Critique of Behe and Snoke (2004) to be Published

The best thing about that,

They call it the BS model.

Its going to be sweet I tells ya.

I still think you guys should have just submitted.

I'd be interested to see Behe's response, bearing in mind his rather novel way of responding to criticism and evidence countering his views.

Just a thought:

Won't it be utterly amazing if it one day turns out that Ian, Steve and Reed, upon learning that the editors of Protein Science had asked Michael Lynch to respond to Behe and Snoke (2004), immediately put themselves in contact with Michael and tried to be ever so useful, offering in so many words to help his fingers find their way around his keyboard? Why, I know I'd be simply shocked to find that out!

Maybe we won't find that out, but something about this post says otherwise.

Michael Lynch on ID Two factors have facilitated the promotion of ID. First, IDers like to portray evolution as being built entirely on an edifice of darwinian natural selection. This caricature of evolutionary biology is not too surprising. Most molecular, cell and developmental biologists subscribe to the same creed, as do many popular science writers. However, it has long been known that purely selective arguments are inadequate to explain many aspects of biological diversity. Building a straw man based on natural selection alone makes it easy for opponents to poke holes in evolution.

Michael Lynch to respond to Behe ... immediately put themselves in contact with Michael and tried to be ever so useful, offering in so many words to help his fingers find their way around his keyboard?

— neurode

Serious question: It seems to me that although the "issues" that IDers raise are ideologically rather than scientifically motivated, they do sometimes suggest intersting avenues of investigation. My question is, are these areas that are being/have been/would have been investigated anyway? Are these areas of investigation that are not scientifically fruitful, but a mere distraction? Or is it the case that, however unscientifically motivated, ID sometimes motivates some inquiries that provide interesting new data? I don't mean to imply that ID will have all been worth it if only we can build a mousetrap without a spring or something; I just wonder--do they ever push research in an interesting direction with the questions they pose?

So, according to Lynch, most molecular, cell, and developmental biologists subscribe to the caricauture of evolution called "evolution by natural selection" alone. What! Most biologists believe in a caricature of evolution, rather than true evolution? How regrettable.

— the irrepressible Cordova

Maybe we won't find that out, but something about this post says otherwise.

— neurode

What is a caricature of evolution by IDists is an accepted creed by many biologists.

But features of the genome, such as genomic parasites or non-coding introns, which aren't so evolutionarily favourable (nor obviously 'intelligent' innovations), can be more readily explained by models that include random genetic drift and mutation as substantial evolutionary forces.

— Lynch

Greg: The central "issues" raised by ID proponents ultimately have to do with the overall nature of reality, and the primary source of order in the various patterns it displays.

The problem: some definitions of "science", the nominal purpose of which is to study reality (aka "nature"), exclude certain possible features of reality from scientific consideration on an a priori basis, and are thus oxymoronic. However, I regret to inform you that you are highly unlikely to get any garden-variety ID critic to admit that the overall nature of reality, and the primary source(s) of natural order, are accessible to science as they conceive it.

On another note, Bayesian Bouffant apparently considers himself to have been semantically victimized by an "ambiguous antecedent" in my last post, namely, "Michael". In other words, Bayesian thinks that I might have meant that Ian, Steve and Reed may have wanted to help Michael Behe rather than, or in addition to, Michael Lynch.

First, this confirms for all to see that the verbal milieu, i.e. language, favored by Bayesian is strictly context-free, each of its expressions properly standing alone and requiring no interpretation in light of context. And given that this would make language accessible even to readers with memory capacities of no more than one sentence, it suggests that Bayesian possesses every bit of the acuity which he was already credited.

The problem: some definitions of "science", the nominal purpose of which is to study reality (aka "nature"), exclude certain possible features of reality from scientific consideration on an a priori basis, and are thus oxymoronic. However, I regret to inform you that you are highly unlikely to get any garden-variety ID critic to admit that the overall nature of reality, and the primary source(s) of natural order, are accessible to science as they conceive it.

Rilke's Granddaughter: "Science does NOT exclude anything but those things it cannot investigate - are you stating that ID is inherently untestable?"

No, I'm stating that to meaningfully use the term "science", we need a comprehensive account of what science is, including its proper domain of inquiry and range of application.

Regarding the former, you say that science excludes only "those things it cannot investigate". However, in order to decide what science "cannot" investigate, we need to logically establish the boundaries of science independently of any particular scientific theory or preferred model of science.

Since this has not yet been accomplished, we are regrettably unable to exhaustively characterize what science does or does not exclude. This means that the issues ultimately addressed by ID theory cannot be summarily excluded from science.

In other words, any reasonable definition of science makes science contingent on its domain of inquiry, reality. To instead make reality contingent on a preferred mode of scientific inquiry is to engage in a logically unacceptable kind of circular reasoning.

But haven't there been a preponderance of critiques of ID literature that shoot holes through Dembski's CSI and Behe's Irreducible Complexity, etc, etc..

The issues addressed by ID theory (what is that theory again? I think you have "theory" confused with "proponents") have been countered many times. these "issues" have been measured and found wanting.

"No, I'm stating that to meaningfully use the term "science", we need a comprehensive account of what science is, including its proper domain of inquiry and range of application."

I'll make it simple for you then.

1) Make a prediction about some observation from the natural world

2) Test the prediction using some form of experimental procedure

3) Publish the result and importantly, have your experimental predictions repeated by other researchers

4) Repeat from step 1 now with the new information in mind.

This is very simple and is the basis for ALL science. ID fails at step 2, because not only do they lack a theory, they don't even have the beginnings of a proper hypothesis (which is really quite sad after all this time). They think science works like this:

1) Say "Goddidit" and then hide behind the same creationist arguments that were broken down years earlier, with new technical jargon so they sound like new 'science'.

2) Don't bother experimentally verifying it in any way, instead whine about 'Darwinist' conspiracies and try to stack school boards to get various idiocy taught (ID proper, failed creationist criticisms of evolution or whatever nonsense is required)

3) Keep whinging through political channels

Without experiments and actual science, as in making testable predictions about the designer, which would require naming said designer incidently. It's little wonder why IDists are so afraid to do such basic science seeing as they are terrified of naming their designer.

Honestly, science isn't hard to grasp or understand. You make predictions based on what you observe and then experimentally test this in a laboratory. What seperates science from witchcraft, quackery, ID and everything else from this point is that those predictions and experiments must stand up to replication by independant parties. If someone else can't replicate your results then it's time to be asking serious questions about the legitimacy of the original paper and its methodology.

However, in order to decide what science "cannot" investigate, we need to logically establish the boundaries of science independently of any particular scientific theory or preferred model of science.

This means that the issues ultimately addressed by ID theory cannot be summarily excluded from science.

Salvador Cordova said:
"So, according to Lynch, most molecular, cell, and developmental biologists
subscribe to the caricauture of evolution called "evolution by natural selection"
alone. What! Most biologists believe in a caricature of evolution, rather than true
evolution? How regrettable."

Yes, it is. Of course, I am sure few of these biologists claim to be experts on the
mechanisms of evolution, vs. topics in their subfields. Didn't the fields mention
give you a clue? Those who claim to have a great insight on evolution, however,
should at least know that natural selection is not all of evolution. For heaven's
sake, haven't they ever read Stephen Jay Gould?

Salvador: "What is a caricature of evolution by IDists is an accepted creed by many biologists."

