“The reason a bike lock works,” explains Meyer, “is that there are vastly more ways of arranging those numeric characters that will keep the lock closed than there are that will open the lock.”
Most bicycle locks have four dials with ten digits. So for a thief to steal the bike, he would have to guess correctly from among 10,000 possible combinations. No easy task.
But what about DNA? Well, in experiments Axe conducted at Cambridge, he found that for a DNA sequence generating a short protein just 150 amino acids in length, for every 1 workable arrangement of amino acids, there are 10 to the 77th possible unworkable amino acid arrangements. Using the bicycle lock analogy, that’s a lock with 77 dials containing 10 digits.
http://www.evolutionnews.org/2015/10/eric_metaxas_on_1100261.html
I believe this is what Mung has been talking about. I asked Mung:
How many goes do you get? How many bacteria in the earth’s soil?
Mung replies:
Not nearly enough.
I feel this is interesting enough for an OP as it seems to finally touch upon what IDers think the designer actually does that can be investigated scientifically.
For example, if we find in a population a protein that is different to the version in an ancestral population but which still works, the by (their) definition, that is prima facie evidence of the designer at work.
Perhaps we can then take the population with the original protein, enclose it in our most sensitive equipment and attempt to detect the designers actions when it “solves the bike lock” and finds the new protein and somehow makes the required adjustment?
If I were an ID supporter these are exactly the sorts of experiments I’d be proposing, and with money on the table (Templeton) I continue to be surprised at the lack of such endeavours. At the very least they can rule out some levels of possible designer interaction at the macroscopic level.
And Mung, I’d be interested in knowing how many would be enough?
Earlier during his direct testimony, Behe had argued that a computer simulation of evolution he performed with Snoke shows that evolution is not likely to produce certain complex biochemical systems. Under cross examination however, Behe was forced to agree that “the number of prokaryotes in 1 ton of soil are 7 orders of magnitude higher than the population [it would take] to produce the disulfide bond” and that “it’s entirely possible that something that couldn’t be produced in the lab in two years… could be produced over three and half billion years.”
http://www.talkorigins.org/faqs/dover/day12am.html
It’s one of those books on my shelf that I hope to get to one day. =P
Should I move it ahead of writing yet another Weasel program?
Jeez Mung…what is it with you and actually looking things up?
http://www.ncbi.nlm.nih.gov/pubmed/15321723
Heck…Bornagain even references it on UD:
I did read it, Joe. You don’t say evolution is not a search, you merely say that it’s not a search for an optimal organism.
And nothing which followed in any way contradicts your characterization of evolution as a search.
You’re still talking about search spaces and finding genotypes/phenotypes. Just not an optimal genotype/phenotype. If evolution is not a search why do you continue to characterize it as such? Will you be issuing a correction at Panda’s thumb?
Oh…and once again for the record: yeah…he did. And once again, you’re wrong.
And BTW Mung, to further add insult to injury, it’s bad enough that Axe made the dubious claim, but the fact is ID proponents (such as Meyers) keep misusing Axe’s claims to draw bogus conclusions. This nicely illustrates the issue:
http://pandasthumb.org/archives/2007/01/92-second-st-fa.html
Robin,
Do you agree with what Art Hunt says in this paper? That the chance of getting a successful 100 aa protein fold is 10^10 to 10^64. Based on this range of numbers what is the mechanism that would allow a bacterial flagellum to evolve?
colewd,
One that doesn’t work like that.
Allan’s quite right. I’ll just add, one that isn’t “searching” for a bacteria flagellum
ETA: Actually, I think KC answered your question quite well in the PT comments:
http://pandasthumb.org/archives/2007/01/92-second-st-fa.html#comment-108626
No correction is needed. As I explained above, the reason for focusing that post on a search was that Dembski, Ewert, and Marks, whose paper we were critiquing, characterized it that way.
So if evolution “is” a search, then … what?
And if evolution “isn’t” a search, then … what?
You need to tell us. You’re fixated on getting people to characterize it as “a search”, but you never explain what follows from that. Without such an explanation on your part, we’re playing word games to no purpose.
If they were unique in all of biology then perhaps you might have a point. Then the only way for them to exist must be that the designer plucked them specifically out of a near-infinite selection.
http://www.pandasthumb.org/archives/2006/09/flagellum_evolu.html
But you don’t have a point, no.
