In this case, perhaps no net increase in fitness would result from the faster alleles. So natural selection may not produce perfection, but you'd at least expect it to get rid of obviously deleterious genes, wouldn't you? Maybe not Here are a few reasons why natural selection might not produce perfection or faster cheetahs: Lack of necessary genetic variation Selection can only operate on the available genetic variation.
Search Glossary Home. Support this project. Selection, not perfection. The "bad" gene. This mechanism is proposed to allow faster genetic adaptation to stressful conditions and to explain why mutations appear directed to useful sites. Analysis of the HSM reveals that it requires implausibly intense mutagenesis 10 5 times the unselected rate and even then cannot account for the behavior of the Cairns system. The assumptions of the HSM predict that selected revertants will carry an average of eight deleterious null mutations and thus seem unlikely to be successful in long-term evolution.
We conclude that temporary general mutagenesis during stress is unlikely to provide a long-term selective advantage in this or any similar genetic system. If I understand well, whether this model is good or bad, it is based on the general idea that some biological beings especially bacteria, I believe have adaptive mechanisms that can help the search for some new functional information always, however, of the microevolutionary type.
I am convinced, for example, that the whole plasmidic system in bacteria is strongly adaptive. And we have a special example of that kind of adaptation in humans, which works on somatic immune cells and not on germ cells: the antibody maturation process, which I have discussed in detail here:.
The problem is that adaptive systems require a lot of complex functional information: they are indeed examples of objects with a huge amount of specific complex functional information. The advantage they can get in a random search is traceable to their functional information, which makes the random serach less random. We are, here, exactly in the context of the principle of conservation of information, many times discussed by Dembski and Marks. You get what you inputted first, in a different form. First you have to find this alleged evolutionary theory.
Then you have to read it to see what it actually says. Work in progress… stay tuned. There is no doubt about it. And if you consider that, to me, it already looked like designed systems, say 10 years ago, and irrefutably so, you can imagine how great is my conviction now! Both negative and positive selection results in the removal of certain organisms from the population. Those removed organisms contained unique information that is lost forever. What a horrible thought! Which brings me to a more general claim: natural selection positive or negative leads to loss of information and is therefore detrimental to evolution.
I would say that this results in a defense of the existing information certainly not in the generation of new information. Of course, the cost of it is the loss of any new information in the individuals that are eliminated. Therefore, it is definitely against evolution by random variation, because any random variation that is a first step toward something new, but reduces the existing function, will be selected against. Moreover, the individual being selected against could have been hosting other potentailly beneficial variations, and those too will be lost.
This is probably a very minor effect, but it is real. But, on the other hand, the elimination of the old population with the old trait is certainly a loss of information, in at least two important senses:. That can be the case in some forms of antibiotic resistance, for example. So, the originaol trait could be the more functional in a standard environment, and if it is completely erased by positive selection uder extreme pressure, that useful information will be definitively lost.
Is two or more beneficial trait have to expand at the same time in a population, from different parts of it, there will be competition: the expansion of one trait may mean the loss of the others. So, you are completely right about negative selection. You are partly right, IMO, about positive selection, because we have to ackowledge that, in some cases, for example in some microevolutionary contexts, the expansion and fixation of a new beneficail trait is a gain of functional information.
The problem is that positive selection is really rare, especially at molecular level, while negative selection is all pervasive. And beneficial mutations are extremely rare, while negative or neutral mutations are all pervasive. But, in the end, the strongest argument against the power of positive NS remains, IMO, the one that I have tried to emphasize throughout this thread:. For NS to have a chance with complex information, such a ladder of simple gradual selectable variations should exist for each example of complex functional information, IOWs for each existing protein.
As far as we know, it exists for none. And there is no reason at all for such a ladder to exist. It does not exist for language, it does not exist for software, it does not exist for proteins. It does not exist for any functional unit where the function depends critically on the final configuration of many bits and is not present unless that functional configuration has been completely implemented. This is, IMO, the true and final argument against the power of NS to build up complex functional information.
One trait was negatively selected and another positively selected under strong selective pressures, but then in some cases things went back to square one under the opposite conditions and so on? How did some of those changes turn cyclical? Origenes: natural selection positive or negative leads to loss of information and is therefore detrimental to evolution. So, not only am I completely right about negative selection, but negative selection is by far the prevalent form of natural selection.
Do you hear that my evolutionist friends? So, positive selection, on its own, not considering other factors such as drift, reduces information. This, on its own, is bad for evolution because it reduces the search capability of evolution. The lesser of two evils, between a rock and a hard place or between Scylla and Charybdis. No, I was thinking more of the classic cases of microevolution, like simple antibiotic resistance, or the relative expansion of drepanocytosis and thalassemia alleles in malaria zones.
