You mean his definition of "theory" is the NAS definition of hypothesis, right?  Hypotheses are a part of science aren't they?

Not quite.  One would not teach all conceivable hypotheses in a science class, only those that have some reasonable body of evidence to support them.

How about as part of a "philosophy of science" class?

Absolutely.  ID would be an entirely appropriate subject in such a class, as well as many other types of classes.  It is a political and a religious subject, not a scientific subject.

Quote from: Broken

Behe's "irreducible complexity" argument is a useful critique of evolution. Behe has helped draw attention to the question of the evolutionary origin of the molecular machinery found in living organisms today. This is certainly not all his doing, but he has been a positive factor.

However, for each of Behe's irreducibly complex systems, a simpler system using the same proteins has been found. For the bacterial flagellum, the bacterial Type III Secretory System has many of the same protein components. In fact, for almost any type of flagellum,  similar systems exist with secretory functions or virilence (infection) functions.  

 Agreed, 'simpler' systems can be observed... but that's not the question that was asked, now was it? What has been  asked is whether a credible model exists which could demonstrate how these complex systems, which are irreducibly complex, could have possibly evolved?

"Irreducibly complex" means, by Behe's definition, a system which can not work if any component is removed. Behe's argument is that any such system would have to evolve all at once (it is irreducible), but since such a system is so complex, it is statistically impossible for any chance mutation to have produced it.

The counter-evidence to Behe's examples of irreducibly complex systems is that there are simpler systems which do perform useful functions and these systems use the same proteins as Behe's examples. So Behes systems are not irreducibly complex: the individual parts of his systems are indeed useful. So, the examples he gives did not have to evolve all at once, they could have evolved from simpler precursors.

For example, the vision biochemical pathway Behe considers "irreducibly complex" is made from a rhodopsin protein, a membrane protein, and a G-protein for signalling. All of these proteins, or very similar proteins, exist in systems performing other functions. So, the vision pathway arises from recombining existing protein modules into a new function. This is evolutionarily probable, whereas the entire system arising all at once is not.

 How does a complex system evolve, when you yourself have shot that concept in the foot by stating that genetic mutation, or 'deleted' genetic material, is actually what is observed?  Stating that some 'similar' systems exist is not in doubt, but all this amounts to is little more than hopeful speculation,  light years away from being a credible model of  explaining  how it occured.

I gave one very simple example of what is observed: a single nucleotide deletion. The are also single nucleotide insertions and single nucleotide replacements. There are many other more powerful means of genetic change. For example,

1) Genes and other strings of DNA are observed to be copied from one part of the genome to another.

2) Virus genomes are observed spliced into our genomes (and genomes of other species).

3) Duplicate copies of genes are often observed.

Mechanism 1 allows protein modules to be "reshuffled" into new configurations. Occasionally, some of these reconfigurations prove useful. The evidence for this is that the same protein modules show up in a multitude of proteins of unrelated function. The cause of mechanism 1 are genetic "parasites" called transposable elements which copy themselves from one place to another in the genome. Half of the human genome is made of these transposable elements.

Mechanism 2 allows viruses to bring new genetic material into a cell's genome. There are observed cases where the virus genes have been co-opted by the host organism to perform functions useful to the host. For example, humans can digest complex carbohydrates with their saliva because of a virus which implanted itself in the amylase gene.

Mechanism 3 allows two copies of the same gene to evolve down separate paths. For example, hemeglobin is made from two nearly identical protein modules.

As far as the missing genetic information in primates and humans, it is completely possible that an intelligent designer would realize that these species would be able to recieve vitamin C through dietary means. Wouldnt it in fact be redundant to have the ability to produce it?. You only claim it is a defect.

If an intelligent designer decided we and the apes did not need a vitamin C gene, why didn't he just leave it out altogether? Why give us the same vitamin C gene he gave all other mammals, and then break that gene? How does that make any sense?

Quote

 Is there empirical evidence to prove it was ever there in a common ancestor? Is there empirical evidence for a common ancestor?

The common defect is evidence of common ancestry. Very strong evidence, since it is difficult to come up with a plausible alternative.

 Difficult to come up with a plausible alternative, or just a plausible alternative that doesn't allow a Divine Foot in the door...?

If the broken vitamin C gene is the work of an intelligent designer, that designer looks rather unintelligent. Less intelligent than we humans, for example.

Quote from: Broken

However, for each of Behe's irreducibly complex systems, a simpler system using the same proteins has been found. For the bacterial flagellum, the bacterial Type III Secretory System has many of the same protein components. In fact, for almost any type of flagellum,  similar systems exist with secretory functions or virilence (infection) functions.  

"Irreducibly complex" means, by Behe's definition, a system which can not work if any component is removed. Behe's argument is that any such system would have to evolve all at once (it is irreducible), but since such a system is so complex, it is statistically impossible for any chance mutation to have produced it.

