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

For the sake of clarification 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. I maintain that the paper 1 does not provide evidence for mutation’s ability to create novel structures, as it does not provide sufficient details on the beneficial mutations that reportedly occurred. As a response Con quoted the following segment: "Because of the high mutation rates of cloned microsatellites, all populations had already accumulated substantial variability after 90 generations. Analysis of the bacterial culture in subsequent generations allowed us to follow the shifts in allele frequency at the cloned microsatellite locus..." The mutations that the authors are discussing here are not the ones that provided benefit. The authors inserted microsatellites into E. coli lineages, and as the microsatellites mutated, they recorded the percentages of each microsatellite allele that was present in the population in order to track different lineages: “The high instability of microsatellites rapidly generates different alleles in dividing cells. These alleles at a single microsatellite locus are sufficient to trace clonal lineages” … “In a multiallelic system such as microsatellites, however, directional selection increases only the frequency of the allele associated with the advantageous mutation. Hence, it is possible to trace adaptive events in a growing bacteria population by the significant increase of one microsatellite allele.” If there was a rapid increase in one segment of the population, then they inferred that specific group had experienced a mutation (separate from the microsatellite) that provided benefit. Notice the authors used the word “the allele associated with the advantageous mutation”, and not “causing” or “providing”. Even still, the only data paper 1 provided in the section Con quoted was that the rate of mutations were high, and there was substantial variability and shifts in allele frequency. These are not very descriptive. The details needed for an informative display of mutation’s ability to create novel structures are again: the change in the DNA code that occurred, the phenotypic alteration, and how this increased the bacteria’s fitness. These are all absent. The following is an example of a mutation described with relevant details. It is taken from paper 2: “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. How this provided advantage - the ability to grow in the presence of an antibody, I1 mAb, at concentrations that inhibit viruses without this mutation. This is a great example of a beneficial mutation described in detail. Paper 1 did not provide such info on their reported mutations. Another quote that Con provided from paper 1 describing the details of the code change that occurred: “"a plasmid vector (pBR322)" which exhibited allele frequency variations from mutations.” This is referring to the plasmid vector that carried the microsatellites and not the beneficial mutations. Also “allele frequency variations” is not very descriptive. Con asked me why I don’t regard new DNA strands as the form the mutations took. My answer is that if a mutation occurs, then by definition a new DNA strand will exist. That is implied. Mutation means a change in code, so to say that a mutation took the form of a new DNA code provides no new information. I stated that the authors of paper 1 inferred mutation rather than directly observed it. Con responded by saying that the authors directly analyzed the mutation’s effect on fitness. The authors did in fact measure the mutations’ effects on fitness. This is different however from observing the mutations directly. Mutation is a cause, fitness is an effect, the two are related but separate entities. The methods used by the authors were to track different bacterial lineages, each with their own signature alleles. If one bacterial line suddenly became more prominent, then the authors determined that that group had spontaneously increased fitness. The authors explained this by inferring that a beneficial mutation happened: “A striking shift in allele distribution becomes apparent after generation 270, where a single allele with 33 repeats has markedly increased its frequency during 90 generations (Fig. 1). This pattern is consistent with an advantageous mutation in the cells carrying the allele with 33 repeats.” “A novel advantageous mutation arose during the propagation of this replicate, and the frequency of a former inconspicuous allele increased significantly.” Con stated that not all mutations lead to phenotypic change, which is true. Con then said that such mutations lead to genetic change that influence fitness. This is false. A change in code (genotype) only has an effect on fitness if there is a corresponding change in the physical features (phenotype) of the organism. There are so-called silent mutations, which are changes in the genotype that have no effect on phenotype, and thus no influence on fitness. For example, let’s say within bacteria A’s DNA there is a segment of code that reads TAT. This signifies the amino acid (protein building block) Tyrosine. A mutation occurs in bacteria B which now has the sequence TAC instead. This would be a silent mutation, because TAC also codes for Tyrosine. The protein that would result in either case would be identical. There would be no difference in fitness between bacteria A and B. “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... Con stated that novel structures were created since DNA was changed, and so the altered DNA could be considered a “new structure”. The purpose of this debate is to look for mutation’s creative ability to generate novel structures, for example the formation of eyes in a species that previously had none. DNA is not a novel structure in this regard, as E. coli already had DNA. When Con writes that the altered DNA is “new” they are technically correct, but that is a different usage of the word “new” than the topic of the debate. I could take a baseball, write my name on it, and say that I have a “new” baseball. While what I’m saying would in a sense be true, it’s not like I created a baseball where before there was none. Con claimed that I conceded the debate when I wrote this: “Con pointed out that the topics of the two other articles they provided address this part of my intro: "supporting mutation as a major force that drove evolution." This is true, they do.” What I wrote is that they address mutation as a force that drove evolution, that’s it. Con said that I acknowledged that the studies showed evidence that mutation was a major force that drove evolution. If you read my quote you will see that is a vast overstatement. Even still those papers do not address the specific focus of this debate which is: To assess the evidence for mutation’s ability to create novel structures. It is not intended to address the other ways that mutation effects evolution. I already admitted that my intro could have been written better to make this clearer, but that is the topic nonetheless. Those papers being referenced, the first two that Con provided in round 1, do not center on this issue. I have to apologize, but since I am running short on time I will have to wait till the final round to compose responses for papers 2 and 3 that Con provided.