Potential falsifications of the theory of evolution

I have already answered this question multiple times. If my previous replies were not satisfactory I doubt another reply will be. I have already done this as well. Just for kicks, here are the two experiments that laid the foundation for our understanding of random mutations with repsect to fitness:Page not found – UF ICBRhttp://profiles.nlm.nih.gov/BB/A/B/F/J/_/bbabfj.pdf

Transposons do not repair DNA. Nowhere in any of Shapiro's papers did I read anything that would indicate that transposable elements are part of DNA repair. If anything, they have a penchant for doing away with the function of a gene once they insert.

You really need to work on reading comprehension. We believe that the complexity of the cell is the result of evolution which is a non-random stochastic process due to the non-random mechanism of natural selection acting on random mutations. Would you say that Zeus creates lightning bolts, or is the naturalistic explanation satisfactory?

The problem we seem to be having is that you don't understand what the scientists are saying, and through this misunderstanding you project your own biases. You see "non-random" somewhere in a sentence and you automatically assume that the use of this word indicates that mutations are non-random with respect to fitness. You even use quotes that are related to gene expression and then claim that it is talking about mutations.When your opinion is based on something other than your ignorance of the subject at hand we can actually start to discuss the science.Edited by Taq, : No reason given.

The point that we have made in multiple threads is that no evidence can falsify ID because ID is not science. Once again we have and ID supporter playing the Argument from Ignorance card in support of an unfalsifiable belief. But we can show that the work he cites demonstrates that mutations are random with respect to fitness, which you and shadow seem to ignore.Even more, since you and shadow want to cite Shapiro's work as evidence for ID it is incumbent on you to demonstrate how Shapiro's work evidences ID. Still waiting for that. Earlier in this thread Shapiro's authority on the subject was cited by shadow as support for his argument. I now see that the tune has changed once Shapiro says something the ID crowd disagrees with.

You keep making the mistake of extrapolating these processes beyond what Shapiro actually states. Shapiro argues that the timing of mutagenesis is engineered, but he does not extrapolate this to mean that the mutations themselves are deterministic. Created by what? Are you saying that Shapiro's work does not support ID, or is at least unrelated to the claims made by ID supporters?

This is a perfect example of what I have been referring to. Shapiro argues that these natural engineering systems use exon shuffling instead of point mutations to find novel functions which produces a higher probability of finding beneficial adaptations compared to just point mutations. This is what Shapiro means when he states "certain changes are non-random with respect to their potential biological utility." He does NOT say that mutations are non-random with respect to fitness. He says that processes like exon shuffling make the chances of finding biological utility (aka beneficial adaptation) more probable.However, the process of mutation involved in exon shuffling is still random with respect to fitness.

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Perhaps the most important aspect of evolutionary change by natural genetic engineering is that it employs a combinatorial search process based upon DNA modules that already possess functionality. . . Mixing functional domains in new combinations is far more likely to produce a protein with novel activities than is the modification of one amino acid at a time.
Mobile DNA and evolution in the 21st century - PMC
(Shapiro 2010 Mobile DNA paper)

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Notice that he calls exon shuffling a "search process". This is neo-Darwinism 101. This is how evolutionists have always described random mutation (with respect to fitness) coupled with natural selection.Non-random mutations (with respect to fitness) would not need to search for anything. The precise mutations needed to overcome a specific challenge would be pre-programmed into the engineering systems, and only those mutations needed to overcome the challenge would be produced. It all depends on the context of non-random. Again, you keep changing the context and pretending that non-random applies to all contexts. It doesn't.Did you read those two experiments I cited for you? I think it would be really helpful to discuss those experiments if you have time.

So the only one claiming that mutations are non-random with respect to fitness is you, and without any evidence to support the assertion.If you want to claim that mutations are non-random with respect to fitness then it is incumbent on YOU to cite the evidence necessary to conclude that mutations are, in fact, non-random with respect to fitness.What you have now constructed is a negative argument which is a logical fallacy. You have started with an assumption and until that assumption is completely ruled out you will not budge from this assumption. This is not how science works. How so, just out of curiousity? For the purposes of this question I am assuming that you are NOT an ID supporter so don't worry about getting your head bitten off.

From the viewpoint of an actual biologist, I would never call Shapiro's thesis "direct". It's a lot of showmanship. Frankly, there is nothing wrong with this per se. There needs to be a bit of salesmanship in every scientific paper. In fact, I have seen papers that are actually quite thin when it comes to actual scientific content but due to the style of the writing (aka showmanship) it was accepted for publication in a prestigious journal.What I see in Shapiro's papers is a lot of terms that were invented simply to make Shapiro's work seem more original. Everything he discusses is already known and described by terms already in general use amongst biologists. Instead of using these well known terms he invents his own (e.g. natural engineering systems). It would be like me describing the aerodynamics of a wing as the "fluidic engineered dynamos of turbulent lift", and then write an entire textbook as if I am describing a whole new field of physics. Why not just call it aerodynamics?At the same time, I don't want to discount Shapiro's contributions as it relates to his actual original research. He does quality lab work with well designed experiments.