Believing something because that was the way it was taught "way back when"
is somewhat excusable, except for a lack of curiosity about some of the
major issues in biology outside their field. Attacking a caricature when it
is known to be a caricature AND you should know better is totally inexcusable.

Comment #44617 Posted by neurode on August 24, 2005 11:35 AM (e) (s) The problem: some definitions of "science", the nominal purpose of which is to study reality (aka "nature"), exclude certain possible features of reality from scientific consideration on an a priori basis, and are thus oxymoronic. However, I regret to inform you that you are highly unlikely to get any garden-variety ID critic to admit that the overall nature of reality, and the primary source(s) of natural order, are accessible to science as they conceive it.

Most ID advocates state that their focus is on detecting evidence of design in nature, without regard to who or what the designer might be. However, ID advocate William Dembski in his book "The Design Inference"[1] lists a god or an "alien life force" as two possible options.

Comment #44649 Posted by Tracy P. Hamilton on August 24, 2005 01:07 PM (e) (s) Salvador Cordova said: "So, according to Lynch, most molecular, cell, and developmental biologists subscribe to the caricauture of evolution called "evolution by natural selection" alone. What! Most biologists believe in a caricature of evolution, rather than true evolution? How regrettable."

Joseph O'Donnell may be a bit off the track when he writes that "science isn't hard to grasp or understand."

The nature and methodology of science is in fact a very involved and difficult topic. Contrary to what Joseph seems to believe, most scientists are not trained to function adequately on this level of discourse.

For example, what sort of hypothesis is one permitted to formulate, and what kind of prediction is one permitted to make? What sort of experiment is one permitted to run, and how is one permitted to run it (for example, can one use mathematical simulations that correspond to reality only at certain junctures, but not at others)? How are experimental outcomes to be interpreted? What are the limits of scientific confirmation? And what are the proper editorial criteria for scientific publication?

These issues really are important, and I'm afraid that until Joseph realizes this, he has little business laying down the law for ID.

Flint says that "scientists attempt to bring the scientific method to bear on matters that method is inherently incapable of addressing, on a regular basis."

I'm pleased to say that I'm in full agreement on this point. However, simply "going out and making the effort to do the investigation" does not provide sufficient grounds for restricting the domain of scientific inquiry.

ID predicts order in nature, specifically in the biological realm. Neo-Darwinism also predicts biological order, but only as predicated on a restricted form of nature itself; hence, it relies on the order already implicit in "nature" (as they define it) prior to its biological manifestations. The difference: in its most fundamental form, the ID hypothesis is about the primary source of this order and the process by which it arose, while neo-Darwinism simply addresses (e.g.) statistical transformations of this order once it is given.

For reasons already given above, it would be premature to say that the primary source of biological order, and the means of its generation, cannot be scientifically investigated.

However, simply "going out and making the effort to do the investigation" does not provide sufficient grounds for restricting the domain of scientific inquiry.

it would be premature to say that the primary source of biological order, and the means of its generation, cannot be scientifically investigated.

For reasons already given above, it would be premature to say that the primary source of biological order, and the means of its generation, cannot be scientifically investigated.

— Neurode

The nature and methodology of science is in fact a very involved and difficult topic. Contrary to what Joseph seems to believe, most scientists are not trained to function adequately on this level of discourse.

ID predicts order in nature, specifically in the biological realm.

good carl zimmer article about new research into why people behave as essentialists. http://www.corante.com/loom/archives/2005/08/24/the_kanisza_virus.php

Essentialism, of course, being the mistake behind the 'A fly doesn't give birth to a horse' line of creationist thinking talking.

Flint: "Not so. The domain of scientific inquiry is established by this very process."

Translation: "The domain of scientific inquiry, that is, objective reality, is established by the (frequently over-restricted or wrong-headed) process of scientific inquiry."

Reality exists prior to any particular formal definition or informal conception of science or its methodology. Therefore, although science often attempts to define its own domain in practice, it can at best describe that domain to some imperfect level of accuracy. Reality is not actually subject to the inaccuracy of any particular description of it, and cannot thereby be limited without danger of fatal circularity.

Joseph, I'm afraid you're just not getting it. The issue is "what can be interpreted as evidence of the ID hypothesis?" ID proponents cite biological order as evidence of their hypothesis, and I assure you that observations of biological order are highly replicable.

"But wait!" you ejaculate. "Neo-Darwinism already owns that evidence!"

I regret to inform you that neo-Darwinism owns nothing of the kind. As I've already attempted to explain, it owns the evidence only within the range of its hypothesis, i.e., with respect to the order implicit in already-existing organisms and its causally restricted model of nature. Unfortunately, you have not yet established that this amount of order suffices to explain evolution, unless you simply regard evolution as a mere set of statistical effects revealing nothing about intergenerational transformations of biological form and function.

On the other hand, the ID hypothesis owns the evidence within the range of its hypothesis, which has to do with the primary source of order in biology and nature at large.

I strongly suggest that you turn down the arrogance on your end, lest I turn it up on this end and make you look even worse than you already do.

Can we please stay on topic?

Joseph, I'm afraid you're just not getting it. The issue is "what can be interpreted as evidence of the ID hypothesis?" ID proponents cite biological order as evidence of their hypothesis, and I assure you that observations of biological order are highly replicable.

On the other hand, the ID hypothesis owns the evidence within the range of its hypothesis, which has to do with the primary source of order in biology and nature at large.

I strongly suggest that you turn down the arrogance on your end, lest I turn it up on this end and make you look even worse than you already do.

steve:

"A caricature version of a given theory is likely still more useful than Puff Of Smoke, or POS, Theory."

Actually, The Puff of Smoke hypothesis can generate testable predictions:

Prediction 1. At least some mutations will be accompanied by a puff of smoke.

Test 1. Look for tiny puffs of smoke inside cells and see if there are now new genetic sequences.

If this is, in fact, observed, we should also be able to identify the residue of the smoke and the look for that residue inside other cells. If this residue is then identified in other cells that also have new genetic sequences, the hypothesis will be confirmed.

Prediction 2. At least some speciation events will be accompanied by a puff of smoke.

Test 2. All smoke that is not readily identified as coming from a known source should be investigated to see if there are any new species at that location.

If this is observed, we should also be able to identify the residue of the smoke and then look for that residue elsewhere to see if it is accompanied by speciation events. If the traces of the puff of smoke are non degradable, or degradable in a predictive fashion, we may also be able to do atmospheric studies to estimate the rate and time frame of speciation events. (Considering that this could conceivably give a lower level limit to species creation, YEC's would also be very interested in this type study).

So, here we are, the POS hypothesis makes testable predictions. I breathlessly await the announcement of funding for these projects by the ID scientists. Considering that the ID movement has fairly deep pockets, this announcement should come anytime now.

Shenda

Reality exists prior to any particular formal definition or informal conception of science or its methodology.

Therefore, although science often attempts to define its own domain in practice, it can at best describe that domain to some imperfect level of accuracy.

Reality is not actually subject to the inaccuracy of any particular description of it, and cannot thereby be limited without danger of fatal circularity.

Won't it be utterly amazing if it one day turns out that Ian, Steve and Reed, upon learning that the editors of Protein Science had asked Michael Lynch to respond to Behe and Snoke (2004), immediately put themselves in contact with Michael and tried to be ever so useful, offering in so many words to help his fingers find their way around his keyboard? Why, I know I'd be simply shocked to find that out!