OMagain,
A multi protein complex with perhaps 20 to 30 proteins that need to assemble together in both charge and shape in order to control the movement of a flagellum. Since these proteins need to bind other proteins I hypothesize that they would require specificity at the high end. So the project is to get the genome lined up so all these proteins can assemble in order and make these motors repeatably every 20 minutes. So now we need to evolve the proteins that make all this timing work. 10^64 chance to evolve one. Estimate 4^40000 nucleotides to line up pretty precisely. Whats the mechanism you propose?
Which one?
OMagain,
Everyone. These proteins need to bind with multiple proteins. These are not single substrate enzymes.
colewd,
You are rehashing your version of Hoyle’s fallacy, which was dealt with thoroughly on the “Genetic Algorithms:” thread in February. In light of our previous interaction there, I found this
rather revealing. Why use the word “hypothesize” when you really mean “speculate without evidence”? Because it sounds better?
You appear to be PRATTing.
DNA_Jock,
This is the best you can do to explain that given rarity of protein folds there is a real identified mechanism that can explain the flagellar motor? This is not Hoyle’s argument it is based on the rarity of protein folds in the scientific literature.http://pandasthumb.org/archives/2007/01/92-second-st-fa.html The genome is a sequence and this is a real advantage for generating diversity but it sucks at finding function in a random search. So what possible mechanism could produce a 30 protein complex? Do you think it is unreasonable to assume that proteins that have to bind in multi protein complexes are at least as sequence specific then single site enzymes in Art Hunts paper?
colewd,
It isn’t clear what you mean by “lined up”, to begin with. Do you mean that the genes themselves have to be in some particular order, or do you just mean that a number of sequences somewhere in the genome have to have a particular sequence of bases?
If the former, huh? If the latter, are you demanding a particular set of proteins with sharply constrained sequences? If so, wouldn’t the actual target be anything that gave motility, whatever the set of proteins and their sequences? And why assume that maximum specificity is required initially rather than being tuned by selection?
Wouldn’t the “target” be anything that somehow proved useful in any way, whether it be motility or any of countless other marginal advantages?
I agree there is an odor here of “this is what was stumbled on, therefore this is what must have been the initial target.”
There must be any number of ways to cobble together two proteins such that the total is greater than the sum of the parts.
John Harshman,
I mean that the genome needs to be organized so the bacteria can sequentially build the motor. This requires coordination of transcription factors and specific location of DNA sequences. Do you have another idea?
I think the 10^64 is required (based on Art’s) analysis just to get the flagellum to assemble for function. DNA jock is right here I am making an assumptive leap but none the less it is intuitive to me that multi protein complexes require lots of specificity because they must bind at multiple sites. If proper binding does not occur the flagellar is non functional and function is required for selection.
The bigger issue is even if we reduce the probabilities for single protein formation this structure is very unlikely to form with a stochastic mechanism. I do think Meyer’s lock analogy is appropriate to get people to understand the magnitude of the sequential nature of the genome and proteins and the challenge it creates for stochastic evolutionary processes.
colewd:
Are you saying that some specific structure is unlikely to evolve, or that any useful change of any kind is unlikely? My intuition is that the odds of getting THIS bridge hand are small, but the odds of getting SOME bridge hand are quite high.
Mung,
From the PT post by Joe and me:
How do you suppose search acquired so many scare quotes (bold face added here)? Point 6 makes it plenty clear that they’re well deserved. Why did we not keep using them? Well, after a certain point, one reasonably expects the reader to have gotten the point. It’s just tedious to keep using them.
No, it doesn’t.
That’s not how it works inside a cell.
Probably that’s an accurate description of how you assemble a car (coordination of “factors” and “specific location” etc) — dunno, been a long time since I’ve been in an automobile factory — but it’s not how the cellular chemistry works. The DNA doesn’t need to be in any specific location. And the cell doesn’t “coordinate” transcription factors.
Well, you could use the term “coordinate” if you insist, but it’s not as if there’s a shop foreman with a predetermined flowchart that tells certain assembly lines when to stock up.
colewd,
There are at most 3 dimensions in space to go at …
You extend an argument on enzymes to arguments on structural proteins. The first is bogus in any case, the extension simply makes it double bogus. That sounds like … perhaps I should get out for a round of golf. Or, as I like to call it, a directed hole search.
