The Instigator
myrrh
Pro (for)
Tied
0 Points
The Contender
MagicAintReal
Con (against)
Tied
0 Points

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

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Voting Style: Open Point System: 7 Point
Started: 2/14/2016 Category: Science
Updated: 1 year ago Status: Post Voting Period
Viewed: 795 times Debate No: 86575
Debate Rounds (5)
Comments (10)
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myrrh

Pro

Evolution happened. What I am contesting here is one of its primary purported mechanisms, mutation. The intention of this debate is for Con to provide peer-reviewed studies supporting mutation as a major force that drove evolution. 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. I will be reading the studies and evaluating what was discovered/concluded. Con should understand the content of the studies well enough to defend its explanatory power in regards to the topic of this debate. The full text of the papers must be available. For the sake of my being able to respond within the time frame, and to allow us to have a thorough discourse on each article, Con can provide a max of three studies. I am aware that there are vasts amounts of info out there on this topic, so choose wisely.

To further specify what I am looking for: something larger scale/a more complex development than a difference in the color of butterfly wings. For example the creation of a new structure that progresses the development of eyes in a species that previously had none.

I welcome and appreciate anyone who will accept the role of Con.
MagicAintReal

Con

I'd like to thank Pro for instigating this topic.

First, we need to clear the resolution up a little, because of some ambiguity with respects to the word "mutation."

There is a difference between a somatic mutation and a germline mutation.
A somatic mutation doesn't occur in sperm or egg cells, so it is not heritable.
A germline mutation however, occurs within sperm/egg cells, and that altered gene can be passed on.

somatic mutation - a change in the genetic structure that is neither inherited nor passed to offspring.
http://ghr.nlm.nih.gov...

germline mutation - the presence of an altered gene within the egg and sperm (germ cell) such that the altered gene can be passed to subsequent generations.
http://ghr.nlm.nih.gov...

So, I hope it's clear that I'm supporting the position that GERMLINE mutations, not somatic mutations, are a primary mechanism of evolution, because somatic mutations do not contribute to genetic variation, the key to evolution.

I also need to point out that germiline mutations are the ULTIMATE source of genetic variation, so when studies mention genetic variation, as a reader, one should understand that germline mutations were likely responsible for that.

gene variation - genetic variation can refer to differences between individuals or to differences between populations. Mutation is the ultimate source of genetic variation.
http://ghr.nlm.nih.gov...

mutation (germline) - a change in a DNA sequence, usually occurring because of errors in replication or repair. Mutation is the ultimate source of genetic variation.
http://evolution.berkeley.edu...

I need everyone to understand that genetic variation is essentially contingent on mutation as a driving force, and that genetic variation is the cornerstone of biodiversity, so my burden, as it were, is sort of a proof of principle.
I have to show that a principle of evolution is a major force that drove evolution.

*Peer-Reviewed Studies*

1. According to a PNAS published study on the effects of mutation on evolution and selection, researchers concluded that increased mutation led to more biological fitness, so phenotypes (characteristics) that were newly developed by mutations led to greater success within specific constraints.
More mutation, increased fitness.

"In the case of mutation rates, Liberman et al. (61) showed that for period 2 and symmetric selection, increased mutation rate is always favored, and the mean fitness at equilibrium is an increasing function of the mutation rate."
http://www.pnas.org...

2. Another PNAS published study mentions that the evolution of characteristics among organisms and the diversity there within are a direct result of NOVEL mutations, that is to say, new information was created by mutations alone and this leads to biodiversity.

"Phenotypic evolution occurs primarily by mutation of genes that interact with one another in the developmental process...the evolution of phenotypic diversity of different phyla has occurred by a continuous process of novel mutations and elimination of preexisting less-fit genotypes."
http://www.pnas.org...

3. Another PNAS published study indicates that beneficial mutations drive evolution and, in E. Coli, the researchers were able to use the mutation rate to predict the overall beneficial mutation rate, which indicates that mutations are not only creating novel, advantageous phenotypes, but mutations are also driving the evolutionary success of E. Coli bacteria.