— neurode

Sen McCain endorse ID:

http://www.azstarnet.com/sn/politics/90069

When will the madness end?

Sorry. I was unable to post this on the bathroom wall. Perhaps under the Bush sticky . . .

No, I'm stating that to meaningfully use the term "science", we need a comprehensive account of what science is, including its proper domain of inquiry and range of application.

Hi Sal.

1. What is the scientific theory of intelligent design, and how do we test it using the scientific method?

2. According to this scientific theory of intelligent design, how old is the earth, and did humans descend from apelike primates or did they not?

3. what, precisely, about "evolution" is any more "materialistic" than weather forecasting, accident investigation, or medicine?

4. do you repudiate the extremist views of the primary funder of the Center for (the Renewal of) Science and Culture, Howard Ahmanson, and if so, why do you keep taking his money anyway? And if you, unlike most other IDers, are not sucking at Ahmanson's teats, I'd still like to know if you repudiate his extremist views.

Steve Reuland: "Well I would certainly be shocked, given that I've never had any contact with Lynch. Perhaps instead of insinuating conspiracies, you could just, you know, ask whether or not we'd collaborated with him?"

Pardon me, but I did allow for either case.

It's just that when authors A, B and C decide not to publish because author D has been queried on the same topic, it suggests that A, B and C expect D to hit all of their major points. Otherwise, why shouldn't they go ahead and publish? This seeming expectation of redundancy then suggests the possibility - but only the possibility, mind you - of communication between {ABC} and D. (As Reed admitted, you did somehow learn that Michael Lynch had read your piece.)

In any case, this list contains enough examples of people putting words and thoughts into the mouths and heads of others to place my remarks not too far out of the mainstream.

neurode continiues his misdirection with: In any case, this list contains enough examples of people putting words and thoughts into the mouths and heads of others to place my remarks not too far out of the mainstream.

And who cares? Let's say, arguendo, that all these guys are text-messaging as we key, plotting who will say what and how. All that matters is what they, individually or together, independently or as a result of a cabal, eventually present in response to Behe and Snoke's arguments.

You would do your position much better by responding to Lenny Flank's #44685. He posits, in an admirably cogent and straightforward manner, exactly what the challenge is to ID if it wishes to establish itself as sciene. (If I was dictator of this blog, I'd add that post to the "must read" list.)How do you, as a defender of ID, meet that challenge?

Flank's queries are of infinitely more relevance than handwringing over which evolutionary scientists are talking among themselves about which ID proponents. So, how do you answer Flank's #44685?

In any case, this list contains enough examples of people putting words and thoughts into the mouths and heads of others to place my remarks not too far out of the mainstream.

Comment #44669 Posted by shenda on August 24, 2005 02:53 PM (e) (s) steve: "A caricature version of a given theory is likely still more useful than Puff Of Smoke, or POS, Theory." Actually, The Puff of Smoke hypothesis can generate testable predictions: Prediction 1. At least some mutations will be accompanied by a puff of smoke.

I notice that there are a few people who come around this site with views that conflict the majority. Sal, WAD, etc.

I also notice that, when he does post, Sal seldom lasts more than one or two exchanges before he quits.

Perhaps the defense advanced by these posters would be something like "we try to talk reasonably with the PTers, but they're all so vitriolic that ANY normal person would leave in disgust." I don't care--WAD does no less, in fact probably does even more to thumb his nose at his critics.

Has anyone ever thought of keeping a site meter on these IP addresses as to how many posts they put up in a single thread? It seems that the PT policy of not deleting posts simply because they conflict with what's generally agreed upon by board members is a happy one--dissenters like Sal don't seem to have the gumption to post more than once or (maybe) twice. On WAD's blog it's the opposite--dissenters are happy to engage him, and his policy of deleting posts seems to be necessary.

On the other hand, there are some like neurode on this thread who wave their hands long enough to ignore literally dozens of requests for an actual testable idea, while he implies that those who challenge him to drop the doubletalk and say something coherent "look bad". I've noticed this particular gradeschool-level metaphysicist has repeated this performance maybe a double handful of times. Of course, he STILL hasn't produced a testable idea for some reason...

ID predicts order in nature, specifically in the biological realm.

— neurode

Flint says that "scientists attempt to bring the scientific method to bear on matters that method is inherently incapable of addressing, on a regular basis." I'm pleased to say that I'm in full agreement on this point.

On WAD's blog it's the opposite---dissenters are happy to engage him, and his policy of deleting posts seems to be necessary.

Does that tell us that there isn't a God who doesn't hear or chooses not to grant prayers? No, of course not, but that's not a matter that any scientist has attempted to bring the scientific method to bear on.

While you may be right, what I read was that these experiments were constructed for the purpose of finding evidence of a working god.

the experiment---a greatly expanded and tightly controlled replication of the small Byrd study---is elegantly simple. Each of three conditions engages several hundred patients at five leading medical centers who are about to undergo coronary bypass surgery. (All consent to participation.) Teams of intercessors--people of faith who, one presumes, hope to show the power of prayer while supporting the seriously ill patients---will pray for two of three groups of bypass patients. One group will know it is being prayed for. Patients in the other two groups will either be prayed for by the volunteer intercessors or not, but will not know which condition they are in. The research is currently underway. Data collection will continue until early 2001 and the announcement of results will occur sometime in 2002.

Neurode (#44665) - you state that"ID proponents cite biological order as evidence of their hypothesis". Herein lies the difference between scientists and ID proponents. Scientists look at that order and ask how it arose. They then do research to unravel the mechanisms. And believe me, these mechanisms exist. ID proponents look at that order and state that a designer did it. One of these approaches is intellectually lazy and disingenuous, the other is science.

Complex systems theory and models demonstrate all of the time just how apparent design can arise from a collection of "bits" Order from disorder, and disorder from order.

Also, I suggest that you would have the same success at identifying "supernatural" design as you would identifying randomness.

The telephone grid is like a living body by virtue of its enormous scale and intricacy but also because it is remarkably reliable (~99.999%). The great majority of service interruptions occur not because of the failure of individual parts---such failures occur at a rate comparable to the genetic mutation rate in living things, mostly without obvious consequences---but simply because the phone companies decided it wasn't worth the money to build a big enough system to withstand the occasional overload. In other words, the fragility of the system is planned. Its robustness is not. It is a side effect of the way the system evolved. During the long, piecemeal process of its development, defects and failures continually occurred and were responded to with various ad hoc expediencies. As a result, the grid, like the genetic, metabolic, and developmental systems of living things, looks like a crazy guilt or, if you're old enough to catch the reference, like a Rube Goldberg contraption. Nevertheless, it works in the sublunary world better than any rationally designed system whose structure, though elegant, would probably be hopelessly brittle.

All of which suggests an Argument from Non-Design. To put things simply: We know that living things were not designed. After all, they work. (The information in this bit is from Andreas Wagner. The argument is my fault.)

Oh, and I forgot about self organisation, where internal feedbacks maintain an apparent order without the need for outside "direction or guidance".

ID predicts order in nature, specifically in the biological realm

Predicting what an intelligent designer would create requires a cognitive model of the designer, or knowledge of the designer's goals, or something, but ID is entirely silent on such matters. The ID inference is entirely in the other direction -- complexity purportedly implies designer. The IDists have no grounds for any inferences in the other direction -- i.e., predictions. An intelligent designer might be like John Cage, who wrote "chance music", as well his famous 4'33" piece, consisting of 273 seconds of silence in three movements. Or the intelligent designer might work in far more mysterious ways than that. Who can know the mind of God -- when it is unspecified?

