Potential falsifications of the theory of evolution

If you can not deal with the human and chimp data then you can not explain any other species. The human genome is one of the most studied genomes out there, and the chimp genome has also been studied extensively. Both have been sequenced. We have an extensive hominid fossil record. The wealth of data makes the human/chimp relationship an ideal species pair to study, wouldn't you agree?

I will try not to go line by line, but rather an overall dissection.Firstly, a mutation is any change in the DNA sequence. This includes point mutations, deletions, and insertions. Movement of a mobile DNA element into another part of the genome IS a mutation. Moving a gene out of one genome and into another is mutation, as in the case of HGT. Shapiro does argue that point mutations alone can not produce the changes we see, and I agree with him. However, you can't change the DNA sequence of a genome and not call it a mutation.Secondly, DNA regulation and DNA sequence are separate (but intertwined) things. All life has gene regulation, at least that I am aware of. The example that most undergraduates are exposed to is the E. coli lac operon discussed here. By using this system E. coli are able to adjust the expression of their beta-galactosidase gene in with differences in concentration of both glucose and lactose, as well as the metabolic state of the E. coli. There is nothing "intelligent" about it. There is no independent decision making. Either the regulatory proteins bind to the promoter regions or they don't, dependent on the presence of lactose and cyclic-AMP. The DNA regulatory response is automated.Of course, this is in a relatively simple prokaryote, but the same holds true in eukaryotes. The only difference is the number of DNA bindings sites and the proteins that bind to them, the number of genes under regulation, and the number of stimuli that cause changes in gene regulation. The difference is an increase in numbers, not a difference in kind. Also, changing gene expression through time and space is the fundamental force that guides embryonic development.The punchline here is this. In order to get a different response to the same stimulus you need a different DNA sequence. It is the mutation of promoters and regulators that can drive the evolution of morphology in complex animals.Finally, mutations are random with respect to fitness, even in the examples given by Shapiro and in line with neo-Darwinian theory. Shapiro correctly argues that mutations are not random with respect to position in the genome or through time. The rate of mutation does change through time and there are mutation hotspots. However, this doesn't change the fact that the result of these mutations is beneficial, neutral, and detrimental. You still need selection of these mutations in order to drive evolution.One of the examples that Shapiro uses for "targeted mutagenesis" is the development of antibodies. This also offers a prime example of what I am talking about. Early in your life your immune system creates millions of B-cells, each of which produces a single antibody. Each antibody is the result of shuffling many domains into just a few. You can think of it as being dealt a five card hand from a deck of 52, and it is just as random as shuffling the deck and passing out cards. After this occurs the B-cell expresses the antibody on it's surface and then just sits there. If and when an antigen comes along and binds to one of these antibodies it activates the B-cell that has the antibody exposed. This activation causes the B-cell to proliferate and a high rate and pump out massive amounts of this antibody. At the same time, the B-cell targets the antibody genes for higher rates of mutation. B-cells with mutated antibodies that bind more strongly to the antigen are turned on even more, producing even more specific forms of the same antibody. Most importantly, the B-cell does not know which mutations will improve binding and which will not. The genes are randomly changed and then passed through selection.Even our immune system uses the mechanisms of random change followed by selection, one of the systems that Shapiro considers to be "intelligent". So what would happen if the B-cell used set responses to immunologic challenges? We would be toast. Our generation time is just too long compared to that of bacteria. If we only produced antibody A against E. coli, for instance, it would be a simple matter for E. coli to come up with the 1 in 10 trillion mutation that gets around that antibody due to the massive numbers of E. coli that can be produced in a short amount of time. We would go extinct without a random and dynamic immune system.Also, you seem to be hung up on the idea that gradualism is the be-all-end-all of the theory of evolution. It isn't. Even Darwin himself voiced doubt that gradualism was the only route. Only if ID theory posits that the cell is the source of the intelligence, and that this intelligence was produced by evolution.

So are these movements random with respect to fitness? Does every single movement of a DNA element result in higher fitness, or do these movements also result in neutral and detrimental mutations?

