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Mutations can generate new information: Affirmative Opening.

Introduction A comparatively new claim from creationist circles is Mutations cannot generate new information. This claim is rather confusing to a biologist though, and it immediately brings up some questions: How does one define new? How does one define information? Attempting to answer these two questions usually brings the problem of this claim into the spotlight. When considering what is an appropriate functional definition for new and information, we must ask what is important new information in terms of evolutionary theory? What would we expect natural selection and other evolutionary processes to be able to generate to fit our current model of evolution? I could define new information as anything I wanted but it is a nonsensical argument if the definitions dont capture an essential ability of evolutionary power. In other words, I can claim that evolution cannot create X or Y, but if it isnt essential to evolution to be able to create X or Y, then it doesnt matter. Some basic information about genetics might be useful to some readers here: A mutation is considered a change in the nucleotide sequence, a nucleotide being one of 4 chemical bases in DNA. A group of 3 nucleotides is a codon, which codes for an amino acid, which is a chemical molecule. Amino acids are created by codons until they are told to stop. The structure that combination of amino acids creates (from start to stop) is called a protein. A gene is usually defined as either a protein, or a group of proteins that create or influence a trait or many traits (I will use the latter), with a trait being a characteristic of an organism think spots on a cheetah or the thickness of a turtles shell for examples. Keep in mind that rarely do we find a one gene one trait relationship. Often genes are pleiotropic, meaning they influence multiple traits. Consequently, a trait is often influenced by multiple genes. Ill revisit these definitions again briefly when they come up. That being said, I submit that the only proper definitions for new information are as follows: a Addition of genetic material (nucleotides/codons/amino acids) b Addition of new proteins c Addition of new traits (genes) If the Negative cares to argue that another definition should be used, I expect an argument on why its a required ability of evolutionary power to create the proposed new definition. I expect this definition and explanation to be very well-described and thought out, as the nature of formal debate limits the ability of prolonged discussion. I plan on giving evidence of the fulfillment of each possible definition throughout the remainder of this case. Note that the definitions are progressive - meaning that they increase in complexity as the list goes on. Definition B requires mutations to be able to fulfill definition A, for

instance, and the third definition requires all definitions to be fulfilled (the creation of a new gene [C] requires the creation of new proteins [B] and therefore genetic material [A]). Because of this, Im going to focus on introductory and hypothetical examples for the first two definitions, to try to give the reader a theoretical understanding of these rather basic genetic functions. The last definition is more complex, and Ill be citing some specific studies to back it up. I want to note that an increase in the number of proteins isnt explicitly required, as the newly added proteins can simply be modifications of old ones, but some the examples I give show both an increase in variation and raw numbers, and how the genome increases in size is well known. Finally, at the end of this argument I want to provide some examples of what I mean by a nonsensical definition of information - again meaning one that has no bearing on evolutionary success. I find this to be essential to the discussion, so it is important that readers understand why these are poor arguments for what information is. 2 Definition 1: Addition of new genetic material (nucleotides) This one is perhaps the most simple to establish to a layman, and I suspect most will agree with this claim mutations, by definition, cause a change in the nucleotide sequence. Think of a nucleotide as a building block of DNA, -there are 4 in DNA, symbolized by A,T, G, C. We describe chunks of DNA just as sequences of these bases. Every 3 nucleotides form an amino acid called a codon. These amino acids work together to create proteins and determine how they fold. Common mutations such as point mutations (change in a nucleotide) or insertions (addition of a nucleotide(s)) Lets take this sequence for example: We start with 9 nucleotides: ATA TAT TGA Some point mutations occur: ACA GAT TGA An insertion occurs: ACA GAA TTG A Another point mutation: TCA GAA TTG A Another insertion: TCA GAA TGT TGA It is not a leap of faith by any means to state that TCAGAATGTTGA is more varied than the original ATATATTGA. The claim that it has more information because of increased nucleotides (meaning more things can be coded for) is relatively straightforward. The amount of nucleotides has increased from 9 to 12, adding an additional amino acid. Since every three pairs codes for an amino acid, we started with gene that codes for a protein that was comprised of the amino acids Isoleucine Tyrosine-STOP (TGA codes for the termination of a chain). Four incredibly small mutations changed that protein into one comprised of Serine-Glutamic Acid Cysteine --STOP. We added an additional codon and completely changed the structure of the protein. In other words, we have managed to create new nucleotides, new codons, and new amino acids.