"Given an approximate substitution rate for beneficial mutations per generation, a population size after transfer, nine generations per growth cycle, and a mean selection coefficient, we obtained 4 X 10^-9 per cell generation as an estimate for the beneficial mutation rate."
http://www.pnas.org...

I reject the resolution, because without germline mutations, genetic variation would likely not be so variant, and evolution would lack a major driving force.

Your thoughts, Pro?
Debate Round No. 1
myrrh

Pro

I would like to thank MagicAintReal for accepting the role of Con.

In the third article provided, http://www.pnas.org..., what the authors of the paper did was to showcase a new method they developed of tracing lineages within E. coli strains. They created ten different lineages using 1 cell to start each line, making each at the beginning genetically uniform. They transformed each ancestor cell with a plasmid containing microsatellites, which are repetitive strings of DNA that are highly susceptible to mutation. Because of this the cell lines would quickly differentiate genetically, and the authors were able to track which microsatellite alleles were present at what percentages with subsequent generations. They closely monitored these percentages, and when one allele displayed a significant increase in prevalence, they inferred that the cell line that had that allele experienced a beneficial mutation.

This is not necessarily a demonstration of mutation creating significant novel biological structures. The exact genetics of the mutations that occurred are not closely analyzed nor described in detail, as this was not the purpose of the paper. Beneficial mutations were assumed, not directly observed. It is possible that a novel structure that provided an advantage was created. However another possible scenario is this: there are genes that inhibit the expression of other genes. This kind of regulator gene experienced a mutation and became inoperable. The other gene that was previously being prevented from expression was now free to, and provided the cell with greater fitness in this specific controlled environment. This is an example of a beneficial mutation without the creation of a wholly new physiological process. To determine what type of beneficial mutations took place is unknown based on the findings of this experiment.

The other two articles provided, http://www.pnas.org... and http://www.pnas.org... are review articles. The first one concerns the effects that random and assymetric selection has on recombination, mutation and migration. In the second article the author sets out to: "I will first consider phenotypic evolution controlled by multigene families, because there is a large amount of interesting data, and the interpretation of new findings in this area is relatively simple. I will then discuss the evolutionary changes of protein-coding and regulatory regions of genes in relation to phenotypic evolution and their implications for the general theory of evolution."

While both of these articles are related to the topic of the debate, they do not directly address it. They are review articles and thus their topic is very broad and references numerous studies. As I mentioned in the comment section I am looking for single case studies, ones that deal specifically with the creation of significant novel biological formations via mutation. Again if you find in these review articles mention of such studies you could choose those to provide for this debate. The first article provided, http://www.pnas.org..., was a single case study.

I would like to ask Con to provide two more case studies.
MagicAintReal

Con

Here's Pro's checklist for "the intention of this debate," which requires Con to provide:

1. "peer-reviewed studies supporting mutation as a major force that drove evolution." Check.
http://www.pnas.org...
http://www.pnas.org...
http://www.pnas.org...

2. "a demonstration that mutation is able to create significant novel biological structures that allow for macro evolution to take place." Check.

From the E. Coli study,
"[W]e repeated the spread of beneficial mutations. Replicas were inoculated with cells that had been frozen at least 90 generations before a statistically significant adaptive event could be identified..."

The result?

"A novel advantageous mutation arose during the propagation of this replicate, and the frequency of a former inconspicuous allele increased significantly."

Novel structures were created and these ALLOW for macro evolution to eventually occur.

3. "[Con's understanding of] the content of the studies well enough to defend its explanatory power in regards to the topic of this debate." Check.

See my entire round 1 on peer reviewed journals.

4. "the full text of the papers." Check.
All of my sources are full texts with URLs that end in .full

5. "a max of three studies." Check.
http://www.pnas.org...
http://www.pnas.org...
http://www.pnas.org...