We all get to translate Shapiro's words. What we are complaining about is the the quality of the translation. If you translate something so that it means the opposite of what the author intended then it is a poor translation, wouldn't you agree? Shapiro doesn't like being quote mined. He doesn't like having his statements pulled out of context so that they mean something different than he intended. Or are you saying that Shapiro should be OK with Behe distorting his own words? All of the mechanisms that you and shadow have referenced are natural mechanisms. Increased transposon insertion as a response to environmental stress is a natural mechanism. It is fully within naturalism. What Shapiro is arguing for are additional natural mechanisms which produce the variation needed for the process of evolution.

Can you please explain how the lac repressor is an intelligent being? Can you explain how the actions of the Lac repressor are not natural? Since the evidence points towards evolutionary processes I think Shapiro is well grounded in his conclusions. Why don't you read his papers and tell us. You are the one claiming that his papers support ID, so surely you have those quotes handy. Then why would Behe cite Shapiro as supporting ID if Shapiro's opinion opposes ID? No, it requires research, something that the ID crowd avoids.

We do have evidence that Hox genes duplicated and diverged through evolutionary mechanisms.The problem I have with the constant reference to "Darwinian evolution" is that no one uses the theory put forward by Darwin. It has changed quite a bit in the last 150 years. Shapiro is beating a dead horse. What Shapiro is arguing against is the myopic view that point mutations are the primary driver of evolution. I agree with him. Let's use heliocentrism as an analogy. Let's say that Galileo, the father of heliocentrism, put forward the statement that the Earth moved about the Sun in a circular orbit. Through time we discovered that the Earth does not follow a circular orbit, it follows an elliptical orbit. Have we just falsified heliocentrism? Perhaps we have falsified Galilean heliocentrism, but have we falsified heliocentrism itself?Let's go even further. Galilean heliocentrism also incorporated gravity at some point and proferred the mechanism that the Sun pulled on the Earth which resulted in the observed orbit. Later on it was found that the gravitational pull of Jupiter also influenced Earth's orbit. Have we falsified heliocentrism once again because the original formulation did not include Jupiter's influence on the orbit of Earth?Now that we have falsified Galilean heliocentrism on two points can we now suggest that the Sun actually orbits the Earth? Can we now argue that it is invisible fairies pushing the planets around in the night sky?

The fact that Behe asserts that Shapiro's findings suggest Intelligent Design when Shapiro's findings suggest nothing of the like. A process whereby heritable variation is created that is independent of fitness, and then this variation is passed through selection. Again, you are confusing origin with action. The activity of these mechanisms is completely natural. No outside supernatural entities are required for DNA regulators to bind to DNA. The mutations that these processes produce are still random with respect to fitness, in line with neo-Darwinism.Also, Shapiro states quite clearly that we don't know NOW how these systems came to be. In classic ID fashion, this is mistranslated into "we can never know, therefore magical poofing". Obviously, you do given your next statement: How does "I don't know" equate to "God . . . err, the Intelligent Designer did it"? You are putting your own biases into Shapiro's statements. That is not what Shapiro is saying. What Shapiro is saying is that cells increase their random mutation and DNA recombination rates when they encounter environmental stress. These changes are still random with respect to fitness. The intelligence of these systems is within the systems, not from an ouside source. According to Shapiro, it is "lucky DNA recombination event, wait awhile, lucky DNA recombination event, wait awhile, and a million years later something has happened". Are you willing to accept that?