Maybe the emergence of nylonase from beta-lactames could figure too, even if I think that was a microevolutionary event in the context of the adaptive plasmidic system in bacteria. Regarding Galapagos finches, I never discuss phenotypic shifts whose molecular cause is not known. And I am not sure that the molecular cause of those shifts in finches is known. Frankly, I have never been interested in that topic, which often seems to be mere propaganda. First, we must know as well as possible what happens at the molecular level, then we can discuss phenotypes.
I have attempted to formulate your argument against NS in premises and a conclusion. Let me know what you think. In all statements. Anything can be functional, because for practically anything we can define some function. And one of the fundamental aspects of my approach to funcrional complexity is that we are free to define any possible function for an object, and to measure the complexity linked to thet function.
The details of my definition of functional information and functional complexity can be found in this OP:.
Artificial intelligent selection can select any possible function. NS has very limited power, as discussed in this whole thread. Definitely, it cannot generate new complex functional information, of any kind. AS is much more powerful, because it benefits of the information inputted in the selection itself. IOWs, the rewarding takes place through a symbolic recognition. The rewarding itself, therefore, is not intrinsic in the system, but requires addition specific information implemented in advance.
That said, we can understand why AS is much more powerful than NS. AS, if well implemented, can find its function thorugh RV with some ease. Even apparently complex functional information can be found in that way, because the complex functional information is the result of the complex functional information already implemented in the system. For example, the famous and infamous paper by Szostak about finding an ATP binding protein in a pool of random sequences is, obviously, a paper about successful AS discuised as a paper about NS, as I have argued many times, almost always arising angry reactions from someone.
Which clearly demonstrates that, if we already know a phrase, we can extract it by gradual RV, using the phrase as an oracle for our AS. Brilliant, indeed! Darwinists have always tried to disguise artificial selection as natural selection, and they will go on doing so, because they have no arguments in favor of NS as an explanation for complex functional information, and they desperately need to invent something! After the arguments in my post 40, I think I have made clear that we should not be interested in a model of evolution, but rather in a model of some specific explanation of how evolution generates complex functional information.
Which is exactly what the authors have tried to effect. A lab experiment is always a simulation. It is not direct observation of what happens in the wild. Therefore, it can never be complete. That is correct. But we should understand better what was implemented by the authors, and what was simply observed in the system. Here is a brief description of the method:. Accordingly, it is possible to mutagenize an entire gene or merely a segment of a gene.
So, this is a good point in the simulation, because the authors use an artificial method which can be considered an acceptable simulation of single mutations that occur in nature as the result of errors in DNA duplication. That is good methodology. That, again, was done by the authors.
So, in a sense, this is Artificial selection, not Natural Selection. But here the methodology is correct.
Limits to natural selection. Nick Barton1* and Linda Partridge2. Summary. We review the various factors that limit adaptation by natural selection. Recent. There are many reasons why natural selection may not produce a "perfectly- engineered" trait. For example, you might imagine that cheetahs could catch more.
The authors chose to select for infectivity, which in phages is essetnially the same thing as reproductive power. So, this type of srtificial selection for the same property that would allow natural selection in the wild is appropriate, and it can be considered an acceptable simulation for NS. These are not elements simulated by the authors, but rather the natural response of the experimental set to the simulation.
And antibiotic resistance is a perfectly natural example of neo-darwinian mechanism, often invoked as one of the very few examples of the powers of NS. So, if such a fixed landscape is good for malaria resistance reasonings, and even for Larry Moran, I would say it can be good for us too. Genetic drift occurred naturally in the system, and was not simulated at all. So, we go back to the first point: they only used single mutations, or at least the kind of mutations that can arise in error-prone PCR.
Why that? The simple truth is that sucvh a kind of artificial random mutations is probably the best we can do to simulate RV in the lab. All depends on what you believe about the relevance of different types of variation as explanations of the generation of new complex functional information. As I have tried to argue, in regard to the generation of new complex functional information, all kinds of ravdom variation events are essentially the same: tghey just test one single state in the search space. However, if you really believe that the specific type of random variation event can change significantly the results, you should try to find somne support for that idea in the experimental literature.
I would be happy to consider any examples of that. In the meantime, I would like to briefly compare our paper to another famous paper, the one by Szostak about a functional ATP binding protein from a pool of random sequences. The main reason, of course, is that it uses AS as a simulation of NS. But it is not AS for an equivalent of what would ne naturally selected, like in the rugged landscape paper where infectivity is selected. It is important to observe that the orinal sequence in the original random pool presented only very weak ATP binding, and certainly was not naturally selectable.