6. "larger scale/a more complex development [from mutations]...creation of a new structure" Check.

See #2 on the checklist.

#1-6 is Pro's entire list of requirements for Con, and I have fulfilled all of them.

More importantly, I have fulfilled the resolution that there is enough evidence to support mutation as a primary mechanism that drove evolution, and the PNAS confirms this.

Now on to Pro's contentions:

On the E. Coli study, Pro claims:
"This is not necessarily a demonstration of mutation creating significant novel biological structures."

My response:
I was referring to the "Selective Sweeps Are Reproducible" section of the study where they found that "a novel advantageous mutation arose during the propagation of this replicate."

Novel mutations are significant biological genetic structures.

Then Pro continues:
"Beneficial mutations were assumed, not directly observed."

My response:
Did you read this part of the study, Pro?

"these experiments demonstrated that our method reliably identifies beneficial mutations with low and high fitness effects in growing E. coli cultures."

Fitness is not an assumption; it's a measurement of the number of offspring that survive to reproductive age.
The experiments showed, by fitness, that the beneficial mutation identification methods were accurate.

Pro looks at my other PNAS articles and claims:
"While both of these articles are related to the topic of the debate, they do not directly address it...they are review articles and thus their topic is very broad and references numerous studies. As I mentioned in the comment section I am looking for single case studies, ones that deal specifically with the creation of significant novel biological formations via mutation."

My response:
The topic of the debate is about whether or not there's evidence that shows mutation driving evolution, and the two titles of the studies are:
a. Evolution in changing environments: Modifiers of mutation...
b. The new mutation theory of phenotypic evolution

To me these directly address mutation driving evolution, despite them being "review" articles, because of the studies' conclusions from so much evidence supporting the resolution.
Nothing in Pro's checklist from round 1 mentions that the studies cannot be review articles, or cannot reference numerous studies, so Pro's appeal to the comments section can be overlooked.

Then Pro requests:
"I would like to ask Con to provide two more case studies."

My response:
Pro, your checklist is very clear in round 1 that "Con can provide a max of three studies."
So, to avoid violating the agreed rules of the debate, I will not, because I have already reached that maximum.

I don't much appreciate Pro trying to expand Con's burden by requiring that the already peer reviewed full text studies, which satisfy Pro's round 1 checklist, be only single case studies,because the difference between a single case study and a multi case study has no impact on the resolution of evidence.

Evidence isn't only single case studies; multi case studies affirm the resolution just as sufficiently as single case studies do.

Pro, it's not fair to make a rule in round 1, max of 3 studies, and then request that Con violate the rule.

Pro, have I shown enough evidence that mutation drove evolution with the items required on your checklist?
Be honest.
Debate Round No. 2
myrrh

Pro

The authors of this paper http://www.pnas.org... do state that novel advantageous mutations occurred. However they didn't go into any detail as to what form these mutations took or how they provided advantage. The reason I think the authors inferred beneficial mutations rather than directly observed them was because their method " tracking the allele frequencies of injected microsatellites" did not involve actual analysis of the beneficial mutations. The mutating microsatellites themselve are most likely not involved in the changing code providing advantage, as they take up a very small percentage of the genome and often mutate without having any effect on the host as microsatellites are non-portein coding.

To describe a mutation and its benefit would have the following info: the exact change in the DNA code, what category of mutation that occurred (insertion, deletion, transpositional, etc.), and the phenotypic alteration that resulted from it. None of those details were provided in this paper, which leads me to believe they were never determined. If they were the authors should have been eager to share their findings.

Because analysis of the mutations was not given I cannot gauge whether or not novel structures were created. As explained in round 2 there are mutations that provide benefit but do not create novel structures. Other such examples of this are: the color of moth wings or the size of finch beaks. Both are famous examples from biology textbooks and neither are incidences of novel structures being created. The two body parts at play " beaks and wings " already existed before the mutations happened. What is going on is an alteration of an already existent formation. The example I gave in my opening text concerning eyes would be a new structure being formed. Other examples would include the synthesis of hearing organs or ATP synthase, the potential list is effectively endless.

