Potential falsifications of the theory of evolution

No one is claiming that they did. Why can't the intelligence within the cell come about through natural means such as evolution?

Because such systems offer a Hail Mary pass, to use an analogy. In stressful environments accumulating some slightly deleterious mutations in order to get the beneficial mutation to survive the stress is preferable to going extinct.

Precisely. This is why I keep asking for the context for the randomness of the system. Using the lottery example, the lottery is not random with respect to time since it occurs at the same time on the same days each week. The lottery is not random with respect to all numbers since the results fall within a set of numbers, not all numbers from 1 to infinity. However, the lottery is random with respect to the tickets sold. That is, the results are random with respect to the winner just like random mutations.And to carry on with the lottery example, during times of stress the cell responds by buying more tickets. This increases the number of losing tickets, but it also increases the chances of getting that lucky winner. Therefore, the rate at which the cell buys tickets is not random. It is environmentally guided. However, the tickets themselves are random with respect to the "winning number". The cell that hits that winning number is then selected for, the role that NS plays in this whole process.

Only if you left out natural selection, which you did in the previous post. We can at least observe the mechanisms that are being put forward for the evolution of these systems. This can not be said for intelligent design. I agree. The next step is designing a research program to find these answers. Evolution offers a way of designing experiments to figure these answers out. ID does not. With evolution we can use phylogenies to tease out the basal systems and look for modifications in different lineages. A similar thing has been done with homeobox genes by comparing homologs in simpler eukaryotes such as cniderians and sponges to homeobox genes in more complex animals like us. What they found is that duplication and subsequent divergence of homeobox genes allowed for more complex developmental pathways. What research has ID done along this same vein? None.

What do you think this means with respect to adaptation? Do you think this means that the cell is able to specifically mutate a specific gene, and that gene only, to overcome specific environmental stresses? You first need to ask what Shapiro means by "random".Also, it is the combined mechanisms of mutation and natural selection that add up to evolution. You might as well ask whether uplift of the Colorado plateau or water erosion were the primary means for creating the Grand Canyon. As it turns out, they are different mechanisms but both were required for producing the Grand Canyon. That's like asking if rain can come about other than by means of moisture falling out of the sky. Mutation is, by definition, genetic change. They are one in the same.Edited by Taq, : No reason given.

It only shifts the importance of where the random mutations occur, such as in gene regulators or in transcription factors. Natural selection is unaffected.

I will repeat this once again. Hopefully it sinks in this time.When you say that a system is random you ALWAYS need to describe the context within which the system is random (or nonrandom for that matter). You can't simply state that something is random without describing what the randomness relates to.For example, would you say that the Powerball lottery is random? When you say that it is random, what context are you referring to? Is the Powerball lottery non-random because the drawings occur on the same nights at the same time? Is the Powerball lottery non-random because the winning numbers are always between 1 and 50 and not other numbers? When you say that the Powerball lottery is random, what are you referring to?Mutations are the same. When Shapiro refers to non-random mutations are they non-random with respect to time, to genomic position, to fitness . . . what exactly are mutations non-random with repsect to? This is a very basic question that MUST be addressed.The Modern Synthesis states that mutations are random with respect to fitness. Let me restate that again. Mutations are random WITH REPSECT TO FITNESS. If Shapiro states that mutations are non-random with respect to TIME then he is not disagreeing with the Modern Synthesis. Then you should also know that definitions in science are very precise and require context. Randomness in mutations is no different. I don't doubt his qualifications. What I disagree with is the salesmanship that he is using. Then let's try to get an idea of what Shapiro means by non-random from his papers before asking. The answers are in the paper, but perhaps not as obvious to those who are not familiar with the science. When Shapiro says that mutations are non-random he is saying that mutations are non-random with respect to genomic features and time. He is not saying that mutations are non-random with respect to fitness.For example, transposon activity is related to the state of the cell so at specific times there will be higher or lower rates of transposon mutagenesis. Also, transposons tend to insert upstream of active genes, so transposon mutagenesis is not random with respect to genomic features. However, the process of transposon mutagenesis has no way of knowing which insertions will benefit the cell. Therefore, transposon mutagenesis is random with respect to fitness as the Modern Synthesis states.