The counter-evidence to Behe's examples of irreducibly complex systems is that there are simpler systems which do perform useful functions and these systems use the same proteins as Behe's examples. So Behes systems are not irreducibly complex: the individual parts of his systems are indeed useful. So, the examples he gives did not have to evolve all at once, they could have evolved from simpler precursors.

Yes, I had a look at your Type III secretory system... Please tell me you're not serious! What possible connection can you make between this system and a  propulsion-system,which the flagellum is? As I have a little background in electromagnetic/motor theory,it is clearly evident to me what  the design and purpose of the flagellum is. If you are familiar at all with it's design, please tell me which part, if this is not a case of irreducible complexity, could be absent, and still allow this system to perform its funtion?  The argument that because this Type III system 1) Performs a function, and 2) uses the same proteins, so 3) this must be a precursory system is like arguing that 1) lawnmowers have parts that contain aluminum,and lawnmowers perform a function,
2) the Space Shuttle has parts that contain aluminum, therefore,
3)  lawnmowers are precursory to the Space Shuttle

Good try, Broken, but I believe this might have to go into the 'just-so-story' bin...

Sorry I took so long responding...

Did you in fact read the article on the Type III Secretion System (TTSS) I linked to? It was rather long, so let me sum up the major points.

The core proteins of the bacterial flagellum is a TTSS. To explain the evidence that the flagellum evolved from the TTSS, let me describe what the TTSS does.

There are many varieties of TTSS found in gram-negative eubacteria and some archea bacteria. The TTSS is used by bacteria to infect plants and animals, including us. For example, salmonella bacteria use a TTSS.

A bacteria forms a TTSS in a multi-stage process. First, roughly seven proteins collect at the bacteria's outer membrane and form a hollow baseplate and a hollow tube attached to the baseplate leading to the bacteria's surface. A second set of proteins then passes through the tube and assembles into a hollow needle which protrudes from the bacteria and contacts the target cell to be infected. A third set of "effector" proteins then passes through the needle and enters the host cell. The effector proteins attack the target cell and open it up so the bacteria can digest it.

To construct a flagellum, a bacteria again starts with a hollow baseplate and hollow tube leading to the bacterias surface. A second set of proteins then passes through the tube and forms the hollow flagellum filament. A third set of proteins attaches to the baseplate to form the motor.

So, the assembly process of the flagellum and TTSS are highly similar. The proteins of the baseplate and initial tube are highly similar. The staging of the assembly process is highly similar. Both systems assemble a hollow tube projecting from the surface of the bacteria. The proteins for both the flagellum and the TTSS are escorted to the baseplate tube using the same "chaperone" proteins.

The difference between the two systems is that the flagellum has motor proteins for mobility and the TTSS has effector proteins for infection. However, bacteria with flagellum can also infect cells. In fact, they need the flagellum to attach to the cells they are targetting. This has been shown by mutating the flagellum genes so no flagellum is grown. Bacteria missing flagellum cannot infect target cells, even if they are in contact. The fact that flagellum still have infection function is further evidence that they are related to the TTSS infection system.

It would appear that the major event in evolving flagellum from the TTSS is the attachment of a motor to the TTSS base. Is the motor, by itself, irreducibly complex? This is somewhat difficult to answer since the exact structure of this motor is still unknown. However, it is known to be a ring structure proton motor, with a stator and a rotor like a man-made electrical motor. Are there other bacterial motors similar to this ring-structure proton motor?

The most similar proton motor is F1F0-ATP synthetase. The rotor of this motor is highly similar to the flagellum rotor. Furthermore, F1F0-ATP sythetase has many homlogous structures with the TTSS, which appears to use F1F0-ATP sythetase structures to push the export proteins up the TTSS needle. So it would appear that proton motor components had already been co-opted by the TTSS.

In any case, the evidence is strong that the flagellum and TTSS have a common ancestry. Since the TTSS has fewer parts than the flagellum, it is clear that the flagellum is not irreducibly complex, but can be reduced to a TTSS and a proton motor (possibly F1F0-ATP synthetase), both of which have useful biological function.

*

I notice you did not answer my questions on the ID explanation for the vitamin C mutation common to humans and apes. Are you admitting that there is no answer?

Here is another question for you. Presumably, the Designer designed bacteria and viruses along with everything else. What is their purpose? Furthermore the Designer gave us defenses against these same bacteria and viruses. And then He gave the disease organisms counter-measures against our defenses. And then gave us counter-counter-measures. Why would the Designer be "playing both sides of the chess game", so to speak?

Yes, I read your link, Broken. Has it been demonstrated in any laboratory to be possible? I understand that a flagellum has only 30-40 genes, so why hasn't anyone done it using a suitable bacterium?