When the authors say novel mutation that means something different. A novel mutation simply means a change in the genome that hasn't occurred before. This may or may not create novel structures. In the end this paper lacks solid evidence for Con's position as the paper does not provide information on the mutations that occurred and thus we do not know whether new structures were created or rather an already existent formation was altered. Even if a novel structure was made and this is what the authors mean by "novel mutation", we cannot see the extent of its explanatory power in regards to the topic of this debate because again there are no details.

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. However, in my intro the very next sentence reads: "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." In this regard they don't. I should apologize because my intro was a bit misleading, as it is possible for mutation to have an effect on evolution other than just the creation of purely novel structures. Also I should have stated in the intro that I was looking for single case studies and not review articles.

The reason that I strongly prefer single case studies is that within the confines of this debate I do not have enough time to appreciate review articles. The difference between single case studies and review articles is that single case are primary sources, and review are secondary. To gauge a primary source one just has to read and understand the experiment that was carried out. However with secondary sources, to truly interpret their credibility one needs to go through and read the primary sources that the author referenced in order to validate how the review author interpreted/portrayed the primary source findings. Simply put I do not have enough time to read through every case study that are referenced in review articles.

That being said I do appreciate Con's participation in this debate and apologize for disregarding two of the articles they took the time to find and present, partially due to my intro not being written as well as it should. With two more rounds to go I again ask that Con provide 2 more case studies.
MagicAintReal

Con

Thanks for that, Pro.

I maintain that the studies that I have presented have not only allowed me to meet my burden, but have negated the resolution, and this affirms that there IS, in fact, enough evidence to support mutation as a primary mechanism that drove evolution; the evidence can be found in this debate, in my round 1 and 2.

Pro has issues with my studies:
"The authors of the [E. Coli study] do state that novel advantageous mutations occurred. However they didn't go into any detail as to what form these mutations took..."

My response:
Let's be clear that Pro is in fact conceding that the study shows novel advantageous mutations, a requirement for Con from round 1.

The study did go into detail about the form the mutations took:
"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 took the form of genetic variability, that is to say, genetic structures that were not there before mutation had appeared after mutation, and these mutations created measurable variability within DNA strands; this is the form the mutations took.

Pro, why don't you regard new DNA strands as the "form these mutations took?"
To me, variations in genetics are new genetic forms that mutations can take.

Pro continues:
"The reason I think the authors inferred beneficial mutations rather than directly observed them was because their method 'tracking the allele frequencies of injected microsatellites' did not involve actual analysis of the beneficial mutations."

My response:
Pro, please listen.
Beneficial mutations are mutations that lead to FITNESS.
Fitness is measured by the number of offspring that make it to reproductive age.
The E. Coli study that you don't find to be proof of mutations driving evolution CLEARLY STATES:

"these experiments demonstrated that our method reliably identifies beneficial mutations with low and high fitness effects in growing E. coli cultures."

The authors DID actually analyze the mutations' effect on FITNESS, which is an analyzable measurement of benefit, because one can count offspring that make it to reproductive age.

So, Pro teaches us how to describe a mutation and its benefit:
1. "the exact change in the DNA code"

*The study clearly states, "a plasmid vector (pBR322)" which exhibited allele frequency variations from mutations.

2. "what category of mutation that occurred (insertion, deletion, transpositional)"

*The study wasn't attempting to find HOW these mutations occurred.
The mutations occurred, and the study attempted to show their effects on fitness, not how the mutations occurred.

This study focused on WHAT the effects of the mutations, regardless of category, on E. Coli genetic variation are...insertion, deletion, and transposition could all be culprits for the types of mutations that occurred, but whether or not these mutations lead to fitness was the intent of the study.

3. "the phenotypic alteration that resulted from it."

