain the conclusions of the study. Even us scientists get a little confused with the terminology at times, but the conclusions are usually straightforward.
quote:
A 300 amino acid sequence has 20^300 different combinations. My understanding is that a large number of those sequences will not code for a protein useful to the organism.
Maybe not in the present, but possibly in the future. Also, it is possible that those proteins were used in the past. Recently, a group of scientists looked through the human genome and found 8,000 pseudogenes. These are genes that were previously functional but are now "broken", that is they are no longer expressed or the protein is mutated so that it no longer works. The number of functional genes in the human genome has been estimated at 30,000. This means that for every 4 functional genes there is 1 non-functional gene that hasn't mutated to the point that it is no longer recognizable. This is what we would expect from an evolutionary process, but not really what we would expect if the human race were 6,000 years old. I really can't see how humans could lose about 20% of their functional genes and still be able to function. We can talk about pseudogenes in another thread if you would like, I am merely using them as an example of protein sequences that are not needed but still had a function. Here is the abstract, I have a feeling that others might be interested in this one too:
Millions of years of evolution preserved: a comprehensive catalog of the processed pseudogenes in the human genome.
Zhang Z, Harrison PM, Liu Y, Gerstein M.
Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, Connecticut 06520-8114, USA.
Processed pseudogenes were created by reverse-transcription of mRNAs; they provide snapshots of ancient genes existing millions of years ago in the genome. To find them in the present-day human, we developed a pipeline using features such as intron-absence, frame-disruption, polyadenylation, and truncation. This has enabled us to identify in recent genome drafts approximately 8000 processed pseudogenes (distributed from Pseudogene.org). Overall, processed pseudogenes are very similar to their closest corresponding human gene, being 94% complete in coding regions, with sequence similarity of 75% for amino acids and 86% for nucleotides. Their chromosomal distribution appears random and dispersed, with the numbers on chromosomes proportional to length, suggesting sustained "bombardment" over evolution. However, it does vary with GC-content: Processed pseudogenes occur mostly in intermediate GC-content regions. This is similar to Alus but contrasts with functional genes and L1-repeats. Pseudogenes, moreover, have age profiles similar to Alus. The number of pseudogenes associated with a given gene follows a power-law relationship, with a few genes giving rise to many pseudogenes and most giving rise to few. The prevalence of processed pseudogenes agrees well with germ-line gene expression. Highly expressed ribosomal proteins account for approximately 20% of the total. Other notables include cyclophilin-A, keratin, GAPDH, and cytochrome c.
quote:
Well I don't think natural selection is going to come into play until a useful sequence is reached. Until then you have to rely on random mutation just coming across a useful sequence by chance.
That is precisely right. This is exactly the mechanism that causes evolution. Natural selection can only work with what is expressed, not with what is not expressed. However, once a new protein is expressed then natural selection decides the fate of the gene, it decides whether the new gene will spread out into the population because it confers better fitness or if it will be passed to fewer and fewer offspring because it confers less fitness. Neutral mutations, those that don't have an effect on fitness, will not be weeded out by natural selection either. These mutations will usually be spread into the population in a random fashion.
quote:
Natural selection is perfectly able to improve a protein sequence, or preserve a protein sequence, but it is unable to guide a protein sequence for one function to a protein sequence for an entirely different function.
Why? What evidence is there that backs this up? In my previous post (message 5) I pasted an abstract that argues against this. In this abstract an arbitrary, random sequence was mutated so that it took on a new function, improving infectivity. Also, mutations can cause enzymes to bind to different substrates. Here is one example:
Nuclear magnetic resonance structure of the P395S mutant of the N-SH2 domain of the p85 subunit of PI3 kinase: an SH2 domain with altered specificity.
Gunther UL, Weyrauch B, Zhang X, Schaffhausen B.
Institute for Biophysical Chemistry, Centre of Biomolecular Magnetic Resonance, J. W. Goethe University, Frankfurt, Marie-Curie-Strasse 9, 60439 Frankfurt, Germany.
Understanding the specificity of Src homology 2 (SH2) domains is important because of their critical role in cell signaling. Previous genetic analysis has characterized mutants of the N-terminal src homology 2 (SH2) domain of the p85 subunit of phosphoinositide 3-kinase (PI3K). The P395S mutant exhibits a specificity for phosphopeptide binding different from that of the wild-type SH2. The P395S mutant has an increased affinity for the platelet-derived growth factor receptor (PDGFr) compared to polyomavirus middle T antigen (MT). Solution structures of the P395S mutant of the p85 N-SH2 alone and complexed to a PDGFr phosphopeptide were determined to explain the change in specificity. Chemical shift perturbations caused by different peptides were compared for mutant and wild-type structures. The results show that the single P395S mutation has broad effects on the structure. Furthermore, they provide a rationale for the observed changes in binding preference.
quote:
Then again it could happen by chance via lots of mutations building up and chancing upon a new sequence (but if that was the case wouldn't it be more probable that the gene was damaged eventually?). I just wonder if anyone has done the maths on this or if we simply don't have the numbers to do the maths yet
It would take a lot of changes and creation of new genes. That means that the diversity in organisms that we see today are the result of numerous changes in DNA, at least according to the theory of evolution. As you stated above, natural selection can preserve functionality in proteins, so I would argue that deleterious mutations would be selected against and the non-mutated alleles would be selected for. You may or not agree with me, but I think the mechanism (mutation and selection) can explain why there are so many different and wonderful species here on earth. However, we may have to agree to disagree, but at least you are trying to learn about the science before you discard it. This is the intellectually honest thing to do and you should be commended for it.
To the best of my knowledge, no one is really working on the function of randomly generated proteins. This would be a tough task. Each protein would have to be screened against thousands, perhaps millions, of different substrates in order to deduce its activity or binding capacity. I remember reading a paper about the success of rational mutations having less success than random mutations in creating new functionality. I tried to find it, but it is hiding from me right now. In this paper, scientists had better luck at changing function or deleting function by randomly mutating the gene. The loser was rational mutation, where they tried to deduce the best mutations to get the wanted effect by analyzing the structure of the protein. Anyway, I hope these posts are making things clearer. If not, let me know.