I wouldn't be too sure that there's nothing like that out there somewhere, ts. Something tells me that it's a live possibility.

After all, if we can ignore the excess baggage attached to the basic Prime Mover concept over the years, there's no reason to think that the "Mind of God" is not self-specified and recognizable through a combination of His work, i.e. nature, and His primary tool in constructing nature, i.e. logic.

Thanks to a few centuries of Scholastic abuse and a reactionary conception of science that fails to properly incorporate logic, it has seemed impossible to read this specification. But maybe not forever.

Of course, even if a real theory of the Mind of God were to emerge, or if were it already out there in virtual secrecy, it would remain to be seen whether most ID supporters would run away from it in fright, and most evolution supporters decohere in rage at the very sight of it.

It's an interesting question to ponder.

It's just that when authors A, B and C decide not to publish because author D has been queried on the same topic, it suggests that A, B and C expect D to hit all of their major points.

— neurode

We didn't know that Lynch had crafted a response to Behe and Snoke until a matter of days ago

— Steve Reuland

And, as Mona suggested above, WTF would be in the slightest bit wrong with a collaboration or sharing of ideas between various evolutionary scholars--in response to, ahem, Behe and Snoke's, um, collaboration?

Nothing whatsoever, for cripe's sake!

Perhaps this has already been covered - but here goes.

Neurode: In post # 44657 you claim that ID predicts order in nature.

Please be so kind as to explain what features of observed order are better explained by ID "Theory", or where ID provides an explanation where "evolution" cannot.

And how can ID Theory can guide us in discovering new or previously unrecognized realms of "order"?

It's an interesting question to ponder.

I wouldn't be too sure that there's nothing like that out there somewhere, ts.

I think Lenny's excellent post (44685) does a great job of explaining how science works, but it's slightly off the mark about where ID breaks down. I think ID does not have a proper scientific hypothesis yet.

Suppose an ID'er came along and took Lenny's challenge and actually made a testable prediction. Say for example they predict that there will be a solid cesium core of 2 mile diameter in the center of the moon. That's a prediction and a potentially falsifiable one too. But how the heck did that prediction arise from the ID'ers hypothesis??

For a hypothesis to be scientific it must be able to be understood to the point where people who accept, reject or aren't sure about it (but at least are honest and intelligent) can figure out what sort of predictions it might make.

This is why Lenny asks the ID'ers to fill in step 3 - because nobody (not even the ID'ers) have a clue what predictions flow from their non-scientific hypothesis. The ID'ers simply don't even know how to get past step 1 of the scientific method.

For a hypothesis to be scientific it must be able to be understood to the point where people who accept, reject or aren't sure about it (but at least are honest and intelligent) can figure out what sort of predictions it might make.

I think Lenny's excellent post (44685) does a great job of explaining how science works, but it's slightly off the mark about where ID breaks down. I think ID does not have a proper scientific hypothesis yet.

Another way of looking at it is that the IDiots are envious of the power of science to influence what people think and know about how the universe works. Since the superstitious BS they peddle doesn't have the same ability to convince, they endeavor to pervert the definition of science as far as is necessary to get their crap included in that definition.

... I'm at a loss as to what testable predictions might be inferred from it, and can say why I think it can't yield testable predictions. But to claim that it's therefore not a scientific hypothesis looks to me too much like argumentum ad ignorantiam --- I might be missing something. Lenny charitably gives the IDists the opportunity to tell us what those testable predictions might be; the burden is on them to provide those testable predictions.">

I don't claim that I've proven my point that ID'ers don't have any scientific hypothesis, but they have failed to make any predictions which is evidence that they don't. But I think my point goes deeper as to what is required of a scientific hypothesis, it can't be one in which everyone is ignorant of any predicitions it can make. It also can't be one in which only one person knows how to make predictions.

Suppose that the ID'ers found a person, call her the "Great Sage," that announces a series of testable predictions that are claimed to flow from a sweeping ID hypothesis like "An unknown intelligent designer separately created all living organisms." Suppose for the sake of argument that these predictions were not obvious or currently known, and that real scientists were able to verify the first two predicitions, and the other two presented were too difficult to test for years to come. Sounds like science, doesn't it? But the problem is that the Great Sage is the only person in the entire world that knows how to make predicitions from the hypothesis and can only explain the predictions she's already made by saying that they are obvious because that is what "intelligence" requires. Is that science? I don't think so.

I think that science requires a hypothesis that is detailed enough for at least a few people who don't accept the hypothesis to understand how to make some predicitions from it. If not, then science is in trouble because the ID'ers will be able to lay claim to science simply by making a couple of very hard to test predicitions. Say for example they claim the ID hypothesis predicts that there will be an earth-like planet located between 1.0x10^8 and 1.2x10^8 light years distant from earth that has a flora and fauna essentially identical to that on earth. It's a predicition, it's testable (theoretically), and if false, the ID'ers will agree it kills their hypothesis. Now they got science? I say no!

I don't claim that I've proven my point that ID'ers don't have any scientific hypothesis, but they have failed to make any predictions which is evidence that they don't. But I think my point goes deeper as to what is required of a scientific hypothesis, it can't be one in which everyone is ignorant of any predicitions it can make. It also can't be one in which only one person knows how to make predictions.

Suppose that the ID'ers found a person, call her the "Great Sage," that announces a series of testable predictions that are claimed to flow from a sweeping ID hypothesis like "An unknown intelligent designer separately created all living organisms." Suppose for the sake of argument that these predictions were not obvious or currently known, and that real scientists were able to verify the first two predicitions, and the other two presented were too difficult to test for years to come. Sounds like science, doesn't it? But the problem is that the Great Sage is the only person in the entire world that knows how to make predicitions from the hypothesis and can only explain the predictions she's already made by saying that they are obvious because that is what "intelligence" requires. Is that science? I don't think so.

If not, then science is in trouble because the ID'ers will be able to lay claim to science simply by making a couple of very hard to test predicitions.

Say for example they claim the ID hypothesis predicts that there will be an earth-like planet located between 1.0x10^8 and 1.2x10^8 light years distant from earth that has a flora and fauna essentially identical to that on earth.

I think that science requires a hypothesis that is detailed enough for at least a few people who don't accept the hypothesis to understand how to make some predicitions from it.

I know you all like to use big words and all, but there are simpler ways to consider this matter.

1. Every stinking, flea-bitten, dead-animal-skin wearing, rotten-toothed tribe on Earth had some "religion," often including gods (or at least super-beings, e.g. the Karuk of California).

2. The ancient Jewish people, it seems likely, didn't worship a single God.

3. The universe is complicated.

4. The human brain can't understand it all.

5. Two year old humans have probably been asking "Why?" "Why?" "Why?" for many thousands of years.

6. If a tribe succeeds, it gives credit for the miracle to its god, because the truth is (more often than not) too complicated to explain.

7. An inherently disprovable god ("my god lives in this tree" "well, what happens if we chop down the tree?") isn't likely to last as long. This suggests that infinite, invisible gods are more sustainable.

So, the real truth is that my god gave birth to the god of Abraham, and only made that Yahweh _think_ it was the ultimate. ;)

But what is the likelihood that one tribe's superstitous, changed-with-the-times conception of the world's ultimate authority is right?