*Not all mutations lead to an observable phenotypic change. These mutations however, lead to genetic change that influenced fitness within E. Coli; one can explain the benefits of a mutation WITHOUT any observable phenotypic change.

Pro goes on:
"None of those details were provided in this paper, which leads me to believe they were never determined."

My response:
No, Pro's first detail WAS provided in the studies, and Pro's other 2 details were merely assumptions that Pro made about mutations and benefit; the category of mutation was irrelevant to the mutations' benefit on fitness, and so was phenotypic alteration.

Pro continues to ignore the analyzable measurement of fitness:
"Because analysis of the mutations was not given I cannot gauge whether or not novel structures were created."

My response:
Pro, did the authors of the study provide an ANALYSIS OF FITNESS?
If yes, then they DID analyze the beneficial effects of mutation on E. Coli.

Pro, were new DNA strands created from the mutations?
If yes, then "novel structures were created," because DNA strands are structures themselves.

Pro, did these mutated DNA strands lead to increased fitness?
If yes, then this is CLEAR evidence that mutations drove evolution in E. Coli.

Pro adds:
"A novel mutation simply means a change in the genome that hasn't occurred before. This may or may not create novel structures."

My response:
A novel mutation is a NEW DNA strand, and DNA strands ARE structures...you can't say there was a novel mutation, but not a novel structure, when what you mean to say is that not all novel mutations create observable new phenotypes; DNA is a structure.

Pro keeps at it:
"The paper does not provide information on the mutations that occurred and thus we do not know whether new structures were created or rather an already existent formation was altered."

My response:
Mutated DNA lead to increased fitness in E. Coli, such that the researchers found a positive correlation between increased mutation rates and increased fitness.

Also Pro, you are simply incorrect that the paper didn't provide information on the mutations that occurred...that was the whole paper!

*Voters Please Look Here*

Pro concedes the debate:
"Con pointed out that the topics of the two other articles they provided address...supporting mutation as a major force that drove evolution. This is true, they do."

My response:
Yeah, Pro admits that the resolution has successfully been negated, because Pro acknowledges that the studies I provided show support for mutation as a major force that drove evolution; the idea that there is not enough evidence to show mutation driving evolution has been negated by what Pro said there.

Pro adds to this:
"it is possible for mutation to have an effect on evolution other than just the creation of purely novel structures"

My response:
Ok, then there is no need to satisfy Pro's request for the creation of purely novel structures, because Pro admits that this is not a requirement for mutations to drive evolution...I still have provided them though, because new DNA is a new structure, phenotypically observable or not.

Pro requests:
"With two more rounds to go I again ask that Con provide 2 more case studies."

My response:
Thank you Pro for recognizing the lack of clarity with the requirements first round, and that Pro has somewhat expanded my burden...because of this acknowledgement, I will provide two more studies.

1. http://www.pnas.org...
"Cumulative frequency distributions for beneficial fitness effects associated with single-nucleotide substitutions measured for random and previously described mutations..." were found in the study.

2. http://www.pnas.org...
"the results reported here show an adaptative evolutionary capacity that overwhelms speculation. It should be stressed that each series came from a single infectious particle that rapidly generated all mutations needed for the remarkable gains in fitness observed."

Your thoughts, Pro?
Debate Round No. 3
myrrh

Pro

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.


MagicAintReal

Con

Thanks Pro.
I'm surprised that Pro has taken so much time to analyze these studies in order to misrepresent them to fit what he wants them to say.

I assure you that the PNAS published study called "Fitness effects of advantageous mutations in evolving
Escherichia coli populations" IN FACT demonstrates advantageous mutations by their effect on fitness.
Pro seems to ignore this constantly.

Remember, it's not an inference that fitness has increased if the number of offspring with a mutation that make it to reproductive age increases...it's math.

Maybe Pro should publish his analysis with PNAS...he should tell those researchers that they don't know how to count offspring that make it to reproductive age; he should tell those researchers that they just inferred those numbers.

