There is not enough evidence to support mutation as a primary mechanism that drove evolution.

I will refer to this paper . http://www.pnas.org... as paper 1, . http://www.pnas.org... as paper 2, and . http://www.pnas.org... as paper 3. There has been an issue during this debate, which is that there is a disagreement as to what the topic is. As the instigator of this debate I chose the topic. I stated in my opening text: “Specifically what I am looking for is a demonstration that mutation is able to create significant novel biological structures that allow for macro evolution to take place. ” To try to make what I mean as clear as possible, I offer the following analogy: I am going to distinguish what I will call type 1 and type 2 alterations. Let’s say there is a race car with a steel body. To make the car lighter and faster, the steel body is replaced with one made of aluminum. While a change was made to the car, a “new structure” was not invented. The part of the car at play, the body, already existed. This is an example of a type 1 alteration. Other examples of type 1 alterations: switching from off-road tires to street, choosing a different paint color, etc. Say that an additional improvement was added, this time the installation of a supercharger adding power to the engine. In this instance a new structure that did not exist in the car before was added. This is a type 2 alteration. Other type 2:, the invention of transmissions, catalytic converters, etc. Now for type 1 and type 2 alterations in regards to mutation. The famous differences in size of Darwin’s finch beaks are type 1. As different food sources become more or less plentiful, the average shape of the bird population’s beaks adapt due to natural selection. Larger beaks are better at breaking and eating nuts and seeds, while slimmer beaks are more proficient at catching insects and probing into cacti. Other examples of type 1: different color feathers, variation in claw length, etc. A type 2 alteration would include: the formation of photoreceptors in a green algae cell that previously had none. Other examples of type 2 would be the creation of ears, the flagellar motor, etc. What I am looking for is evidence that mutation is able to create specifically type 2 alterations. This is why it is important that the papers provided give relevant details on the mutations, to determine what type of alterations are occurring. Con there is a difference between making slight changes to a structure that was already present, and to truly create something that did not exist before in any form. I said that the authors of paper 1 inferred beneficial mutations rather than observed them. Con responded that the authors directly observed increases in fitness. This is true, however different from directly observing the mutations themselves. To go back to the car analogy, let’s say a series of races are happening. All of a sudden, at the beginning of race 3 one of the cars is suddenly faster than it was before. One would imagine that this was due to some improvement made to the vehicle. However just making that observation won’t tell you what exact changes were made. You would have to open up the hood and look directly into the mechanics of the vehicle to see what happened. This is analogous to what occurred in paper 1. The authors saw that there were significant increases in the fitness of certain bacterial lines. They then inferred that a beneficial mutation was the cause behind the increase in reproductive output. If they directly observed the mutations they made no mention as to how they did so or what they found. They did not claim to have sequenced the bacterial genomes afterwards (equivalent to “looking under the hood”), nor gave any description as to what genotypic and phenotypic alterations resulted. This is why it more info is needed before this study can support mutations being able to produce type 2 alterations. We simply do not know what kind of mutations occurred. Con needs to provide more info on their hypothetical germline mutation to distinguish how exactly “genetic compatibility” is being increased without altering any phenotype. Are there genetic barriers to conception between members in this species? Is compatibility being increased in some other way? Know that if physical changes are occurring at only a cellular level, that is still a phenotypic change. In the end whether or not a genotypic change that has no effect on phenotype can possibly increase fitness, such would be the exception rather than the norm. Natural selection does not care what code our DNA reads, whether it’s A,T,C or G. What it does care about is how fast you are, your good your sense of smell is, how well you can see at night, etc. These are all physical features, in other words phenotypes. “Silent mutations are mutations in DNA that do not significantly alter the phenotype of the organism in which they occur. ” “Because silent mutations do not alter protein function they are often treated as though they are evolutionarily neutral. ” . https://en.wikipedia.org... “An individual's fitness is manifested through its phenotype, which is affected by the developmental environment as well as by genes” . https://en.wikipedia.org...(biology) “Natural selection is the differential survival and reproduction of individuals with certain traits. It acts on phenotypes. ” . http://www.uic.edu... Con wrote: “Notice, I have not really needed to defend the other papers I provided, because Pro refuses to acknowledge them. ” This is an overstatement of what I actually said, something that Con has done before (see my round 4 response 3rd to last paragraph). What I in fact wrote was that I was running out of time and thus needed to wait till the next round to provide responses to the other papers, which I shall do now. The primary theme of papers 2 and 3 was to observe changes in fitness of RNA viral lineages over time, with paper 2 incorporating single-nucleotide substitutions into a portion of the population. Both studies go into great length describing the trends they discovered as to how change in fitness over time correlated with different statistical models, such as hyperbolic, exponential, log-normal, etc. However I only found 1 cases of a mutation being described in detail, it comes from paper 2 and I have referenced it before: “we introduced the substitution A-3853 --> C in the plus strand (Asp-259 --> Ala substitution in the G surface protein), which confers the ability of growing in the presence of the I1 mAb (MARM phenotype), at concentrations that inhibit wild-type growth. ” The exact code change - Adenine at location 3853 was replaced with Cytosine. The phenotypic result - Aspartic acid was replaced with Alanine in the G surface protein. The advantage that developed - the ability to grow in the presence of an antibody, I1 mAb, at concentrations that would inhibit viruses without this mutation. This adaptation did not occur for the first time during the course of this experiment. It was a previously known variation and the scientists used it as a template ancestor for their viral lines. “This cDNA clone, named MARM RSV, was used as template for the rest of mutagenesis. ” The authors do not go further into how this adaptation actually provides resistance to antibodies, as it was not the focus of their study. An educated guess is possible though. Antibodies are proteins that work by attaching themselves to multiple viruses at a time, immobilizing them and causing them to form clumps. This inhibits the virus’ ability to attach to and infect cells, as well as makes the viruses easier targets for ingestion by macrophages of the immune system. Antibodies attach to viruses at antigen-binding sites, which are on the viral surface and can take a wide variety of forms, notably surface proteins. . https://en.wikipedia.org... Seeing how the mutation caused a change in a surface protein, it is likely that this protein is involved in the antigen-binding site of I1 mAb. Because the antigen-binding site is now different, the connection does not occur as readily and thus the virus gains resistance to the antibody’s effects. If this is the case, then a type 1 adaptation is occurring. A novel structure is not being created, rather an already existent structure, the viral surface protein, is being changed slightly (1 amino acid difference). Thus a type 2 adaptation did not occur. In the end from the three studies that Con provided, only paper 2 gave an informative description of a mutation that confers fitness. The mechanism of benefit had to be guessed though, and if the hypothesis is correct it would only be an example of a type 1 alteration. While Con did provide papers that address mutation as a force involved in evolution, they did not demonstrate that mutations are capable of producing significant novel structures, which was the specified focus of the debate. That being said, I greatly enjoyed this exchange and would like to thank MagicAintReal for accepting and carrying out the role of Con. I also appreciated their provision of extra materials.