We need more archaeology, to help prove that the ancient Jews didn't worship a single God, or any god at all.

La allah. Lo adonai. There is no god.

1. Observe some aspect of the universe

2. Form a hypothesis that potentially explains what you have observed

3. Make testible predictions from that hypothesis

4. Make observations or experiments that can test those predictions

5. Modify your hypothesis until it is in accord with all observations and predictions

What are some good examples of the scientific method being applied to evolution, examples where predictions regarding evolution are made and then tested with experiments (not observations)?

What are some good examples of the scientific method being applied to evolution, examples where predictions regarding evolution are made and then tested with experiments (not observations)?

Why exclude observations? If the hypothesis doesn't fit the observation, then it needs to be modified.

Are there no experiments then?

John, the point you are missing is that science relies on observation and experimentation is a form of observation. You cannot exclude observation and include exeperimentation.

I suggest that you go to the closest collegiate science library and pick up one of the journals with "evolution" in its title then start reading papers. You'll quickly find experiments.

Does evolution make predictions that can be tested with experiments? If the journals are full of predictions based upon evolution and their associated experiments, name a few that really stand out.

Hypothesis: The phenotype of each population is adapted, and is the result of the local balance of sexual and predator selection. Prediction: If the balance of sexual and predator selection is changed, the phenotype should evolve in response. Result: Phenotypes evolved in response to changes in the balance of sexual and predation selection.

I pulled this citation from Pubmed on this topic.

Johnson JB.(2001)Adaptive life-history evolution in the livebearing fish Brachyrhaphis rhabdophora: genetic basis for parallel divergence in age and size at maturity and a test of predator-induced plasticity.Evolution Int J Org Evolution. Jul;55(7):1486-91.

This may not be one of the papers you were thinking about, but reading the abstract suggests to me that it does not address predictions based on evolution (and testing of those predictions through experiments)in the way that I was thinking.

My interest is actually more directed towards the earlier posts regarding the lack of hypothesis and use of the scientific method by advocates of ID. I have seen no hypotheses advanced that offer a means to test ID, so I would agree with those sentiments. However, I have similarly not seen hypotheses and (experimental evidence to test those hypotheses) that supports evolution either.

There are many papers that show how selection can affect phenotypes within a population over time. The paper cited above probably does this.

What I am looking for is a paper that proves Behe is wrong about the evolution of new functions. Behe says that selection can't act upon the various transition stages that exist between the starting point (a duplicated gene) and the final product (a mutated version of the duplicated gene that evolves to express a new product with a new function), because function does not exist (to allow selction based upon that function) until you've reached the final product.

If Behe is wrong, it seems to me that evolution of new functions should be something that one could demonstrate experimentally.

What I am looking for is a paper that proves Behe is wrong about the evolution of new functions. Behe says that selection can't act upon the various transition stages that exist between the starting point (a duplicated gene) and the final product (a mutated version of the duplicated gene that evolves to express a new product with a new function), because function does not exist (to allow selction based upon that function) until you've reached the final product.

ID "theory" cannot make any testible predictions because, at core, it simple has no BASIS for making any. Stated in the simplest possible scientific terms, ID "theory" consists solely of "an unknown thing did an unknown thing at an unknown time using unknown methods". How the hell can ANYONE make any testible predictions from THAT?

John, to help you out, I can think of two experiments to provide evidence for evolution. You won't find many journal articles that address this question exactly, because evolution has been settled science for so long. It would be like Physicists doing experiments to describe Newtonian mechanics, it just isn't considered necessary.
But here are two that you can perform yourself, one for macroevolution and one for microevolution.
The micro one first:
Observe: Antibiotic resistant bacteria seem to emerge and increase in frequency over time when we use antibiotics in a therapeutic setting.
Hypothesis: evolutionary theory posits that new gene functions will arise through mutation and selective pressure.
Experiment: Start with a culture of antibiotic sensitive bacteria, virtually any strain you like will be useful in this experiment. Culture the bacteria while slowly increasing the antibiotic concentration from 0. For example, use Mycobacterium avium (that's the one I study), and gradually increase the Kanamycin concentration from 0 to 200. Eventually you will have "evolved" your culture from antibiotic sensitive to antibiotic resistance, and with a little gussing and checking you can find the gene or genes altered to grant this function (ribosomal parts, acetyl or adenyl transferases etc.). You have just tested microevolution.

Now macro:
Observe that the species cluster into an apparent phylogeny based on phenotypic traits. There have been many such trees drawn. Just for fun you can take an old one of birds, bacteria, apes and humans, whatever you like.
Hypothesis: We learned that genetic information is carried in the form of DNA sequences, and we suspect that these sequences drift over time at a nearly steady rate. We thus hypothesize that the pattern of similarity of sequences of essential components, such as ribosomal RNA, certain subunits of the F1/F0 ATPase, superoxide dismutase, etc. will objectively produce the same tree as that of the more subjective phenotypic analysis. This would be a test of macroevolution.
In fact, both of these have been performed numerous times, as have countless other methods of testing the tenets of evolutionary theory. The theory has grown to include the various complex ways that things evolved, but has maintained the central tenets of the synthesis pretty well.
Now John, what have IDists demonstrated to prove their theory?

By new functions I mean a new complex molecular machine or enzymatic pathway that didn't exist before. Behe lists many examples, such as the pathway for purine biosynthesis or the pathway for blood clotting.

Behe argues that you can't evolve these systems using the tools of evolution (mutation/selection) because the genes that they evolve from (intermediates) have no function that would allow for their selection over time to produce the final product (the molecular machine or pathway). I may be paraphrasing his idea here, but I don't think I've misunderstood the point. If he is wrong about this, then I think he should proven wrong by an experiment that demonstrates macroevolution.

Behe goes on to infer the existence of an intelligent designer to account for complex molecular machines. Let's not go there. What about the point he makes suggesting a flaw in our thinking of how these complex systems arise (not worrying about his alternative explanation)? How do they come about through evolution? I think he has made a valid point that should be answerable through some experiment.

I would agree that DNA sequence analysis is very compelling evidence to argue in favor of macroevolution. However, it is consistant with evolution rather than a proof. To my mind, a proof would involve setting up a system to measure macroevolution in real time.

I don't have an experiment in mind to offer up, but I would expect that some type of bacterial system would be required. Maybe a simple version would be somthing like the microevolution system mentioned by sanjait, but with some modifications.

I would agree that DNA sequence analysis is very compelling evidence to argue in favor of macroevolution. However, it is consistant with evolution rather than a proof. To my mind, a proof would involve setting up a system to measure macroevolution in real time.

Russell - that is the best analogy I have heard in a long time. I'll be recycling it for sure.

Cheers

By new functions I mean a new complex molecular machine or enzymatic pathway that didn't exist before. Behe lists many examples, such as the pathway for purine biosynthesis or the pathway for blood clotting.

Um, wasn't a possible mechanism for the latter known when Behe first proposed IC and later got more evidence supporting it?

Observed Instances of Speciation by Joseph Boxhorn Copyright © 1993-2004 [Last Update: September 1, 1995] http://www.talkorigins.org/faqs/faq-speciation.html

And the Salvadorites shall see it, and be grieved; they shall gnash with his teeth, and melt away: the desire of the wicked shall perish in Dover.