Pro said:
"I maintain that the paper 1 does not provide evidence for mutation's ability to create novel structures"

Then later Pro said:
"The altered DNA could be considered a new structure...if a mutation occurs, then by definition a new DNA strand will exist...when Con writes that the altered DNA is "new" they are technically correct."

My response:
There it is.
Pro agrees that altered DNA is a new structure, and on this subject, I am technically correct, so on the issue of new DNA being an example of a new structure, both Pro and Con agree; this study shows that novel structures were created by mutation, and it was with these novel genetic structures that THE NUMBER OF OFFSPRING THAT MADE IT TO REPRODUCTIVE AGE (fitness) INCREASED irrespective of inference.

Pro agrees even more:
"The authors did in fact measure the mutations" effects on fitness."

My response:
Again!
Pro concedes that the authors MEASURED, not inferred, the effects of mutation on fitness.
Given Pro's concession on this and the direct quote from the E. Coli study,

"these experiments demonstrated that our method reliably identifies beneficial mutations with low and high fitness effects in growing E. coli cultures,"

there is in fact enough evidence to support mutation as a primary mechanism that drove evolution, in E. Coli bacteria.

Pro gets errant:
"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."

My response:
This was when I figured out that Pro is in fact neither a scientist, nor well-versed in biology, despite his overly-critical assessment of the paper.
There is no rule in biology that says that only phenotype changes can have an effect of fitness. NONE. Germline mutations affect fitness in E. Coli bacteria, phenotype change or not, and Pro has not given us ANY reason to doubt that, in fact, Pro has conceded that mutations led to new genetic structures AND that this study measured the fitness of such.

Pro, imagine a germline mutation that allows an organism to be reproductively viable, but has no discernible phenotypic change...only a genetic mutation that allows for the organism to be more reproductively compatible with other members of its species. This would increase fitness and there would be no observable phenotype change.

Finally Pro gets errant again:
"The specific focus of this debate...is to assess the evidence for mutation"s ability to create novel structures."

My response:
Nope.
Nice try Pro.
The resolution claims that there is not enough evidence to support mutation as a primary mechanism, and makes no mention of novel structures...the novel structures thing is just Pro's unscientific way of determining mechanisms of evolution.

Either way, novel structures were created by mutation in E. Coli, so Pro can no longer move the goalposts in this debate. I negate this particular resolution.

Notice, I have not really needed to defend the other papers I provided, because Pro refuses to acknowledge them.
They are however, evidence for mutation driving evolution, and Pro cannot find any more ways to misinterpret scientific findings published by PNAS.

Also, I must remind everyone...MUTATION IS THE ULTIMATE SOURCE OF GENETIC VARIABILITY, AND THIS IS A FACT OF BIOLOGY.
http://ghr.nlm.nih.gov...

Mutations-->fitness-->evolution.

Pro?
Debate Round No. 4
myrrh

Pro

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.

Vote Pro!

MagicAintReal

Con

Thanks for the debate Pro.

I'll respond to Pro's last round, and then conclude this mobile goalpost of a debate.

Pro posits:
"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."

My response:
This analogy of cars :: organisms always fails, because cars are made by an external, non-genetically related entity.
ALL organisms are descended genetically from a pre-existing organism, so new genetic structures descend genetically too.

On a car, any new structure would have to be created non genetically, mutually exclusive to pre-existing structures.
Cars don't reproduce cars, so cars don't reproduce new structures for cars.

Also, by putting a different, aluminum structure on to the car, the car now has a new structure.

Pro adds:
"Now for type 1 and type 2 alterations in regards to mutation."

My response:
Now for some BS that's pseudo-scientific and irrelevant to mutations' effect on driving evolution, the resolution of the debate.

Pro just made up this idea of type 1 and type 2 alterations, and readers should not find it to be a coincidence that Pro did not provide sources that show this arbitrary distinction between alterations.