But, even more strikingly, the final protein with strong ATP binding still was not naturally selectable at all. No other source of variation is tested. So, a paper which not only is inappropriate in its chosen methodology, using a completely wrong simulation of NS, but also shares the obvious limits which are probably shared by any current lab experiment about NS. So, what was the result of that in the academic response? Was the paper criticized for its inappropriate methodology? Were the limits in the basic experimental settings clearly outlined by scientists?
Beware, this discourse is not intended for you, of course. I have full certainty of your good faith and honesty. But my point is that you seem to share the general bias, of course unintentionally. However, we have tested only one form of random variation, single nucleotide subdtitutions.
It is possible that other kinds of variation, like recombination or others, could change the results. The role of recombination has been indeed suggested. Unfortunately, we can draw no conclusions about that, because we did not include recombination, or other types of variation, in our simulation. Further research is certainly needed to assess that important point. The result is that when I cite correctly the conclusions derived from their data, that single substitutions and natural selection cannot find the wildtype, darwinists immediately say:.
What would still be true? Who says that? What facts support that statement? Is this some dogma, or what? However, when I find a good paper which presents good data and reasonable intepretations, I give it serious consideration. Have they or anyone else done any testing to see how well the theoretical model they use corresponds to reality. But I think that darwinists should be very eager to falsify those results, if they really understand what they mean.
The paper is an important one. The paper was published in Finally, you present some detailed criticism about the model itself. We should be able to read and understand well, at least, the:. Regarding your objection to the fit shown in Fig. So would I. The curve was probably computed on the raw data. And it does not seem a bad fit, looking at the figure, at least IMO. However, my little understanding of the model itself, and the lack of more details about the raw data, prevent me from being able to judge the statistical aspect about which I would probably be more competent.
So, I can only say again: I accept the model as it is, with the caution that we always must have about any scientific model, and I have no specific reason to think that it is wrong or grossly imprecise. However, your insistence in doubting those results is IMO some evidence that you have really understood their meaning. Well, the authors did. Also, you want a discussion about negative selection acting in favor of, or neutral toward, evolution?
Negative selection removes deleterious mutations. This means that at the very least, it will maintain the current fitness state of a population, and therefore be neutral. So, at the very least, negative selection is neutral. By culling deleterious mutations, negative selection constantly holds a population in a state that is primed for further adaptation…. You hem and haw about forests and trees, but you are apparently still missing the point. In the end both processes contribute to the improvement of fitness for a species. You are obsessed with staring at amino acid sequences, but are missing the bigger picture.
However, in biology there is almost always wiggle room. As I said, those examples were not about function. They were pointing out huge changes that can occur in an organism with little to no change in nucleotide sequence. And once again, your attempt to just sweep these under the rug do not look good on your part. Your use of the word new here I assume means you are asking for a sequence that is unlike other before it.
As I said, the original evolution of a protein and and the evolution of one protein from another are two completely different processes. They are entirely different. It does this through a transfer of energy, also just like any other enzyme. I should probably stay out of this — gpuccio and ET can defend themselves, and this thread is really better as a discussion between gpuccio and Gordon…. In simple English, this quite literally is working against evolution. Thank you for the help. It is really appreciated. Really interesting stuff.
Nothing is taken for granted throughout the work, and the only valid mode of escaping from its conclusions is, by either disproving the fundamental Propositions, or by detecting fallacies in the subsequent reasoning. First, bringing two molecules near each other and in the right orientation to catalyze a reaction is not specific to ATP synthase. Heterozygosity estimates used to calculate effective mutation rates were corrected for ascertainment bias see SI Text and excluded genes that were captured by 4 or more independent mutations, a signal of hotspots and mutation rate heterogeneity. If you get anything out of this, ET, please let it be the fact that how a protein originally evolved and how proteins have evolved from other proteins are two very different questions. I agree with you that having some detailed model of what happened in evolutionary history is an ongoing task, and that there are a lot of different approaches to that, and different models, including, I would say, different design models which, although ognored by the official academy, are part of the scientific thought just the same. How do morphogens create concentration gradients to establish positional information in developing tissues?
I have been busy with my commitments but I did notice that you addressed my question. Thank you very much. I will give this OP and the thread underneath a good read as soon as I can. Many Thanks! Are you familiar with neutral theory? It is claimed that this theory has become central to the study of evolution at the molecular level. This theory is based on the notion that selection works against evolution. There are many quotes to be found, see for instance here :. First of all, thank you for commenting. It seems that this time you try to make some arguments. So I will happily answer you.
You are really wrong and unfair here. I have read alla that you have said with hreat attention, and answered point by point, in detail. I appreciate that you seem to have accepted that negative selection and positive selection are two different processes, even if we agree that they share the eliminative character. Negative selection is a process. Regarding evolution, the question here is if it acts in favor or against evolution, or if it is not involved in it.