This message is a reply to:
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CreationMan
Inactive Member


Message 8 of 75 (85122)
02-10-2004 4:59 PM


Ya'll missin' the point
Ok you guys are toally missing the point. Even my creationist brother whom I agree with is missing it. Can mutations be beneficial? YES!! It is rare but it can happen. Wingless beetles on the Galapagos Islands have shown that. But the question is:
Have there ever been mutations shown to INCREASE NEW information in the genes. I.E., Information causing a reptile arm to turn into a bird wing. Yes if you have a duplication mutation which causes an extra finger to be expressed in the phenotype there is an increase of info, but it is NOT NEW info. There is NO scientific evidence to show that new information has arisen by mutaions in a genome. And new information cannot arise out of nowhere, (that's a scientific law) That shows that macro-evolution is IMPOSSIBLE.

"The Fool has said in his heart, 'There is no God'"
Mario (Creation Man)

Replies to this message:
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Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 9 of 75 (85132)
02-10-2004 5:16 PM
Reply to: Message 8 by CreationMan
02-10-2004 4:59 PM


Re: Ya'll missin' the point
CreationMan writes:
And new information cannot arise out of nowhere, (that's a scientific law)
You are talking through your hat - there is no such law. Here is a link to Shannon's original paper on information. Notice that the law you describe is not mentioned therein.
What *is* mentioned is that the greatest source of new information is a random number generator. Which is pretty much the source of mutation.
--Percy

This message is a reply to:
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CreationMan
Inactive Member


Message 10 of 75 (85135)
02-10-2004 5:31 PM


Info
It is a scientific fact that information can only arise from information and ultimately from a teleonomic (intelligent) source. No where has matter ever been observed to give rise to information.
INFORMATION CAN ONLY ARISE FROM INFORMATION AND ULTIMATELY FROM A TELEONOMIC SOURCE.
If you disagree provide me with a scientific example of the opposite happening. You can't, and you won't find one either. So happy hunting.