If this numerological approach were correct, all mutation, and non-silent error tolerance in translation, would be impossible. They aren’t, therefore it isn’t.
Likewise, proteins would not be able to fold. Yet they do.
Despite the fact that we covered colewd’s faulty “intuitions” re protein-protein interactions on the Genetic Algorithms thread, they re-appear here as if nothing had happened.
In the “leaping fully-formed from its father’s forehead” department, I found his demand that the system be able to “make these motors repeatably every 20 minutes” very revealing.
Why on earth would that have been necessary?
DNA_Jock,
Got to keep up with the production line!
It does seem very cart-before-the-horse, to have the modern replication rate a prior constraint. Still, you can’t have a decent Salmonella infection without a decent rate of manufacture. Cheers, Designer!
Still no evidence that the designer is a bike thief.
iirc, DEM define what they mean by search. The scare quotes are gratuitous. And in the context of the DEM paper what is important is whether evolution meets the definition of a search as given by DEM.
Flint,
I am saying that the current identified mechanisms are almost certainly not the cause of how this structure evolved. We need a very long DNA sequence with high precision to emerge in almost infinite sequential space. This is not doable with a stochastic process in less than an almost infinite time frame. My answer is we don’t currently know how this evolved.
hotshoe_,
Do you really mean this?
Flint,
The chance of getting some bridge hand is 100% and if all proteins folded into their required function despite the RNA code that was translating them there would be no probability issue. This is not the case and as you build a multi protein complex amino acid specific arrangement becomes important so the shapes work together. If I need the last piece of the flagellar motor how many possible aa sequences would get me that piece. If there were 100 aa in the protein and 1000 combinations would create the sequence then 10^127 searches to find one of those combinations. The argument for the current mechanism is that most combinations would work but most the research says that functional protein space is rare.
So, let’s see if I’ve got this right…
Argument from Incredulity + Morton’s Demon ~ gods of the gap = Therefore Jesus!
Ho hum…not a particularly exciting approach to understanding the world, but I suppose it works for some folk…
Robin,
My argument is we don’t know what the mechanism is and current speculation is almost certainly wrong. The design argument is only an inference at this point.
I’m not sure why this is being ignored, but the only space being explored is the space of sequences one mutation away from whatever is current. Mutations come in many types and sizes, but any mutation that doesn’t kill the offspring of prevent reproduction is a candidate for change in functionality.
Thornton has looked intensively at several related proteins and shown they are just a few mutations removed from a common ancestor. Fully compatible with observed rates of mutation.
Axe asks the wrong question. He shows the difficulty of mutating from one modern protein to another modern protein.
First of all, this involves at least twice as many changes as diverging from a common ancestor. Second, it implies that the current state was a target.
Axe is either an idiot, or he is dishonest.
And Mary and Joseph.
What does “required” mean in this case? Required for THIS bridge hand, or required for ANY bridge hand?
What do you mean by “the last piece of the motor”? As I understand it, the flagellum was a sort of unexpected, accidental modification of a secretory system. So did the “last piece” create the “required” motor, or did it wreck the “required” secretory system? Or is it possible you can grasp that there are no requirements, because there is no goal.
Most combinations probably would not work as a flagellum, so you must calculate how many USEFUL modifications exist – and here, we’re talking about every possible useful modification of everything the organism MIGHT do if it were different! And that is your actual search space. You are still calculating the near-impossibility of the bullet falling to the ground precisely where it did, and concluding that bullets can’t fall too the ground, it’s too impossible, so some unknown process must be at work.
Yes I really mean it. Why wouldn’t I?
What part of this do you think is dubious? Do you guess that I misunderstood or mis-stated something?
I think he is neither, but he is blind. He has, IMO, done his level best to understand what evolution is, and shown that evolution can’t work that way. He KNOWS, beyond any other possibility being able to occur to him, that evolution consists of something that exists, changing into something else that exists. The concept of changing into something new lies beyond his model.
The sad thing is that all he has to do is show that something that exists can change without killing the organism. The nature of the change simply does not matter, ANY change and he has shown an evolutionary mechanism.
He knows about Thornton and Lenski, and persists in doing research that has no point. If a physician behaved that way, it would be actionable malpractice.