Are you saying that negative selection is not involved in evolution? Where is your logic? You are completely and blatantly ignoring the reason why negative selection acts against evolution. You are reaching conclusions without even starting a debate about the issue! Nobody denies that negative selection imperfectly helps preserve the already existing functional information. I have said that many times, and very explicitly. If you want to argue that such a preservation is the premise for further evolution, I agree.
But that does not mean that negative selection has any active role in promoting evolution, IOWs in the generation of new functional information. If it were for negative selection, information would at most remain the same as it already is. Absolutely not. As already said, the simple argument for the role against evolution played by negative selection is that it acts by opposing change, if change is deleterious to the existing function.
That implies acting against evolution, because evolution need change, and in many cases that change will ne deleterious for the existing function. Now, both A and B, individually, are slightly deleterious mutations which is a very common case , but their mutual interactions makes them beneficial. It can happen. But if the deleterious effect of each individual mutation is strong enough to trigger negative selection, then the probability of having both mutations in a certain evolutionary time in the same individual becomes essentially zero, because whatever the first mutation is that takes place A or B , it will be eliminated by negative selection.
Whatever you say. Professor PZ Meyers deserves a special mention:. The bottom line is that you cannot easily explain most increases in complexity with adaptationist rationales. You have to consider chance as far more important, and far more likely to produced elaborations. Again, this sounds only like a political slogan and nothing else.
Certainly not like an argument. You are certainly free from the devil, I would say: no details at all in what you say. Just political slogans and propaganda. It is absolutely true that prokaryotes are by far the most successful kind of living beings, in regard to fitness and reproduction! As PZ says, no need for eukaryotes, least of all for metazoa. These fans of chance should really do some math about probability, a task they seem to abhor, instead of simply relying on the goold old NS in case of difficulties!
In many cases, a single mutation can completely erase the function of a protein. It depends on what is the aminoacid that changes, IOWs the functional information in that aminoacid site. And I am not sweeping anything under a rug. I am only saying that new complex functional information cannot be generated with small changes in information. We should learn biology in order to understand what the Neo-Darwinian folks are trying so hard to tell us. Also you seem to be obsessed with sudden appearance of large amounts of functional information in protein families.
You may want to consult with a specialist that could treat your obsession problem before it gets out of control. Or better yet, try to understand evolution and thus all your obsession issues will disappear magically.
The exact molecular mechanisms that determine the correct number of ribs, or the correct size or form of parts of the body, are still poosrly understood. Maybe some of them are relatively simple at the molecular level, but I doubt it. But, again, I do discuss molecular examples of comple functional information where the functional complexity is understood and can be measured. Like ATP synthase beta chain, just to go back to one classic example.
As I fully understand the breadth of what destructive random variation, even simple, can entail, I wanted to clarify that, instead, constructive functional random variation, when simple, entails almost nothing. If you agree that simple random variation cannot entail any relevant complex result from the point of view of functional information, then we seem to agree.
I will continue not to be amazed at the power of destructive random variation: whoever has destroyed a house of cards with a very slight movement knows that concept all too well. On the other hand, whoever has built a house of cards with a single, slight movement, is certainly a remarkable individual! I would not like to confuse your perspective, but the simple reason is that it is not clear what you mean. Now, we have about protein superfamilies in the SCOP database , which are completely unrelated at the levels of sequence, structure and function.
Lots of functional information here! Now, what is your model for the origin of that sequence? How was that highly specific sequence found? If that is the case, please read what I said in my post 5, to EugeneS. I paste here the relevant part for your convenience:. Of course, we have the protein superfamilies, already cited, which are a very good example of groups of proteins which are completely unrelated at sequence level, and also at structure level and function level.
Most of that new information appears in proteins that alredy existed in pre-vertebrates, abd which alredy exhibited some sequence homology with the human form of the proteins. But the fact is, a lot of new human conserved information is added in the transition to vertebrates. No other enzyme works by force of pressure. If you think I am wrong then go ahead, show me. The only reason it happens is because it is squeezed on- pressure does it. So you lose regardless of any semantic mistake you think I have made.
Without ATP any proto-organism would have to be tethered to an energy source until a mechanism to make ATP could just happen. But that begs the question- how did blind and mindless processes figure out that ATP would be the best currency for life? The exact molecular mechanisms that determine the correct number of ribs, or the correct size or form of parts of the body, are still poorly understood.
The problem is that, with neutral variation, the probabilities of getting function are exactly the probabilities of a random walk, because it is a random walk and nothing else. Genetic drift, as I have said many times, does not change anything, because it is random: any mutation has the same probabilities as any other to be fixed. So, a purely neutralist intepretation is exactly the same as saying that, say, ATPsynthase beta chain came into existence by simple change. IOWs pure magic,. GPuccio: The problem [with neutral theory] is that, with neutral variation, the probabilities of getting function are exactly the probabilities of a random walk, because it is a random walk and nothing else.