The results of experiments are not consistent with non-random, deterministic mutations. The results are consistent with random, non-deterministic mutations. This is made clear in the two experiments I cited (twice) for you earlier. The mutations conferring phage and antibiotic resistance occur in a random generation in the absence of either phage or antibiotics. When these mutations occur they are either neutral or slightly deleterious (in the case of the tonB mutations conferring phage resistance). These mutations are not produced in response to the presence of either phage or antibiotics. In fact, these same mutations can be produced in the absence of the entire cell. They can be produced with nothing more than a DNA template and the required polymerases and cofactors.

The Luria-Delbruck paper is going to very hard to understand for the layman. That is why I linked to a webpage that boiled it down. However, the Lederberg paper is actually written in a very straightforward manner that you shouldn't have too much trouble understanding.It is also worth mentioning that Luria and Delbruck won a Nobel Prize primarily for the work described in that experiment.Edited by Taq, : No reason given.

Again, there seems to be a disconnect here. Of course an organism's fitness is determined by the mutations in it's genome. No one is arguing otherwise. What we are saying is that the processes that produce these mutations have no way of determining which of the mutations they produce will increase or decrease fitness. These processes are blind as to the effect of these mutations on fitness. This is what makes them random.

I can see that. We often see ID supporters jump to conclusions like this. The lottery is engineered and it is random. I have used an engineered transposon for random mutagenesis before. It would also be outside the realm of the scientific method. Scientific conclusions do not make absolute statements of truth. Conclusions are always tentative and based on the evidence at hand. So far, all of the evidence is consistent with random mutations with respect to fitness.

It wasn't. The emergence of the nylonase enzyme (nylC) was the product of an insertion mutation in a plasmid carried by the bacteria. We know this because we have the parent populations and daughter populations. The nylon oligmers that the bacteria are now able to utilize as a food source did not exist until the 20th century, well after the flavobacterium existed.

I just found a paper by Shapiro that should help illuminate the subject at hand. It actually ties together several things that I have been talking about, including the Lederberg paper that I mention in previous posts. Shapiro uses the plate replica method to demonstrate that DNA fusions resulting in beneficial adaptations are unrelated to specific selective pressures. They specifically looked at the appearance of reverse lacZ mutants that were capable of digesting lactose.

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Our results unambigously demonstrate the formation of araB-lacZ cistron fusions encoding active hybrid B-galactosidase molecules in the absence of arabinose and lactose substrates. The fusions were obtained by the sib selection technique [my note: this is the Lederberg plate replica method] (Cavalli-Sforza and Lederberg, 1956) and characterized by PCR analysis and B-galactosidase assay (Table V). This demonstration means that there was no requirement for selective substrates (arabinose and lactose), and that the sharp transition (observed by three different laboratories) from normal growth conditions, where no fusion formation by MCS2 was detectable, to selection conditions, where fusion formation was observed at surprisingly high frequencies, was a response to carbon source depletion. . .

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This view of how selection-induced mutations are triggered in the araB-lacZ system is an example of what we have described previously as the operation of natural genetic engineering systems (Shapiro, 1992, 1993b).

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[this was transcribed from the .pdf so any spelling or grammatical mistakes are mine and should be assumed to be random with respect to spelling ]

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The paper can be found here:http://www.ncbi.nlm.nih.gov/...95473/pdf/emboj00069-0222.pdfSo the same randomness of mutations established by the Lederberg and Luria-Delbruck experiments is the same randomness seen in the genetic engineering systems that Shapiro actually studies. The paper also goes on to mention that the same results are produced by the Luria-Delbruck fluctuation method.In addition, this paper really spells out how Shapiro views "random" mutations and genetic engineering systems. A perfect example is this quote:

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In other words, much genetic change is not a stochastic ongoing process, controlled at the level of selection or mutation fixation (reference deleted), but instead involves the regulated assembly of specific cellular complexes. The physical and biochemical events needed to produce an araB-lacZ fusion are too elaborate to occur by an accidental breakdown in the normal replication process (reference deleted).

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So Shapiro sees two different sources for random mutations: the breakdown of the normal replication process and specific cellular complexes. IMO, he does a disservice in other papers referring to the former as random and the latter as non-random, even though both are random according to the standard assays used to determine the randomness of mutations with respect to fitness.