Done what in the laboratory? Quite a bit is known about bacterial flagellum from laboratory experiments, but there are still quite a few unknowns about the details of the motor operation, gene regulation, the assembly process, and how the flagellum helps the bacteria infect other cells.

 Let me ask you this in regards to the vitamin c issue... how would natural selection explain an apparently disadvantageous mutation like loss of vitamin c production in some primates and humans? Kind of goes against the grain, doesn't it?

Apes and humans have a lot of vitamin C in their diet since they eat fruits and vegatables. They don't need to produce it internally, unlike carnivorous mammals (for example). Vitamin C deficiency (scurvy) is quite rare, unless you spend prolonged time at sea. Therefore, the vitamin C gene is unnecessary for survival. Unnecessary genes degenerate, since there is no selective pressure to retain them. So, what is the ID explanation?

Here is another ID puzzle for you. Why would the Designer use viruses to design humans?

Here is an example. Most mammals can only digest complex carbohydrates in their intestines, since the necessary enzyme, amylase, is only produced in the pancreas.

On the other hand, primates (humans and apes) produce amylase in their salivary glands, allowing them to digest complex carbohydrates much more quickly than other mammals. Now, the salivary gland and the pancreas are closely related, both being glands in the digestive tract. What is different about humans and apes that activates the amylase gene in their salivary glands?

Researchers found that the amylase gene in primates has a virus genome inserted in the gene regulator. This virus is what has changed amylase gene regulation so the gene is turned on in both the salivary gland and the pancreas. Primates have acquired a genetic advantage due to a fluke viral infection.

What is the ID explanation for this? Does the Designer use viruses to do His handywork?

Look, Broken, nobody's arguing the fact that mutations do exist, they are seen all the time. But mutations cause a loss of genetic material, not an addition to it. So how do you then get from a simple organism to a far more complex one via loss of genetic code? If it could be observed to occur on a large scale basis in nature,IC and  ID would be dead in the water.

Quote from: 8d82thebone

Look, Broken, nobody's arguing the fact that mutations do exist, they are seen all the time.

Let me rephrase what I said.

What is the probability of the exact same mutations showing up in in exactly the same genes in all primates by random chance? Basically, zero.

If you want to get into odds, that's up to you... what are the random chances of a single functoning protein forming on its own? Less than zero; but if it suits your argument, then of course all of a sudden it becomes a fact...

And again, no one is arguing that genetic information can change within a species. Microevolution falls short as a suitable explanation for how life appeared in the first place. I watched an interview where Richard Dawkins was asked whether he could name a single instance where an increase in genetic information was known to have been responsible for the appearance of a new species, and he was basically left speechless. That says it all to me.

Needless to say, Dawkins now checks the credentials of those who ask to interview him.

I don't understand.  Why do the credentials of the person asking the question matter?

Quote from: Broken

Quote from: 8d82thebone

Look, Broken, nobody's arguing the fact that mutations do exist, they are seen all the time.

Let me rephrase what I said.

What is the probability of the exact same mutations showing up in in exactly the same genes in all primates by random chance? Basically, zero.

If you want to get into odds, that's up to you... what are the random chances of a single functoning protein forming on its own? Less than zero; but if it suits your argument, then of course all of a sudden it becomes a fact...

You are confused. Evolution does NOT address how life got started. Evolution does NOT address how life got started. Evolution does NOT address how life got started. Got that?

If you wish to discuss hypotheses on the origins of life, we can do that, but I suspect you of trying to divert attention from the serious flaws I pointed out in ID.

I have answered your critiques of evolution for several posts now. You have not answered a single one of the contradictions I pointed out in ID theory. Your turn to defend your position.

How about the virus which improved a gene example? Or the vitamin C gene mutation example? Or the question of why the Designer would design both disease organisms and the defences against them and the countermeasures to these defenses? Are you just another typical Creationist who ignores all information which contradicts your POV?

And again, no one is arguing that genetic information can change within a species. Microevolution falls short as a suitable explanation for how life appeared in the first place. I watched an interview where Richard Dawkins was asked whether he could name a single instance where an increase in genetic information was known to have been responsible for the appearance of a new species, and he was basically left speechless. That says it all to me.

You must not have read my last post where I listed (for the second time) three different mechanisms whereby genetic information increases. All of these mechanisms are experimentally observed.

If you want more clarification on how these mechanisms work, or you disagree that these mechanisms add genetic information, then I would be glad to discuss it. If you are simply going to ignore all information which disagrees with your point of view, then we really don't have much to talk about.

In terms of protein evolution and the origin of life, I have studied these areas extensively and would be happy to discuss them with you, but we should start a new thread on "life origins", since this thread is about ID and evolution. Let's stick to the subject.

You are confused. Evolution does NOT address how life got started. Evolution does NOT address how life got started. Evolution does NOT address how life got started. Got that?

Hey, sntjohnny, who does Broken sound like here?  I'll give you one guess.