Because none of them involve a supernatural mechanism or outside intelligence. A new theory of evolution. So where did we go when Darwin's own suggestions on the mechanisms of heredity turned out to be false after the discovery of Mendelian genetics? We moved to a new theory of evolution, the Modern Synthesis. Where are we going with all of these new findings? Towards a new theory of evolution.You seem to think that the theory of evolution is set in concrete or something. It isn't. It is ever changing as it incorporates new information. However, nothing we have found thus far has put the major tenets in doubt, those being that mutations are random with respect to fitness and that these mutations are affected by natural selection to one degree or another. We observe lucky chaos that is then filtered through natural selection. When transposon activity is induced by environmental stress, as discussed by Shapiro, it is complete chaos within the genome. They insert all over the place. Some of these insertions are neutral, some are beneficial, and some are detrimental as with all mutations. Random with repsect to what? Unguided with respect to what?Does natural selection guide a population towards higher fitness? Yes. Is natural selection intelligent? No. Do gene regulators guide protein expression? Yes. Are gene regulators intelligent? No. Is gene regulation a smart way to do things from a backwards looking teleological position? Yes. Does this imply that an intelligence constructed the system? No.Can I say that the lottery is not random because the numbers are always between 1 and 50 instead of any number as a truly random process should be? Is the roll of the dice in Craps non-random because 7 is a more common result than 12? Both of these processes are random WITH RESPECT TO THE BET. Mutations are the same. They are random with respect to fitness. Mutations are not random with respect to time and genomic space, but they are random with respect to fitness. When you say that something is non-random you need to supply the context, otherwise it is meaningless. They got that purpose from the process of evolution, the same process that gives purpose to evolved antibiotic resistance in bacteria and evolved beta-galactosidase enzymes and nylonase enzymes. So how do you explain mutations that cause disease? Do parents purposefully give their children hemophilia by specifically and purposefully choosing the mutations that will give them hemophilia? Do parents purposefully create chromosomal rearrangements so that their children will have Turner or Down's Syndrome? Do cells purposefully become cancerous by changing their DNA arrangements and methylation patterns? Then please cite an example where DNA is mutated in a specific manner every time it is challenged with a specific challenge that always results in a beneficial change that is the inherited by the next generation. Shapiro doesn't cite a single example of this. You say you don't buy the argument and then you prove my point in the very next sentence. Nice job.

I interpret this as the theory of evolution needing to incorporate the idea that selection acts on the interaction of many genes, not a single gene in isolation. Also, mutations that change the interactions between these genes, be it in changing genomic position or a change in a gene regulator, plays a large role in selectable variation. When a gene is turned on and to what extenct is as important as the actual protein sequence of the gene itself. The problem I see with this interpretation is that you are taking specific types of selection and mutation that Shapiro talks about and apply it to all selection and all mutations. This is a big mistake, IMHO.Edited by Taq, : No reason given.Edited by Taq, : No reason given.

That's my take on it too. Sometimes he sounds like a high schooler who comes home with a proud look on his face while he tells everyone how light can be both a wave and a particle as if it was earth shattering news. I don't want to say that Shapiro's article is much ado about nothing because it is important, but it is hardly new. He never seems to get beyond his own descriptions of these systems to the more important questions within the theory of evolution. Of course, this is only a review article so generalizations are expected.For example, he makes a big deal of the tendency for transposons to insert up stream of genes and act as gene regulators. Well, that is great and all but what does this mean with respect to evolution and fitness? What if this results in the gene being turned on when it should be off, or overexpressed? What if this gene is involved in the cell cycle? What if the disregulation of this gene results in unrestrained replication along with a lack of cell contact inhibition? I believe they call that cancer.Shapiro is a good salesman, I will give him that.Edited by Taq, : No reason given.

It is tangential to the issue of the randomness of mutations. What Shapiro is talking about is the old paradigm of one-gene, one-feature. This is where variation is primarily driven by point mutations in genes, and each mutation is modular or singular in it's actions. Biology has left this paradigm in it's rear view mirror well before Shapiro published the article in question. Biology has switftly adopted the Evo-Devo view of evolution where gene regulation plays a very important role in evolution. With the DNA revolution it was finally possible to link embryonic development (Devo) with the evolution of DNA sequence (Evo), and with it came the understanding that gene regulation plays a very important role in overall fitness.To put this in plainer terms, Shapiro is beating a dead horse and trying to look fancy while he is doing it.