Indeed, but to be fair, this is an improvement on the probabilities faced by adaptionist neo-darwinism. That is, in as far as neutral theory is able to steer away from natural selection. As we both agree, with Larry Moran, natural selection generally acts as a break on evolution as a blind search. So, again, it seems that neutral theory attempts to improve on that. However, an unassisted search, a random walk, is a modest improvement:. The operative phrase is, of course, given enough time. Let us limit the task facing our monkey somewhat. How long will he take to write this one little sentence?
The scenario is staged to produce a string of gibberish letters, assuming that the selection of each letter in a sequence of 28 characters will be random. Unassisted search will not work for even moderately sized problems [1, 2]. Monkeys at a typewriter eventually generating the complete works of Shakespeare is simply impossible. Simple combinatorics show the universe as modeled by science today is not sufficiently old nor big enough to support the search for even a hand full of pages [3, 4].
Gpuccio 92 and rest of discussion by all above. Enjoying this post. Thanks for your contributions again here at UD. Question, does Neutral Theory solve the problems Darwinist must overcome for a blind, unguided process of random mutations and Natural Selection? Neutral Theory by Kimura was an attempt to address real world problems that Haldane appropriately identified at the time.
An attempt to get around the cost of substitution and reproductive rates for mammals. For example between chimps and humans. There was not enough time and generations for enough variation and positive selection to take place. I guess it was a valiant attempt to solve a real world problem of time theoretically. But did it? Origenes is right. Dembski is right. To rely only on random walks to explain proteins, or any other form of complex functional information in biology, is utter folly!
Highlighting in block quote see 2 …. F-class Pump: functions to power the synthesis of ATP from ADP and Pi by movement of protons from the exoplasmic to the cytosolic face of the membrane down the proton electrochemical gradient. Rotation of protein shaft couples proton flux. Alpha and beta subunits arranged alternatively around a hydrophobic shaft that is formed by the Y subunit. As the shaft rotates, e- are accepted and this acceptance allows the conformational change for the shaft to rotate.
Beta unit accepts ADP and Pi and rotates into loose state. Turns again to open state and releases ATP. ATP is released every 3rd turn. This is critical because, without oxygen, they will accumulate and the concentration gradient needed to run the ATP pumps will not allow the pumps to work. They both go through an antiporter to do so. Update link: ADP and Pi squeezing. More than bits of functional information which can be dated almost at the beginning of biological history, and have remained the same through billions of years!
I would argue that holding a population in a state of relatively high fitness is essential to evolution and primes the population for further evolution. Now, what does this plot look like? I think it resembles a bell curve, do you? What will happen if we plot the next generation? The curve will probably be ever so slightly shifted to the right, right? Now, do you think there is a steep drop-off on the left side of the curve where a certain low-level fitness is culled from the generation?
Or do you think there is a gentle slope and then eventually a short drop? Now the question becomes this: How prevalent are slightly deleterious mutations versus mutations that immediately trigger negative selection. You seem to think that mutations immediately triggering negative selection is the rule, while slighlty deleterious is the exception.
That is not the case. What if I told you that publications were extremely biased toward these types of mutations? The slighlty deleterious mutations are much more difficult to study and much more difficult to draw conclusions from, at least conclusions that are significant according to the almighty p-value.
This is unfortunate, but it is the current state of research in biology. The fact that you can take a population of millions of cells, mutate each one at a different place, and still get the majority of them to grow and divide happily is a testament to the amount of change that is tolerated by biology.
ET, this will probably be the last time I respond to you. Your post 99 is essentially meaningless. I think it deserves at most a couple of very simple corrections:. Indeed, it makes it more difficult. I cannot be more clear than that, then you can say whatever you like. In population genetics, a selection coefficient, usually denoted by the letter s, is a measure of differences in fitness. Selection coefficients are central to the quantitative description of evolution, since fitness differences determine the change in genotype frequencies attributable to selection.
The following definition of s is commonly used. For example, the lactose-tolerant allele spread from very low frequencies to high frequencies in less than years since farming with an estimated selection coefficient of 0. Though this selection coefficient might seem like a very small number, over evolutionary time, the favored alleles accumulate in the population and become more and more common, potentially reaching fixation.
So, as you can see, it is not at all necessary that a deleterious mutation be incompatible with life to trigger negative selection. IOWs, it is enouth that the selection coefficient is negative, slightly negative but not insignificantly negative for negative selection to act.