Definition 2: Addition of new proteins. So weve established that mutations can increase the amount of nucleotides, codons, and amino acids - but what about proteins? Our example from Part 2 still only creates a single protein, after all. New proteins are simply created when codons are added after a STOP codon. Remember, the STOP codon simply tells the process that this particular protein is done being translated - a new protein starts up after the STOP codon. Lets revisit that protein we looked at: TCA GAA TGT TGA = Protein consisting of a Serine-Glutamic Acid-Cysteine chain. Lets say that sequence undergoes a mutation that causes a duplication of the last 3 codons. TCA GAA TGT TGA GAA TGT TGA This results in an additional protein being made - the final GAA TGT TGA now codes for a Glutamic Acid - Cysteine protein after the original protein has been made. Mutations have now increased both the variety and the amount of proteins available. Its important to note that while there is a set number of amino acids that codons can create, the amount of protein variety is theoretically endless because it relies on the sequence and length of amino acid chains.

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Definition 3: Addition of new traits. Now that weve established that new proteins can be created, can we establish that new traits can evolve in the genome as well? This one needs to be approached in a different manner than the last two definitions, something this complex needs to be shown with experimental evidence, small examples of the process wont suffice. Remember that a trait is defined as a physical character of an organism, and also recall that genes are often pleiotropic they affect several traits, and traits are often affected by several genes. A theoretically simple example can be made though a new protein is created by copying a chunk of codons with a stop codon at the end, and that new protein undergoes a mutation which changes the structure of it, either by coding for a new amino acid or changing the ones currently being produced. That new protein makes a physical change such as a protein that binds to destructive molecules that threaten the organism, therefore neutralizing them (like an antibody). There has been a new trait created the ability to neutralize a specific type of molecule. Its also important to note that an increase in the amount of genetic material isnt a requirement of evolution or a new trait. A modification to current genes can create variation without adding new genes. The variation is what allows evolution to progress, and an increase in the amount of genetic material just allows more potential variation. That being said, let me provide some

examples of traits that we have observed. - An Apolipoprotein mutated into a form that stimulates cholesterol removal from cells, and possesses an antioxidant that prevents some damage in arteriosclerosis that was discovered in a small community in Italy. (Calabresi et al. 1999, Bielicki and Oda 2002) - In Lenskis long-term E. coli experiment, cells evolved more rounded cells (cell shape is very important to bacteria) and increased cell wall elongation. (Nadege et al. 2008) - E. coli mutated the ability to digest citrate in oxygen-rich conditions. This is particularly intriguing because the lack of this ability in aerobic environments is considered to be a defining characteristic of E. coli. (Blount et al. 2008, Blount et al. 2012) - HIV-1 mutated a new gene known as vpu (Strebel et al. 1988). This gene acts as an ion channel in the host cells membrane ( Klimkait et al. 1990), degrades a host cell receptor (Bour and Strebel 2003), and has mutated to require an additional binding site (Gomez et al. 2005). In subtype M-C of HIV-1, vpu is so dramatically different that the subtype can be defined by it, and acts in a fundamentally different manner than the vpu in other types. (Pacyniak et al. 2005). These are all significant biochemical mutations in the virus. - Two bacteria in a pond next to a nylon factory mutated an enzyme which allowed them to digest the nylon (Negoro et al. 1994, Kato et al. 1995). This is particularly fascinating because Nylon is a man-made material with a unique structure and bonds that has only been around since the 1930s. I understand that these examples are hard to understand with a layman understanding of biology, but that is something that cannot be avoided. Specific examples regarding physical benefits of proteins are always going to require a foundation in biochemistry something that takes 3 years of college chemistry at most institutions to acquire, so its a stretch to think that the fine details of this can be understood fully by laymen, my apologies. Please take full advantage of asking me questions in-between submissions. Ill try my best to respond to a reasonable amount. 5) Bad Definitions of Information Its not really new, its just a modification! Id like now to investigate some of those nonsensical definitions of information that are commonly used. Remember, the most important thing regarding information is that its a required evolutionary mechanism. You can define information as anything you want, but if you dont provide a compelling case on why its essential to evolution to be able to produce it, then it doesnt matter. The first one of these that I want to tackle is the Its not really new, its just a modification! this is summed up well in one of the negations articles on mutations (Doberenz, unknown