"The Fool has said in his heart, 'There is no God'"
Creation Man

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Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 11 of 75 (85137)
02-10-2004 5:36 PM
Reply to: Message 10 by CreationMan
02-10-2004 5:31 PM


Re: Info
CreationMan writes:
If you disagree provide me with a scientific example of the opposite happening. You can't, and you won't find one either. So happy hunting.
Any event. If the event is illuminated, information about that event will be transmitted to your eyes.
--Percy

This message is a reply to:
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Loudmouth
Inactive Member


Message 12 of 75 (85140)
02-10-2004 5:40 PM
Reply to: Message 10 by CreationMan
02-10-2004 5:31 PM


Re: Info
quote:
It is a scientific fact that information can only arise from information and ultimately from a teleonomic (intelligent) source. No where has matter ever been observed to give rise to information.
It is not a scientific fact. See Percy's post above. Random number generators can create information.
Secondly, could you give me an example of what new information at the genetic level would look like? If you don't know what it would look like you can't say it doesn't happen.
But, just for a scientific example:
Nucleic Acids Res. 2000 Jul 15;28(14):2794-9.
Evolution of biological information.
Schneider TD.
National Cancer Institute, Frederick Cancer Research and Development Center, Laboratory of Experimental and Computational Biology, PO Box B, Frederick, MD 21702-1201, USA. toms@ncifcrf.gov
How do genetic systems gain information by evolutionary processes? Answering this question precisely requires a robust, quantitative measure of information. Fortunately, 50 years ago Claude Shannon defined information as a decrease in the uncertainty of a receiver. For molecular systems, uncertainty is closely related to entropy and hence has clear connections to the Second Law of Thermodynamics. These aspects of information theory have allowed the development of a straightforward and practical method of measuring information in genetic control systems. Here this method is used to observe information gain in the binding sites for an artificial 'protein' in a computer simulation of evolution. The simulation begins with zero information and, as in naturally occurring genetic systems, the information measured in the fully evolved binding sites is close to that needed to locate the sites in the genome. The transition is rapid, demonstrating that information gain can occur by punctuated equilibrium.
There, evolutionary processes can increase information. If you have a scientific data that refutes this, please post it. If not, then it would seem that it is your own bias that keeps you from seeing the truth.

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CreationMan
Inactive Member


Message 13 of 75 (85142)
02-10-2004 5:46 PM


Mutation
And BTW MUTATIONS HAVE NEVER BEEN OBSERVED YEILDING NEW INFORMATION.
Evolutionary change would require the addition of new information, which is not a feature of the sort of changes one sees in bacteria. Even when a bacterium develops resistance where there previously was none in the population, by mutation (a random copying mistake which changes the genetic information), the change still represents a loss of information. This sounds counterintuitive, but it’s important to recognize that enzymes are usually tuned very precisely to only one type of molecule. Mutations reduce specificity. Hence the enzyme is less effective in its primary function, but it is able to break down other molecules too. In no case have bacteria been observed to become resistant through a gain of new information, i.e., the emergence of a completely new gene that produces a completely new enzyme.
Dr. Lee Spetner (biochemist) said that all point mutations studied on the molecular level tend to REDUCE the amount of information. Not increase it.
Point stated.

"The Fool has said in his heart, 'There is no God'"
Creation Man

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Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 14 of 75 (85143)
02-10-2004 5:47 PM
Reply to: Message 12 by Loudmouth
02-10-2004 5:40 PM


Re: Info
Looks like we have a Dembski or Gitt disciple. Dillan used to say the same thing.
--Percy

This message is a reply to:
 Message 12 by Loudmouth, posted 02-10-2004 5:40 PM Loudmouth has not replied

  
Percy
Member
Posts: 22392
From: New Hampshire
Joined: 12-23-2000
Member Rating: 5.3


Message 15 of 75 (85145)
02-10-2004 5:53 PM
Reply to: Message 13 by CreationMan
02-10-2004 5:46 PM


Re: Mutation
CreationMan writes:
And BTW MUTATIONS HAVE NEVER BEEN OBSERVED YEILDING NEW INFORMATION.
Spetner is wrong. You can understand why by following this scenario.
Imagine a population of organisms, and one of the genes in this population has 8 different alleles (varieties), so the total information for this gene within the population is log28=3.
Now imagine that one of the newly born organisms possesses a mutation at this gene location that is different from the other 8 alleles, yielding a total of 9 alleles within the population, so the total information is now log29=3.12. Since 3.12>3, information in the population has increased.
--Percy

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