Pro's pseudoscience became very clear here.
There are no type 1 or type 2 types of alterations; there are changes that get passed on, and there are changes that don't.

Berkeley does an excellent job of explaining the difference between somatic changes that can be misconstrued as evolution-inducing and germline changes that are the ultimate source of genetic variation.
http://evolution.berkeley.edu...

Pro requests:
"Con needs to provide more info on their hypothetical germline mutation to distinguish how exactly "genetic compatibility" is being increased without altering any phenotype."

My response:
You have misrepresented what I said.
I said without altering any OBSERVABLE phenotype.

What you keep requesting is for a new eye to form from a mutation, which implies a highly observable phenotype change.
So, I pointed out that there could be less noticeable genetic changes, ones that don't change an OBSERVABLE phenotype, that still increase fitness and drive evolution.

Some germline mutations can have a phenotypic change occur AFTER pubescence, like the acidity of sperm.
If sperm is too acidic, it may not be able to impregnate a member of the species.
Mutations that lead to this acidity would be detrimental.

Mutations that lead to a more compatible sperm PH level, would then allow for successful reproduction and likelier fitness.
These changes would not be observable until reproductive age.

I hope readers actually read the papers for what they're truly worth, and I hope people understand the real mechanisms of evolution, not just pseudo-scientific interpretations of what mechanisms should be.

To conclude this ever-expanding debate, I'm going to try something different.
I am going to negate the resolution ONLY using Pro's words...here we go:

Pro:
"In the third article provided...it is possible that a novel structure that provided an advantage was created...there are mutations that provide benefit but do not create novel structures...as it is possible for mutation to have an effect on evolution other than just the creation of purely novel structures."

Pro:
"If a mutation occurs, then by definition a new DNA strand will exist...Con stated that novel structures were created since DNA was changed, and so the altered DNA could be considered a "new structure"...when Con writes that the altered DNA is "new" they are technically correct."

Pro:
"The authors of paper 1...did in fact measure the mutations" effects on fitness...the authors determined that that group had spontaneously increased fitness....the authors directly observed increases in fitness. This is true."

Pro:
"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.

Paper 2 gave an informative description of a mutation that confers fitness...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."
http://www.pnas.org...
Debate Round No. 5
10 comments have been posted on this debate. Showing 1 through 10 records.
Posted by MagicAintReal 1 year ago
MagicAintReal
Agreed.
Posted by myrrh 1 year ago
myrrh
id say it was pretty good. i made a few too many grammatical errors, esp in the last round.
it would have been a lot better if we couldve agreed on the topic -_-
Posted by MagicAintReal 1 year ago
MagicAintReal
What did ya think of the debate myrrh?
Posted by myrrh 1 year ago
myrrh
debate *on* those
Posted by myrrh 1 year ago
myrrh
This is a review article that makes reference to many different research studies. I am looking for Con to provide 3 specific single-case research studies. You could choose 3 of the studies referenced in that article to focus on and I would debate those.
Posted by MagicAintReal 1 year ago
MagicAintReal
"Phenotypic evolution occurs primarily by mutation of genes that interact with one another in the developmental process. The enormous amount of phenotypic diversity among different phyla or classes of organisms is a product of accumulation of novel mutations and their conservation that have facilitated adaptation to different environments. "

http://www.pnas.org...

Do you want to debate this?
"the driving force of phenotypic evolution is mutation, and natural selection is of secondary importance."
Posted by MagicAintReal 1 year ago
MagicAintReal
Do you have to have a dog or fox face to post here?
Posted by Jedd 1 year ago
Jedd
Well then, I'm in no position to participate. I will spectate, though, this is going to be interesting.
Posted by myrrh 1 year ago
myrrh
I am asking that Con refer to external sources i.e. peer-reviewed journal-published studies.

I have a BS in bio.
Posted by Jedd 1 year ago
Jedd
Are you going to refer to external sources? Because from what you're saying you seem to have a degree in the field.
No votes have been placed for this debate.