date*): Mutations work like thisthey mix up information that is already there, they take away information that is already there, or they add in extra information which is actually already there. Thats the basics of mutations. You cant POOF in new information. You dont have a mutation that turns an average turtle into a karate-chopping, talking, ninja turtle. There is no information in turtle cells that gives them the ability to speak, grow into human-like forms, or perform ninja moves. A mutagena physical or chemical agent causing mutationsdoesnt switch on or create the portion of a turtles brain that allows them to talk, and do so somewhat intelligently, such as drawing conclusions and using basic logic. Turtles cant do thatno matter how hard you try. Evolutionists will try to tell you differently, but you cant get NEW information out of cells. That good ol Person A always had the ability to smell, but it was enhanced. He had the information and the ability to smell, it was just heightened in that hypothetical example. If someones red blood cells are in a sickle shape, we see that the blood cells actually had information to change shape in that way. It wasnt that brand new special blood cells popped up out of nowhere, it was just that the existing information changed. Lets take a look at this claim for a second. First, it is problematic that Mr. Doberenz never actually defines information. Secondly, he seems to be making the claim that nothing new ever gets added to organisms he states that turtles will never have a mutation that turns them into a ninja turtle, and he seems to be claiming that the sickle-cell form already existed in some way, and the mutation merely activated it (unsure of exact claim, to be honest). Well consider the turtle claim first: this is an example of a strawman a fallacy which is based on the misrepresentation of an opponents position. No evolutionist expects a mutation to turn something like a turtle into a ninja, so using the failure of that as an example why evolution isnt correct is nonsensical. Furthermore, hes using that example as what new information is this too is a strawman. If you define new information as large leaps such as a turtle turning into a bipedal ninja, of course we arent going to see new information we wouldnt expect to! Evolution works by gradually changing and improving on current structure, we dont expect a single mutation to give a turtle gigantic cognitive abilities and bipedalism if that were to happen we would expect gradual change over large amounts of time. For instance, to make that turtle walk upright changes to the physiology would be needed that wed expect would evolve gradually wed expect changes to the bone structure by modifying the existing structure, and wed expect changes to the musculature by modifying the existing structure. Demanding examples of new mutations that arent modifications of anything is nonsensical because evolution doesnt claim that completely new things will magically pop in fully formed. This same strawman is reiterated with the sickle cell claim . If someones red blood cells are in a sickle shape, we see that the blood cells actually had information to change shape in that way. It wasnt that brand new special blood cells popped up out of nowhere, it was just that the existing information changed.. As weve already discussed, evolutionists dont think that new things pop out of nowhere so saying that because new things dont pop out of nowhere, evolution is not correct is nonsensical. Also, it is unsure to me exactly what Mr. Doberenz claims by asserting that blood cells already had information to change shape. We know exactly what causes sickle-cell its a single point mutation that changes a hydrophilic amino acid into a hydrophobic one (this is easily found

online). So, when Mr. Doberenz claims that the blood cells actually had information to change shape in that way., what is he asserting? Is he saying that because the genetic code already existed, any modifications to the genome doesnt qualify as new information? Since all genetic material can be traced back to 4 nucleotides in DNA, does this mean all additions or modifications to the genome are not new information because they are still comprised of the 4 nucleotides? I believe that this is exactly what Mr. Doberenz means when he states Mutations work like thisthey mix up information that is already there, they take away information that is already there, or they add in extra information which is actually already there. talking about point mutations, deletions, and insertions respectively. What this boils down to is yet another strawman. Yes, mutations only work on the existing genetic material or add to it by copying the existing genetic material we do not claim or expect it should do anything else. Saying that because mutations work exclusively on existing genetic material they do not add new information, and there evolution is false is a nonsensical claim, because new information is defined as something that we dont expect evolution to do, nor does it need to do for it to be a valid theory. 6) Bad Definitions of Information But that mutation created a loss!! Lets take a look at another article written by the negation, The Domestic Cat (Doberenz, unknown date*): The cat just changed appearance. It was a loss of information as the color was removed from their feet, making it albino on its feet. Mr. Doberenz is asserting that because we can say that the cat lost something, it was a loss in information here is he talking about a cat mutating white boots on its feet the cat has supposedly lost information, because the color has been removed. The problem with this is that it can be applied to everything. You can say that something was lost in every situation. Lets say the opposite happened the cats white boots mutated away and it went back to a single color. Now you can say It was a loss of information as the pattern was removed from their feet, making it just a single color! or It was a loss of information as the second color was removed, making the cat monochromatic!. There is no actual metric here there has been no discussion on whether increased colors or increased uniformity is the actual increase and there is really no way to measure that. Does a cell lose information (the ability to be noncircular) if it becomes more rounded, or does a cell lose information (the ability to be circular) if it becomes less rounded? The problem comes down to the fact that we are arbitrarily assigning some modifications to be losses without really knowing if they are as shown above, you can essentially say ANYTHING is a loss of something, and when you can say that two opposite statements are both losses, than it is contradictory. Such claims of phenotypic changes being losses are therefore useless to this discussion because they cannot be objectively decided. For instance, I am inclined to view the addition of white boots on a cat as an increase in complexity (and it actually is if were using Kolmogorov Complexity, a part of algorithmic information theory (Komolgorov 1963)) but unless an objective (and appropriate way) is decided upon to use, it remains a useless conjecture.