Well, technically you are not offering an argument. Hence my comment. All you are actually doing is saying, I can’t imagine a natural mechanism that could do this and I don’t believe that the mechanisms described in the Theory of Evolution can account for such, so maybe some other explanation is warranted.
Thing is, your feeling and belief doesn’t amount to an argument, let alone a basis for understanding the world around us. Actual research demonstrates quite soundly that no other explanation or account is necessary and that the current Theory of Evolution quite readily covers how protein folds occur, are configured, and are then built into new structures. And you have specialists who have commented here noting that very thing, but for some reason you think that your gut feeling about the probability of protein folds occurring in a given way trumps actual research on the subject and the comments of specialists. See….that’s not actually an argument.
I wonder to what extent he actually can understand what they did. I suppose it’s possible that he knows he’s not disproving any claims anyone has ever made, since every reviewer of his work I’ve read says this, over and over. And it’s likely that his target audience can’t even begin to understand the details of what he’s doing and he knows this. So maybe he’s taking advantage of that ignorance, so his target audience can say “here is real lab-type experimental biology disproving evolution” without any knowledge of what evolution is or what biology is.
But somehow, I doubt he’s that cynical. After all, he goes to a LOT of trouble, far beyond what his target audience would understand or need. You and I will probably never quite understand what drives him.
It’s an argument, just an incredibly unconvincing one.
I have to wonder why this stripe of idiot theists are so goddamned insistent that unguided evolution (random mutation and natural selection) were NOT sufficient to result in lethally infectious microorganisms.
Why are they so stupidly insistent that their designer-god get all the blame?
We have a “million-dollar baby” — 31 days in PICU for E coli 157 infection — and of course E coli have flagella which those fucking idiots insist must have been designed. Designed on purpose! If I hadn’t already been an atheist, our experience would have been sufficient to deconvert me from any form of theism.
You know, god works in mysterious ways, and we can’t possibly fault god for working on bacteria design to destroy a completely innocent two-year old human. God noi!
But at least the type of theists who accept unguided natural evolution have an out when it comes to E coli. It wasn’t their designer-god who specifically set out to create motile bacteria. That, at least, was just an outcome (however likely or unlikely) of billions of years of physics, chemistry, and unguided biology.
Why would any one of them be stupid enough to say to me personally “the Designer is proud of that feature and works hard to ensure that all infectious bacteria come pre-installed with all the latest design features” ???
What do they get out of thinking that they are required to thank god for it when one of their own relatives gets infected and has to be hooked up to all those machines (human designed, to fix god’s mistakes) in the ICU ???
hotshoe_,
What do you think the process is that causes transcription of the gene that codes for the beta catenin protein? Do you think this is an uncontrolled random process?
Fair enough. Maybe I didn’t start reading up the comments list far enough to find the actual argument that Cole is making. It certainly isn’t an obvious argument.
Yes. I think that the order of DNA sequences on a circular bacterial chromosome is not especially relevant to construction of a protein complex. It might be nice if many of them were part of a single operon, but I don’t see why that would be necessary either. If the cell makes a few too many of protein X, that isn’t a big deal.
Great. But do you have any reason to think that? I don’t think you do.
But what if the flagellum began with fewer parts, and parts were added gradually, with all the parts co-evolving their binding as new parts were added? What if binding didn’t have to be perfect to be useful?
I think you’re imagining this “sequential nature” as you explain it. And you are also imagining proteins emerging, as someone above put it, “from the brow of Zeus”. Your model of new protein formation is the tornado in a junkyard model, and that invalidates all those calculations.
There’s a difference between “uncontrolled random process” and NOT “requiring coordination of transcription factors” — which is the phrase you originally used in your comment.
Is that your problem with understanding how cellular chemistry works?
Flint,
This is not what I am arguing. In your case it would be asking what is the cause of the bullet falling to the ground which we know.
What is the cause of a 20 proteins being added to and existing protein complex (if this is true) and becoming a protein driven rotary motor. My answer is we have no idea.
That’s not an “argument” — that’s mere speculation on your own part.
Which I in turn speculate is because you have no idea how cellular chemistry works, no idea how much scientists do actually understand about the “mechanism(s)”, and your entire concept of probability/improbability has been mis-formed by Youtube cartoons created by the plagiarists at the DI.
hotshoe_,
So you are claiming that transcription factors are not coordinated by cellular processes? How would you then explain the cell cycle?