I would change it to:"Do you have an opinion whether mutations are random with respect to fitness per the modern Darwinian theory?"As to random mutations being the primary means of evolution, it doesn't make any sense. It requires both random mutations and natural selection. One mechanism by itself is an incomplete process. You might as well ask which is more important for making bread: kneading the dough or baking the dough. Without either step you don't have bread. Go with this question. I would also like to hear Shapiro differentiate between human decision making and the decisions that cells make. However, I am sure Shapiro will try to sell his idea that they are the same even though there are striking differences.

That is exactly what DNA fingerprinting is based on, the probability that another person other than the defendant will have the same STR pattern as those found in the evidence samples. DNA fingerprinting uses a panel of short tandem repeats (STR's), each of which has several alleles in the general population. For example, a single STR may have 4 alleles spread ubiquitously throughout the population. Therefore, the chances of the crime scene sample matching the defenedant is 1 in 4. By using several of these STR's you get the multiplicative of these probabilities until you get a number that is 1 in several billion. The casinos in Vegas would disagree. Their profits depend on their mathematical models of randomness. Not random with respect to what? Is the lottery not random because the drawings take place at the same time every Wednesday and Saturday? The problem is that you don't understand what Shapiro is talking about. The upregulation of DNA polymerase IV during an SOS response in E. coli is not random. However, the mutations that DNA polymerase IV produces are random with respect to fitness. You need to understand what "random" is referring to.ABE: The lac reversion via the SOS response is actually a good model for explaining randomness with respect to fitness. The earliest studies found that lac+ clones appeared at a higher rate than would be expected from known rates of random mutation. Some of the earliest hypotheses suggested that the E. coli were sensing the lactose in the environment and then producing specific mutations that would result in lactose metabolism. However, further studies demonstrated that this was not the case. The presence of lactose does not increase or decrease the rate at which the lac+ mutations occur. It has nothing to do with the process other than selecting for lac+ clones. The processes which produced these lac+ clones are completely blind to the presence of lactose. Instead, the rate of random mutation and recombination is elevated due to the bacteria sensing DNA damage.The mechanisms that Shapiro refers to are the same. They can not sense the specific needs of the cell. They do not mutate specific genes at specific bases to result in a specific function. Instead, the cell increases the random mutation rate.Edited by Taq, : No reason given.

That is what the research says that he cites. Then mutations are random with respect to fitness. The fact remains that the mutations produced by these systems are random with respect to fitness. The fact that morphological change is due to different mutations in different genes does not change this fact.You also claim that it is not a matter of the cell increasing it's mutation rate, and yet I cited a paper that demonstrated exactly that. Mechanisms cited by Shapiro, such as trasposon mutagenesis, have likewise been demonstrated to be random with respect to fitness.To go back to the lottery example, no one is claiming that the machine which mixes and selects the ping pong balls is the product of randomness. It didn't form by a tornado tearing throuhg a junkyard. However, the results that the machine produces are random with respect to the tickets. I stated that the chances of finding the beneficial mutation needed to overcome the overwhelming environmental stress would be higher, but it comes at a cost. The cost is the accumulation of more slightly deleterious mutations. However, a higher background of deleterious mutations is preferrable to outright extinction, wouldn't you agree? Obviously, it does work as the paper on the SOS response in E. coli demonstrates. If your life depended on getting the winning lottery ticket would you buy one or buy as many as you could, not caring how many of those tickets are losers or how much debt you would rack up? If the alternative is that everyone dies from the disease anyway, why not give it a try? Please cite examples with reference to mutations. You seem to be switching between cellular function and the process of mutation at will with no reason. Show us an example where a specific environmental stimulus evokes a specific mutation, and only that mutation, each and every time. Anything short of this is an ineffecient system, is it not? And this adjustement and adaptation occurs through random mutation followed by selection. For example, Shapiro writes:

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The adaptive benefits of this regulatory capacity are clearest in the cases of DNA changesintegrated into the regular life cycles of organisms (our immune system is an example), but biological utility is also evident in the ability to stimulate variability under conditions where proliferation or survival are threatened.
Letting Escherichia coli Teach Me About Genome Engineering | Genetics | Oxford Academic

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He is talking about the stimulation of variation, not the stimulation of specific adaptations to a given stimulus. Another key quote from the same paper:

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These systems have the capacity to reduce the size of
the genomic search space dramatically and to maximize
the chances for success by using a combinatorial process
based on existing functional components.

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So what does it mean to reduce the search space? He means favoring one type of random mutation over another. In this case, the propensity for the cell to shuffle exons and transcription units. However, these changes are still random with respect to fitness. What Shapiro is saying is that the genetic engineering systems produce mutations which have the best chance of producing a novel function, but obviously chance is still an integral part of the process.

It would be much more appropriate to point to a peer reviewed research paper, preferrably a primary source and not a review article. If you think mutations are non-random then find papers that specifically demonstrate this non-random nature complete with the actual data from experiments. This is exactly what I did to demonstrate that the genetic engineering systems in E. coli produce a higher rate of random mutations through upregulation of DNA polymerase IV, if you need an example.

Non-random with respect to what? I don't know how many times I have had to ask this.Is the lottery non-random because it happens at the same time every Wednesday and Saturday?

Interesting quote from that paper:

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The effects of the TE's [transposable elements] within their host genome can be viewed as essentially neutral, although their proven capacity for causing deleterious genomic rearrangements and the emergence of mechanisms for their silencing in somatic tissues has led many to view them as harmful parasites (several cited papers).

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So it appears that TE's have beneficial, neutral, and detrimental effects . . . almost as if they are random with respect to fitness, hmmmm.

Shapiro is still ducking the main issue, as exemplified in this question: He weazeled out of the question like I suspected he would. What he is saying is that by targeting the upstream regions of genes that the mutations have a better potential for causing beneficial change. At the same time, they also have a higher chance of causing deleterious change, but he doesn't mention that. To use an analogy, retroviruses are like missles that seek out body heat. This gives them a better chance of hitting the enemy, but it also gives them a higher chance of hitting your own troops. The missile itself (analogous to the non-random genetic engineering systems) does not know if it is hitting an enemy or friendly, all it knows is that it is hitting a person.However, he is much clearer in this answer: He does separate non-random from deterministic which is the big clue here. He also states that these non-random processes produce large amounts of variability which again points to the fact that they are random with respect to fitness.As to natural selection . . . Completely agree here. Mutations are the creative process, selection is the purifying process. Together they result in populations adapting to their environment. He considers increasing the random mutation rate in times of stress to be a sentient reaction. Interesting, but I personally wouldn't call it sentient.

Something also struck me as interesting. Shapiro likes to draw analogies between these genetic engineering systems and what molecular biologists do in the lab. He suggests that cells use some of the same techniques that we do when restructuring their genome.As it turns out, molecular biologists do use transposons to create mutant strains. They usually call it random transposon mutagenesis. The whole point of a transposon mutagenesis is to create a library of cells with genes that are randomly knocked out. The choice of transposons is often based on the random nature of their insertion with respect to which genes are being knocked out. If transposons only inserted into specific genes in response to specific stimuli they would be useless in the lab for the purposes of library construction.I have constructed my own transposon libraries. After testing 1700 individual clones for specific enzyme production I finally found the knockout, and that was after dual screening for drug resistance to make sure the transposon was even inserted into the genome. I would have been uberpissed if that transposon was overly biased so that it never inserted into the gene of interest. I was pissed enough that it took 1700 clones to find the one I was looking for.