Works Cited: An * denotes a non-scientific source (Not published, or published in a journal with questionable peer-review).

Bielicki and Oda (2002) "Apolipoprotein A-IMilano and apolipoprotein A-IParis exhibit an antioxidant activity distinct from that of wild-type apolipoprotein A-I." Biochemistry 41, 2089-2096 Blount ZD, Barrick JE, Davidson CJ, Lenski RE (2012). "Genomic analysis of a key innovation in an experimental Escherichia colipopulation". Nature 489 (7417): 513518. Blount, Zachary D.; Borland, Christina Z.; Lenski, Richard E. (2008). "Historical contingency and the evolution of a key innovation in an experimental population ofEscherichia coli". Proceedings of the National Academy of Sciences 105 (23): 7899906 Bour S, Strebel K. (2003) The HIV-1 Vpu protein: a multifunctional enhancer of viral particle release. Microbes and Infection 5(11):1029-39. Calabresi L, Canavesi M, Bernini F, Franceschini G. (1999) "Cell cholesterol efflux to reconstituted high-density lipoproteins containing the apolipoprotein A-IMilano dimer."Biochemistry 38, 16307-14 *Doberenz, Jake. "Intelligent Design: Domestic Cats: So Many Kinds of Cats." Creationist Company. N.p., n.d. Web. 4 Mar. 2013. *Doberenz, Jake. "Mutations and Evolution: Another Evolutionary Fail." Creationist Company. N.p., n.d. Web. 4 Mar. 2013.

Gomez LM, Pacyniak E, Flick M, Hout DR, Gomez ML, Nerrienet E, Ayouba A, Santiago ML, Hahn BH, Stephens EB. (2005) Vpu-mediated CD4 down-regulation and degradation is conserved among highly divergent SIV(cpz) strains. Virology. 25;335(1):46-60. Kato K, Ohtsuki K, Koda Y, Maekawa T, Yomo T, Negoro S, and Urabe I. (1995 Oct). A plasmid encoding enzymes for nylon oligomer degradation: nucleotide sequence and analysis of pOAD2. Microbiology, 141 (Pt 10), 2585-90. Klimkait T, Strebel K, Hoggan MD, Martin MA, Orenstein JM. (1990) The human immunodeficiency virus type 1-specific protein vpu is required for efficient virus maturation and release. Journal of Virology. 64(2):621-9 Kolmogorov, Andrey (1963). "On Tables of Random Numbers". Sankhy Ser. A. 25: 369375 Negoro, S., K. Kato, K. Fujiyama and H. Okada. 1994. The nylon oligomer biodegradation system of Flavobacteriumand Pseudomonas. Biodegradation 5: 185-194 Pacyniak E, Gomez ML, Gomez LM, Mulcahy ER, Jackson M, Hout DR, Wisdom BJ, Stephens EB. (2005) Identification of a region within the cytoplasmic domain of the subtype B Vpu protein of human immunodeficiency virus type 1 (HIV-1) that is responsible for retention in the golgi complex and its absence in the Vpu protein from a subtype C HIV-1. AIDS Research and Human Retroviruses. 21(5):379-94. Philippe, Nadge; Pelosi, Ludovic; Lenski, Richard E.; Schneider, Dominique (2008). "Evolution of Penicillin-Binding Protein 2 Concentration and Cell Shape during a Long-Term Experiment with Escherichia coli". Journal of Bacteriology 191 (3): 90921. Strebel K, Klimkait T, Martin MA. (1988) A novel gene of HIV-1, vpu, and its 16-kilodalton product. Science. 2;241(4870):1221-3.

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