John,

You still haven't defined any criteria for distinguishing "new" from "modified" with respect to your question. This is an important distinction that you need to establish before anyone should attempt the meet your challenge.

Evolution is descent with modification, and thus you need to establish some criterion in your challenge for when a modified function becomes a "new" function.

Furthermore, you mention "macroevolution" but don't define it. "Macroevolution" is a technical term in evolutionary biology that is probably the most misused term by anti-evolutionists. What do you mean by "macroevolution?"

By macroevolution I mean the process by which major novel biochemical pathways (purine biosynthesis, blood clotting cascade)or complex molecular structures (flagella) arise. These kinds of novel molecular pathways and molecular structures are the basis for morphological changes that accompany speciation. If this process is not macroevolution then correct me as to what it should be called. Can an experimental system be designed that would select for a new biochemical pathway or complex molecular structure?

I don't expect to find an experimental system where you see the evolution of an entire pathway or complex structure like a flagella in real time. However, if you simplify the question somewhat, maybe a system could be set up to show the evolution of a single novel function. That would at least be a start.

Here is an imperfect attempt that someone could improve upon.

The bacterial ampR gene confers resistance to ampicillin by producing b-lactamase, which destroys the drug. At some point in time, b-lactamase presumably evolved from some precursor gene (nonfunctional with respect to b-lactamase activity , but presumably functional for some other activity) into its present form.

For the moment, let's assume that we have no constraints on time and resources to do an experiment. We first nonselectively grow up 1 liter of E. coli (that has no amp gene) and then plate 999ml on ampicillin plates. No ampicillon resistant colonies arise. We take the 1 ml of remaining culture and grow up another 1 liter of E. coli nonselectively, and repeat the experiment. We do this experiment over and over again, endlessly. Do we ever get an ampicillin resistant colony out? My guess is that we never evolve a new b-lactamase gene. The reason is that any mutations that occurred in precursor genes that modified the precursor closer to a functional b-lactamse gene were lost upon drug selection because they didn't function. They also would not persist in the unselected cells used to propagate the culture, because there was no selection to maintain them.

Maybe you disagree and would predict that the ampR gene should evenually evolve if time is unlimited. How?

If you agree that the ampR gene never evolves in this system, what is missing in this system that was present in its actual evolution?

By macroevolution I mean the process by which major novel biochemical pathways (purine biosynthesis, blood clotting cascade)or complex molecular structures (flagella) arise.

By macroevolution I mean the process by which major novel biochemical pathways (purine biosynthesis, blood clotting cascade)or complex molecular structures (flagella) arise.

These kinds of novel molecular pathways and molecular structures are the basis for morphological changes that accompany speciation.

Abstract: To establish an experimental system to directly observe molecular evolution, a DNA fragment that confers ampicillin resistance on Escherichia coli was cloned from an archaeal genomic DNA. The activity of this clone was enhanced by 50 rounds of directed evolution by using DNA shuffling. Analysis of the evolved DNA fragments shows that two genetic regions have coevolved: One region, which has no obvious ORF, is essential for the activity, whereas the other, which appears to encode a protein, is not essential but enhances the activity of the former region. Analysis of the evolutionary intermediates shows that negative mutations are effectively removed while beneficial mutations accumulate and illustrates how a protein has evolved over the course of the evolution experiments. Although the mechanism of the activity remains unclear, the evolved DNA fragments also confer resistance to other drugs that inhibit bacterial cell-wall synthesis. The present system would serve as an experimental model to study evolutionary dynamics in the laboratory and provide the concept of screening natural libraries to obtain starting materials for directed evolution.

We devised the following experimental system to satisfy these criteria: an expression library of Pyrococcus furiosus genes is screened for a gene that endows Escherichia coli with ampicillin-resistant (ampR) activity. After the ampR activity is enhanced by directed evolution, evolutionary intermediates as well as finally evolved mutants are analyzed. P. furiosus is a hyperthermophilic archaeon isolated from a marine hydrothermal vent (6). Archaeal cell wall is chemically different from the bacterial peptidoglycan, and therefore archaea are not susceptible to common antibiotics directed against cell-wall synthesis, including beta -lactam antibiotics such as ampicillin (7). Understandably, no beta -lactamase activity has been detected in archaea (8). Thus, the original biological function of the P. furiosus gene, even though it shows ampR activity when expressed in E. coli, should be unrelated to peptidoglycan metabolism or inactivation of beta -lactam antibiotics. Although the number of rounds of screening and selection we can achieve cannot be predicted, this model system might allow us to simulate molecular evolution in the laboratory.

Having isolated a starting archaeal DNA fragment, this fragment was subjected to 50 rounds of directed evolution (Fig. 1). The directed evolution experiment was done as follows: the 1.2-kb fragment was treated with DNA shuffling (1) to introduce random mutations (and also recombinations after the second round). Recombination is a key feature of DNA shuffling because it facilitates the accumulation of functionally positive mutations while eliminating negative mutations (3). The shuffled DNA fragment was ligated to a plasmid vector, and the resulting construct was introduced into E. coli JM109 cells by using electroporation. At each round of screening, a library of 2 × 106-6 × 106 transformants was screened at an appropriate ampicillin concentration, and a mixture of plasmids was prepared from the about 200 largest colonies. The 1.2-kb fragment was amplified from the plasmid mix by using PCR, and a subsequent round of DNA shuffling was done to introduce further mutations and recombination events among the selected mutant genes. These procedures were repeated at increasing concentrations of ampicillin. At the 14th round, the inducer IPTG was omitted from the selection medium, and at the 15th round, the vector pHSG398 (about 500 copies/cell) was replaced with pBR322 [about 20 copies/cell (11)]. These procedures increased selection pressure by decreasing the expression level of the gene and thus enabled us to do further rounds of directed evolution. The evolutionary trajectory thus obtained was not linear but hyperbolic, as is most evident in the 15th to 50th rounds. That is, the evolution decelerated gradually as it proceeded.

I might also point out that penicillin is a modified peptide, and that the chemical reaction catalyzed by the ampR gene product is an amide bond hydrolysis, just like the reactions catalyzed by peptidases, and that the ampR gene bears an obvious family relationship to certain peptidases.

I would say what's missing from John's laboratory simulation that's present in real-life evolution is:

(1) the "large" numbers of organisms and the "large" amount of time envisioned in the laboratory simulation are still infinitesimal compared with the corresponding real-life numbers, and thus so is the number of "trials" available for trial and error, and

(2) In real life evolution, there would be more or less continuous selection during expansion of the candidate genetic material: the ancestral peptidase would have coevolved with ancestral penicillin (probably a relatively weakly antibiotic peptide).

I can't identify a single molecular pathway or structure that distinguishes humans from chimps, but I was never trying to define a species in the first place. If my use of the terms microevolution and macroevolution are not correct, I stand corrected. As far as new vs. modified is concerned, let me return to the experiment I suggested.

A new gene, in the context of the experiment, is one that encodes b-lactamase activity. A modified gene is defined as any gene within the E. coli genome that acquired a mutation after the start of the experiment. We don't know which gene (if any) will eventually mutate to express b-lactamse activity. None of the E. coli genes in the starting strain have b-lactamase activity.

What would one predict to happen in the experiment? Does b-lactamase activity eventually evolve in the E. coli or not?

John,

Please see the paper mentioned in #47211.

What would one predict to happen in the experiment? Does b-lactamase activity eventually evolve in the E. coli or not?