Random with respect to what? You need to be specific here.Is the lottery nonrandom because all of the results are always between 1 and 50 instead of any number? Is the lottery nonrandom because it always occurs on Wednesday and Friday nights?Edited by Taq, : No reason given.

Look who's talking. You have yet to define random as it applies to evolution and to these genetic systems. No one is saying that the genetic engineering systems are random. We are saying that the mutations produced by these systems are random with respect to fitness. That is, these systems produce mutations that are detrimental, beneficial, and neutral. You have shown zero evidence to the contrary. So mutations are nonrandom with respect to time. I agree. Epigenetics does not involve mutations, and epigenetics can not explain the differences seen between species. It is a non-sequitor.So I will ask again. Is the lottery non-random because it occurs at a set time every Wednesday and Saturday night (or whenever it is)?

I beg to differ. As part of the SOS response in E. coli they upregulate the expression of an error prone DNA polymerase that increases the random mutation rate.

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PLoS One. 2010 May 27;5(5):e10862.

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Competition of Escherichia coli DNA polymerases I, II and III with DNA Pol IV in stressed cells.
Hastings PJ, Hersh MN, Thornton PC, Fonville NC, Slack A, Frisch RL, Ray MP, Harris RS, Leal SM, Rosenberg SM.

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Department of Molecular and Human Genetics, Baylor College of Medicine, Houston, Texas, United States of America. hastings@bcm.edu

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Abstract
Escherichia coli has five DNA polymerases, one of which, the low-fidelity Pol IV or DinB, is required for stress-induced mutagenesis in the well-studied Lac frameshift-reversion assay. Although normally present at approximately 200 molecules per cell, Pol IV is recruited to acts of DNA double-strand-break repair, and causes mutagenesis, only when at least two cellular stress responses are activated: the SOS DNA-damage response, which upregulates DinB approximately 10-fold, and the RpoS-controlled general-stress response, which upregulates Pol IV about 2-fold. DNA Pol III was also implicated but its role in mutagenesis was unclear. We sought in vivo evidence on the presence and interactions of multiple DNA polymerases during stress-induced mutagenesis. Using multiply mutant strains, we provide evidence of competition of DNA Pols I, II and III with Pol IV, implying that they are all present at sites of stress-induced mutagenesis. Previous data indicate that Pol V is also present. We show that the interactions of Pols I, II and III with Pol IV result neither from, first, induction of the SOS response when particular DNA polymerases are removed, nor second, from proofreading of DNA Pol IV errors by the editing functions of Pol I or Pol III. Third, we provide evidence that Pol III itself does not assist with but rather inhibits Pol IV-dependent mutagenesis. The data support the remaining hypothesis that during the acts of DNA double-strand-break (DSB) repair, shown previously to underlie stress-induced mutagenesis in the Lac system, there is competition of DNA polymerases I, II and III with DNA Pol IV for action at the primer terminus. Up-regulation of Pol IV, and possibly other stress-response-controlled factor(s), tilt the competition in favor of error-prone Pol IV at the expense of more accurate polymerases, thus producing stress-induced mutations. This mutagenesis assay reveals the DNA polymerases operating in DSB repair during stress and also provides a sensitive indicator for DNA polymerase competition and choice in vivo.

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DNA Pol IV does not specifically target mutations in the lac promoter. It targets DNA breakage, and repairs it with more errors than other polymerases. So while the timing of the increase in mutations is nonrandom with respect to time the mutations produced by this genetic engineering system ARE random with respect to fitness.

I'm not the one with the problem, mate. No, but then evolution as a whole is not random or accidental. It includes natural selection. Evolution is more than just random (with respect to fitness) mutations. It is a two step, stochastic process that includes the non-random mechanism of natural selection.At the same time, we could also look at other natural phenomenon such as hurricanes that are well organized and intricate systems that arise through random interactions in the atmosphere.Also, you are now avoiding the question of whether or not the mutations produced by these genetic engineering systems are random with respect to fitness, the whole point of the recent conversation.Edited by Taq, : No reason given.