Of course I can have both! You make it up. My statement, quoted by you, was:. We are discussing evolutionary times here. If a mutation is so deleterious that it is incompatible with life, then the individual will just not survive. The probability of the trait to survive in its mutated form will be lower than for a neutral mutation. I think that many mutations, probably most mutations, are neutral or quasi-neutral IOWs minimally deleterious, but not enough so that they behave differently from neutral mutations.
I think that many mutations, probably a big minority, are slightly deleterious: enough so that negative selection acts probabilsitcally against them. I think that a few mutations are strongly deleterious, up to being incompatible with life. Those are strongly selected against by negative selection. Maybe not immediately, but in shorter times.
The few that are, are really an exception. However, those few exception can be positively selected, especially in contexts where a veri strong environmental pressure against the previous trait is present, like the antibiotic resistance scenario. They can never generate complex functional information. Corey- Much more has been learned about ATP synthase since But go ahead in live in the past. Heck with mutations and natural selection, negative selection and positive selection.
Hence yours has to be given starting populations of prokaryotes that already have many irreducibly complex systems up and running. So in , scientists were already suggesting the existence of other proteins also using this mechanism. Nor would they have a mechanism capable of creating it if they did find them.
Or do you know that actually thinking about evolution in a sensible way reveals all the faults in your logic and your misunderstandings about biology? Now maybe you realize the fault in your mutations argument: Allowing these slightly deleterious mutations to hang around for any time at all since we are talking evolutionary timescales , it is long enough to account for the low probability of both mutations occurring in the same individual. Just for your convenience, I will now say what I think. You are the poster child for confirmation bias. You make claims about what evolution is incapable of and point to a protein that was fixed in all organisms billions of years ago as support for your argument.
ET, you are absolutely impervious to new information, just like Gpuccio here. Although, Gpuccio is at least smart enough to make the conscious decision to do so. I am very satisfied of the discussion here, because I believe that a lot of relevant aspects have been touched. Gordon Davisson has offered many good arguments, and I have addressed them from my point of view.
I realize that, in the course of the discussion, I have repeatedly tried to focus on one point, which is IMO the strongest, most important argument against the role that NS is supposed to have in the neo-darwinian scenario: the simple fact that complex functions cannot be deconstructed into simple naturally selectable steps.
So, at the cost of being repetitive, I would like to state again that single point here, and to follow it with a challenge. First, I will paste here the summary of the argument that I have already posted at the end of I quote it here entirely, keeping the original emphasis:. Now, just to give another flavour of the argument, I will paste here the brilliant summary that Origenes has made of it at his post 63 I hope he does not mind! Here it is:. That such a ladder exists, in general, or even in specific cases? All those on our side of course, who probably know all too well how to answer, are invited to offer contributions, if they like.
Anyone who could present a case that meets your challenge should be nominated for the Nobel Prize in biology. Too vague to be of any use. You have yet to provide any.
On the other hand I have supported my claim. And I also understand why you would focus on the minutiae of how the binding occurs as you sure as heck cannot account for ATP synthase. Moreover, the evolution of the eye is a rather trendy subject, I would say. Why not try something more original, say the evolution of the ear? I am specially interested in a model for the cochlea and the semicircular canals.
From this we see that if both mutations are almost neutral i. This is consistent with the results for the even-skipped stripe 2 enhancer mentioned earlier. Well, less than 1 million years, in Drosophila, for two mutations that can change the affinitiy of a transcription factor binding site of 10 nucleotides! Our previous work has shown that, in humans, a new transcription factor binding site can be created by a single mutation in an average of 60, years, but, as our new results show, a coordinated pair of mutations that first inactivates a binding site and then creates a new one is very unlikely to occur on a reasonable timescale.
How do I put this politely? Either Corey has a weird sense of humor or he suffers from a massive comprehension blockage. The quotes provided in 74, 75 and 78 are crystal clear. I will not comment on the meaning of the metaphor itself, which frankly eludes me, but rather on its implementation. So, unless in the meantime planes and cars have started to arise from neo-darwinian evolution and I have not realized it, it seems that Corey is using designed objects in a metaphor, however obscure, about neo-darwinian evolution.
Why do neo-darwinists so often resort to designed objects when they want to make examples or metaphors about how neo-darwinian evolution works? OK, this is not another challenge. I am already busy enough commenting on the many answers to the first one! Well, in my case I did deserve to be punished by the distinguished biochemistry professor from the university of Toronto, because I did not ask honest questions.
The only show in town. But that was the hard part, getting from there to an ear is the easy part. You are too easy on me! They are loud in vague philosophical discussions that lead nowhere, but they try hard to stay away from serious scientific discussions, specially with gpuccio, who usually gets very technical, though the Italian doctor tries hard to make it easier for the nonscientific folks to understand as much as possible. We have seen it here. The few who dare to engage in discussions end up running for the doors. Careful please. In addition to simple diffusion, a number of other transport mechanisms have been proposed and are actively being investigated, including shuttling via other proteins, transport via vesicles e.