Russell,
I think we agree that b-lactamase would not evolve in the experiment for the same reason. You answer the second question by stipulating that for the real life evolution of b-lactamase, "the ancestral peptidase would have coevolved with ancestral penicillin (probably a relatively weakly antibiotic peptide)." We now have to assume that penicillin itself evolves, so that we can have a weak selective pressure at the start, allowing for selection of weak resistance. Evolution of b-lactamase works in real life because we have a gradation of selection that starts out low and increases over time.

OK, I could imagine that happening. Does that then mean that all evolution must similarly involve a graded selection that starts out low and then coevolves to a stronger selection over time? Can we apply that same concept to the real life evolution of flagella, the blood clotting cascade, and purine biosynthesis?

Reed,
Directed evolution does something that real evolution does not. Instead of a gene evolving through a stepwise addition of mutations where selection occurs at each step, directed evolution generates all combinations of mutations in the gene at one time. Selection then occurs on genes with combined mutations rather than on intermediates in which each new mutation was selected independently.
Also, did b-lactamase activity arise de novo from unrelated DNA in this experiment? From the abstract, it sounds like what they produced probably isn't b-lactamase activity (no ORF in gene 1, and gene 2 is nonessential but enhances the activity of gene 1). If it is resistance to ampicillin due to some other mechanism that is mediated by the actual DNA fragment (and not a b-lactamase enzyme activity) it is not a model for the evolution of proteins (and complex protein structures and biochemical pathways).

One additional thought regarding the coevolution of b-lactamase and penicillin. In the experiment to evolve b-lactamase, can we now succeed if we drop the ampicillin concentration to a point where 0.1% of the cells survive, and use these cells to grow the culture up again (and repeat the selection)? In other words, we have a less stringent selection now, but it (the drug) doesn't have the capacity to coevolve. Do we get b-lactamase activity eventually?

OK, I could imagine that [penicillin-precursor producing fungus in an evolutionary arms race with penicillinase-producing bacteria] happening. Does that then mean that all evolution must similarly involve a graded selection that starts out low and then coevolves to a stronger selection over time? Can we apply that same concept to the real life evolution of flagella, the blood clotting cascade, and purine biosynthesis?

Directed evolution does something that real evolution does not. Instead of a gene evolving through a stepwise addition of mutations where selection occurs at each step, directed evolution generates all combinations of mutations in the gene at one time. Selection then occurs on genes with combined mutations rather than on intermediates in which each new mutation was selected independently.

— John

Also, did b-lactamase activity arise de novo from unrelated DNA in this experiment?

Reed,
This experiment shows how you can take genes that already confer resistence to ampicillin, and through randon mutations, DNA shuffling and selection, improve their function (for conferring resistance to ampicillin). The system isn't generating b-lactamase activity de novo. Further, the addition of mutations and their reshuffling in vitro is not the same as generating single mutations one at a time (or having a single recombination event) then selecting based upon the phenotype of that single event.

John,

You're doing exactly what I expected, shifting the goal posts to claim that it is just a modified function. The system is clearly generating ampR de novo from unreleated DNA because the starting sequence was obtained from archeans that are neither affected by ampicillin nor exposed to it. There is no reason to expect that this gene exists in Pyrococcus furiosus for ampicillin resistance. Instead it does something else and had the fortitous property to have weak ampR abilities.

This is how nature works.

Please explain to me how you expect your experiment in plating hypothetical bacteria with no capacity to survive on ampicillian to show anything other than we evolutionary biologists already know: extinct populations don't evolve. While you're at it, check out the classic experiment by Luria and Delbruck about mutations and adaptation.

Reed,
Sorry, I thought it was clear when I said

"Do we ever get an ampicillin resistant colony out? My guess is that we never evolve a new b-lactamase gene."

that I was referring to de novo b-lactamase. I was looking for an example that demonstrates how novel proteins with novel functions arise. I am not shifting the goal posts. I just don't see how this serves as an experimental model for evolution.

Ampicillin resistance did not arise de novo in the experiment. It was there from the beginning when they cloned the sequence based upon its ampR phenotype. Whether it was fortuitous or not, it was there. They simply made it a stronger phenotype through mutations generated in vitro, using methods that don't take place in nature. Ultimately they found two sequences that confer a higher level of resistance than the starting clone. Is this an example of evolved IC? How could we know without even knowing what the molecular basis is for the observed ampicillin resistance? Besides, both sequences were present from the beginning as well, so if they represent IC, they didn't evolve de novo.

Although I think this is interesting in its own right, an experimental system to model evolution should turn out novel proteins. Proteins are what make up the vast majority of known molecular structures and enzymatic activities. In this experiment, it remains to be seen whether proteins are involved in the ampicillin resistance observed.

Regarding my hypothetical experiment, I was actually hoping to see someone else tell me how to make it demonstrate evolution. Maybe that can't be done, but I was ultimately hoping to see it taken the next step to show how complex molecular machines and biochemical pathways could arise through evolution. You wont find that in Luria and Delbruck.

John,

Your requirement that the colonies in your experience show zero resistance to ampicillin at the start of the experiment is an abiological requirement. Mutations are random and therefore do not wait to occur until after a selective force is present.

I can tell you what would happen with such an experiment if you were able to engineer the type of population that you demand; it'd die in the first plating, and extinct populations don't evolve.

Ampicillin resistance did arise de novo in the experiment. Pyrococcus furiosus has no ampicillin resistance because it is neither affected by ampcillin nor exposed to it in nature. The experiment did result in a novel protein, since it didn't exist before.

But let's look at your question from a different angle. Start with a single bacterial cell with no ampR ability because we have intoduced premature stop codons into its ampR genes. Plate this cell in the absence of ampicillian and allow it to become a culture of bacteria. Random mutations will occur as the cell grows into a culture of billions of cells. Plate this culture onto a weak concentration of ampicillian and look for resistant cultures. By your defination, any colonies that are resistant have de novo ampR abilities because at the start of the experiment the population had no ampR abilities. Experiment, after experiment has shown that such resistant colonies will exist.

It has become very clear to me that if we are to continue this then we need to go back and you need to provide a rigorous defination of "novel" in the context of protein evolution that does not depend on synonyms of "novel". Perhaps answering this question would help.

If you gave me two proteins--one ancestrial, one descendent--how would I determine if the descendent protein is novel with a novel function?

If you cannot answer that question with detailed and rigorous criteria, then this conversation will go nowhere.

How about one ancestrial protein complex and one descendent protein complex?

The ancestrial protein complex is the type III secretory system (TTSS).

The descendent protein complex is the bacterial flagella.

One can determine that the descendent protein complex is "novel" by virtue of its novel function of conferring motility to the cell. The ancestrial protein complex, TTSS, cannot confer the phenotype of cell motility.

How does the descendent protein complex evolve from the ancestrial protein complex?

An additional cadre of proteins in addition to the TTSS cadre is required for the flagella to function. How do they evolve when selection is based upon motility (and motility is absent until the additional proteins evolve)?

John, that is not an answer to the question since it appeals to a specific example. I don't want an example; I want specific criteria that can be unambiguously applied to any example. Once again,

If you gave me two proteins--one ancestrial, one descendent--how would I determine if the descendent protein is novel with a novel function?

Note that answering the question using synonyms of "novel," i.e. a novel protein is one with a "new" function, is still ambiguous.