According to morphogen gradient theory, extracellular ligands produced from a localized source convey positional information to receiving cells by signaling in a concentration-dependent manner. How do morphogens create concentration gradients to establish positional information in developing tissues? Surprisingly, the answer to this central question remains largely unknown. During development, a relatively small number of morphogens are reiteratively deployed to ensure normal embryogenesis and organogenesis. Thus, the intracellular processing and extracellular transport of morphogens are tightly regulated in a tissue-specific manner.
Over the past few decades, diverse experimental and theoretical approaches have led to numerous conflicting models for gradient formation. A number of studies highlighted the dynamic nature of morphogen read-out and the importance of feedbacks and a network context. Important open problems concern the mechanistic basis of scaling and growth control — as well as the role of Turing patterns. They can even teach us to predict the hottest issues in science. Just search for their latest fairytales. Actually you taught me the meaning of that term.
BTW, Did you notice that this thread has received over visits in about a week? Apparently lots of anonymous readers, onlookers, lurkers attracted to this topic. BTW, gpuccio graciously provided a tremendous hint , but since you responded almost 20 minutes before that comment appeared, your answer did not benefit from it.
Now, why would you claim to want to have a discussion, but then refuse when actually engaged in one? It is about functional irreducible complexity. It is about evolution by means of blind, mindless processes. And yes it is up to the people making the claim that ATP synthase evolved via blind, mindless processes to convince everyone else by using science and not dogma. ID has said exactly what will falsify it. IDists have said exactly what will convince us otherwise.
So good luck with that. We describe two attempts at a quantitative model — one by Sir Fred Hoyle and the other by Dr. Richard Dawkins. While most models modify a previously-existing, functional, complex structure, both of these models are attempts to quantify the ability of evolution to innovate rather than modify. We critique these two models, and present our quantitative model. Specifically, we hypothesize a primitive version of Chlamydomonas reinhardtii, a simple single-celled green alga, which does not yet have a functional eyespot.
We then calculate the probability of developing an eyespot that is functional enough to confer an evolutionary benefit assuming all components are pre-existing, except a few proteins. Amusingly enough, the authors of that paper point out some of the errors made by Dr Behe. Scroll down to just before the conclusion. Okay, got it. That is a plausible explanation. No, the reason is that they lack what is required in order to engage in a technical discussion with someone of the caliber of our Italian doctor.
Been there, done that myself. I know how they think on the other side, because I was there quite a long time too. JVL Amusingly enough Dr Behe has responded to that paper and made corrections to their premises. I find it weird, more than amusing. Do you think that criticizing Behe chnages in any way their experimental results? I appreciate that you are the first, up to now, who has ansered my challenge, even if only to state that you will not attempt to answer it.
I could ask you to give us the answers just the same, for the sake of other onlookers, but I will not do it. After all, sinners cannot beg. Sure, I have only written 12 comments including this addressed to you personally in this thread:. A lot of complex functional information, I would say. This is a form of discussion, too. I confess that I would not be at ease using your own twisted definitions. Human nature. Finally, I point to proteins that IMO are too complex to be explained by your theory, and ask you to explain how they could be explained by your theory.
Horrible, indeed! What kind of dicsussion is this? I should probably just acknowledge that you believe they can be explained. How arrogant of me to ask for clarifications. Even when you give me beautiful explanations about cars and planes, I remain skeptic, and still mention that ugly protein! Even worse, not only that one. In my evil attitude, I have even suggested that you read some of my previous OPs. For example:. Ok gpuccio I have skimmed some of what you have pointed me to , so how about a variation of your challenge:.
Again, all we need is three names, a number of bits, and three dates, and we will have a discussion about that. Another way is for the morphogen to be produced for some limited period of time and then the gradient stabilized. Corey Delvin: Gpuccio, I think this quote demonstrates your misunderstanding of evolution the best:. But that does not mean that negative selection has any active role in promoting evolution. Well of course GPuccio does not think that preservation has an active role in promoting evolution. Why would anyone?
What is unclear about that? Corey Delvin: I would argue that holding a population in a state of relatively high fitness is essential to evolution and primes the population for further evolution. And how is that different from what GPuccio says? What is your point? Can your position even account for the existence of proteins?
I doubt it so perhaps you should start with that. What a great effort! In particular, I will read your response to my question about gene duplication. I have one comment so far. As a matter of fact, in terms of search algorithm capabilities, I suspect recombination will improve the chances! I am not a biologist, as you already know, but I have spent some time doing combinatorial search in operations research and scheduling. There is a simple standard local search, whereby you start from an initial schedule a functional protein in this context and tweak it by removing one job AA in this context at a time.
The neighbourhood of a solution i. The point is that it can considerably increase the neighbourhood your local search is exploring. Now, having said this, I understand that recombination will probably not qualify as neo-Darwinian. Nonetheless, it would be really interesting to hear your further comments on this. The original implementation of Large Neighbourhood Search as a meta-heuristic i. Actually, I know the guy. I met him when I worked as a researcher for University of Glasgow.
Using constraint programming and local search methods to solve vehicle routing problems, Fourth International Conference on Principles and Practice of Constraint Programming, v , Lecture Notes in Computer Science, pp —, All the proteins I mentioned in my post are good examples of informational jumps that are extremely problematic for the neo-darwinian paradigm. What they have in common is that the jump can be demonstrated in the first vertebrates, which is the issue I have focused upon in my last OPs. Jump in functional bits measured as human-conserved BLAST homology between pre-vertebrates and vertebrates:.
This is the best hit among all non vertebrate animal. In this case spiders have better hits than deuterostomia, who have even lower homology, for example:. Saccoglossus kowalevskii hemichordates : 87 bits Branchiostoma floridae cephalochordates : This is the best hit in cartilaginous fish. Callorhinchus milii has very similar values bits. The evolutionary time when this new functional information appeared is in the window between the appearance of the first chordates and the appearance of the first vertebrates, IOWs between the common precursor of chordates and the common precursor of vertebrates, before the split between cartilaginous fish and bony fish because humans derive from bony fish.
While no one can give an exact time window, a reasonable guess is between and million years ago, where:. Therefore, the approximate window of evolutionary time for the generation of the new functional information is: about 30 million years. RodW, your answer was correct.
Nothing else should be added. What were you trying to comment on? Your post is very interesting, but I would like to clarify a few point, and then hear what you think. When we consider the probabilities to find some functional target by a random walk, if our scenario is a new functional isalnd, IOWs a functional sequence which is essentially unrelated to the starting sequence, whatever it is, then our serach is not a neighbourhood search. IOWs, we are in the ocean of the search space, and we have absolutely no reference which can guide the search.
In biology, neighbourhood searchs can be useful only in small tweakings of an existing function, and in that case negative selection can anyway be a problem, as we have discussed here in great detail. However, the real problem for neo-darwinism, and the real point of ID, is generating new complex functional information, like a new superfamily, then the search really has to travel the ocean of the search space.
Which, as you know, is really huge. Indeed, when you start from random sequence libraries, you are already testing isolated points in the search space. The basic protein superfamilies are completely unrelated at sequence level and at structure and function level too , so that a transition from one to anotger is certainly not a neighborhood search.
Recombination has a supposed role in remixing existing information in new combinations, like in exon shuffling. Random variation has many ways to move directly into the ocean of the search space, whatever the starting sequence. For example, any frameshift mutation will change completely the sequence to be translated. Indels, transposon activity, translocations, and so on can change and remix existing sequences. But they do that in a random way. So any state has the same probabilities to be reached. Non coding sequences which become coding sequences a scenario ever more likely for protein origin are another good example of jumps into the full ocean of the search space, because the sequence in non coding regions has no relationships of necessity with its possible meaning if transcribed and translated.
Agian, we are in the field of mere chance. Is the gradient generated only by synthesis, diffusion and degradation? Is really diffusion the main factor here? What is the role of other transport systems, for example cytonemes? How is the gradient controlled and read? What is the risk of error, and what are the systems of error correction? EugeneS: As a matter of fact, in terms of search algorithm capabilities, I suspect recombination will improve the chances! Eugene, you may find these two articles on exon shuffling recombination to be informative. While the hypothesis of exon shuffling does, taken at face value, have some attractive elements, it suffers from a number of problems.
For one thing, the model at its core presupposes the prior existence of protein domains. A further issue relates to interface compatibility. The domain shuffling hypothesis in many cases requires the formation of new binding interfaces. Since amino acids that comprise polypeptide chains are distinguished from one another by the specificity of their side-chains, however, the binding interfaces that allow units of secondary structure i.
That is to say, it is non-generic in the sense that it is strictly dependent upon the particulars of the components. In fact, in the few cases where protein chimeras do possess detectable function, it only works for the precise reason that the researchers used an algorithm developed by Meyer et al. This only serves to underscore the problem. Even in the Voigt study, the success rate was quite low, even with highly favorable circumstances, with only one in five chimeras possessing discernible functionality.
You may want to read carefully what I wrote to you, which is quoted for your convenience. It would not make much sense for me to ask somebody to explain morphogen gradient formation or interpretation. Those are huge topics in and by themselves. Does that sound fast to you? Is there any information on typical rates for other proteins in various organisms with varying gaps in time, or have you calculated any of these yourself?