A criteria that could be applied to any example would be defined by function. A function associated with the respective proteins could be either be enzymatic or structural. The distinction between the ancestral protein (A) and the descendent protein (D) would be based upon and the presence of a specific enzymatic activity or structural function in A that was not present in D. Conversely, D has an enzymatic activity or structure function that is not present in A.

I'm not sure why this is the crux of the question for you. Do you have an alternative criteria in mind that you want to put forth, or do you think no such criteria exist (obviating the need to continue on with the original question as to how the TTCC could evolve into a flagella, or vice versa)?

The TTCC (A) has the function of transporting toxin into host cells. The flagella (D) does not have this function. Conversely, the flagella (D) has the function of cell motility, which is not present in the TTCC (A).

John,

You still haven't answered the question because you've provided no criteria for determining it the activity of protein D is not present in protein A and vice-a-versa.

For instance, A digests lactose, and D digests maltose. Person 1 may argue that D has a novel function because it can digest maltose, whereas Person 2 may argue that D does not have a novel function because it still digests a disacaride.

This is the entire crux of the issue because one can demand that evolution produce novelty and then dismiss any example as just modification. The hierarchical quality of nature helps such word games, e.g. humans are not novel, they are still mammals, and flagella are not novel, they are still secreting organelles.

For any trait that is said to have a new quality, one can still find many qualities that are not new, and dismiss novelty based on them.

And finally,

TTCC (A) has the function of transporting proteins along a tube. Flagella (D) also transport proteins along a tube.

Reed,
You rightly point out that flagella (D) can also transport proteins along a tube. So flagella (D) do have a function shared with the TTCC (A), yet flagella also allow the cell to move (a function not shared by TTCC).

Cells with TTCC alone and no flagella cannot move. Isn't that functional test sufficient to show that protein A lacks the function of protein D (the function of conferring cell motility)? Even if we find many qualities that are not new between the two, why do we have to dismiss the motility function of flagella as new?

In order to dismiss motility in this way, you would have to argue that motility is somehow present in TTCC. If our functional test says it isn't present, why isn't motility in flagella "new?"

John,

The problem is that I previously gave you an example of a gene (D) that could resist >30 μg/ml of ampicillin, and its ancestral gene (A) that could resist ~5 μg/ml. Gene (D) has a function not shared with (A), survivial on >30 μg/ml of ampicillin. However, according to you D did not have a "new" function. This directly conflicts with your flagellum/TTCC argument, and you have not produced any criteria that distinguishes the examples.

If in your example, your ancestral gene (A) conferred ampicillin resistance at ~5ug/ml before its evolution. It then evolved through in vitro mutatgenesis and DNA shuffling to confer 30ug/ml resistance to ampicillin. It evolved from low resistance to higher resistance. I didn't consider it "new" because the requirement was that b-lactamase activity had to arise de novo to be "new". If the 30ug/ml resistance to ampicillin was shown to be b-lactamse activity, then I would call this "new" because no such activity was observed in the starting cells containing ancestral gene A. However, in this example we started with no b-lactamase and we also finished with no b-lactamase activity.

The criteria for this example is that protein A has no b-lactamase activity, and protein D does.

You are calling ampR by any mechanism the same function. I am making a distinction between ampR conferred by the Pyrococcus furiosus gene (we don't know what the biochemical basis is, but it's not b-lactamamse) a different function from that of b-lactamase (an enzyme that cleaves the antibiotic).

I think these examples each now have their respective criteria, defined by a specific biochemical function (or lack of that function).

Perhaps some IDer out there would be so kind as to tell me how ID explains the process by which major novel biochemical pathways (purine biosynthesis, blood clotting cascade) or complex molecular structures (flagella) arise, according to the much-vaunted (but never seen) scientific thbeory of ID? Pick one, any one, and show me how ID "theory" answers it. What, according to the scientific theory of ID, did the designer do to produce it? What mechanisms did it use to do whatever the heck the scientific theory of ID thinks it did? Where can we see any of these mechanisms ina ction anywhere today, doing anything at all? Or does ID "theory" simply boil down to "POOF!!!! God --- er, I mean, the Unknown Intelligent Designer --- dunnit!!!!!!", and are IDers simply lying to us when they claim otherwise?

John,

Are you certain that you want to say that each example has its own unique criteria for determing what is new? If that is true, then it is pointless to provide any examples to you of the evolution of novelty since only you know where the goal posts are.

Reed,

Yes, I am certain that I want to say each example has its own unique criteria for determining what is "new." I gave you those criteria for the two examples we have considered so far. Now, let's get to the mechanism of how these "new" functions evolve.

If you prefer to call them "not new," then let's get to the mechansim by which these "not new" functions evolve.

Lenny,
ID and evolution both suffer from the same problem. They both substitue "Poof" for "Proof." If we looked for an experiment that demonstrates ID, we would have the same problem that we are having now with finding an experiment to demonstrate evolution.

The problem here is, we have a truly stunning wealth of evidence that demonstrates evolution. We also have the "John posture": Evolution does not happen, so nothing can demonstrate it. Show me your best evidence so that I can deny that you've shown me anything.

Yes, I am certain that I want to say each example has its own unique criteria for determining what is "new." I gave you those criteria for the two examples we have considered so far. Now, let's get to the mechanism of how these "new" functions evolve.

— John

I imagine the ability to degrade DDE and nylon would not count?

ID and evolution both suffer from the same problem.

If we looked for an experiment that demonstrates ID, we would have the same problem that we are having now with finding an experiment to demonstrate evolution.

Joseph,
I couldn't find any papers on "nylonase" in Pubmed.
Could you post the reference you're referring to?

Was it this one below?

Negoro S, Ohki T, Shibata N, Mizuno N, Wakitani Y, Tsurukame J, Matsumoto K, Kawamoto I, Takeo M, Higuchi Y.
X-ray crystallographic analysis of 6-aminohexanoate-dimer hydrolase: Molecular basis for the birth of a nylon oligomer degrading enzyme.J Biol Chem. 2005 Sep 14; [Epub ahead of print]

Hey John, are you going to answer my simple questions, or aren't you?

What seems to be the problem?

Lenny,
You are right. We agree. ID theory does not offer any scientific explanation as to how any irreducibly complex systems arose. When you challenged anyone to come up with testable preditions based upon ID, no one did. I can't either.

All I am asking is whether evolution can meet the same challenge you posed for ID. I asked whether evolution can make predictions that can be tested with experiments. Do you know of any?

If not, we can continue to trade posts on how we both agree that ID offers no testable scientific predictions.

I asked whether evolution can make predictions that can be tested with experiments. Do you know of any?

— John

Now, let's get to the mechanism of how these "new" functions evolve.

— John

Reed,
I was hoping you were going to go on to suggest how these five forces could be applied in evolving a TTCC complex into a flagella. No?

Lenny,
I checked out the site to look for predictions made based upon evolution, which could be tested by experimentation.

http://www.don-lindsay-archive.org/creation/evo

The predictions listed aren't predictions in the usual sense, where you make predictions based upon a hypothesis and don't yet know the the outcome of the experiment.

They are more like explanations of how past events gave rise to present observations.

Are there any experimental predictions that evolution makes for events that have not yet occurred (fortelling a future outcome as opposed to a past outcome)?

John,

I'm spending the entire semester explaining the basics of these five forces to undergrads. I don't have the time to provide the same information to you on this blog.