Design inference

Then, the aliens pull out a picture you drew for your mother and hold it up next to the bacterial flagellum, and ask you the same question.

If one thing is more likely to have evolved than another thing, that is an evolution inference.

"But that is a concession that it is possible to infer design."

Can you name anyone who has claimed that it's not possible to infer design?

I say the beak because birds are cuter than E. coli. And because we'd never suspect it. Cagey, those aliens.

You don't think Dembski understands that all design inferences are not equally strong?

Gentlemen,

Darwin's only success was to convince a few devotees that natural selection affected evolution in such a way as to produce novel biological forms. Natural selection before Darwin was seen as a process that actually conserved organismal form (see for example the work of Edward Blyth). I don't think anyone has proven contrary to the early view. In fact, the modern synthesis has done more to convince us of the limitations of evolution, than to convince us of its power of producing entirely new organisms.

Think about it. If genetic entropy coupled with blind selection mostly depletes the informational content in the genome, how can we get new functions. What we need is incremental information, not its degradation. Design theory is very effective in showing why large amounts of information cannot be purchased without intelligence. If, in fact, we can get complex specified information from a totally serendipitous process, then please provide some empirical examples.

Thank you.

Well, it has been very difficult to locate mutations that actually increase the informational content in such a way that it produces novel biological functions. I don't know of one, do you? Perhaps "mostly" is too strong of a word.

My second assertion is perfectly consistant with evolutionary theory. To say that it is a "serendipitous" process is to say that it is a process that does not have any teleology. It is a process that presumably produces "beneficial" effects through the blind selection of randomly occuring mutations. Yup! Pretty "serendipitous," I'd say.

Hello Hawks,

Well, for starters you cannot simply assert that point mutations will increase information. More clearly, indels cause frameshifts which deplete the genome content and substitutions simply "substitute" nucleotide bases (with some reversion), but may also deplete the information content.

You may try gene duplication, but you must keep in mind that they (the duplicates) are also subject to the same mutational effects as any other genes. Moreover, it may only be considered an increase of information if, in fact, the content produces some functional divergence (more on this below). In this sense, it is perfectly acceptable to use gene duplication as proof for the increase of information. As long as the genes are able to attain selectable properties after a number of mutations, it is perfectly fine. However, if we are to invoke major morphological divergence from polyploid organisms, we should be able to see changes at a much faster rate than what Darwin envisioned, and the changes must always confer an entirely new function.

Let me give you an example, or two. Myoglobin and hemoglobin have been said to be tied by gene duplication (i.e. hemoglobin deriving from a duplicate of myoglobin). However, their basic function (i.e. oxygen transport) remains the same, mainly due to regulatory constraints. Should this be considered an increase of information? Hmmm. There is another example that comes to mind. That is, there are some enzymes produced through gene duplication that are capable of breaking down dietary RNA within higher acidity levels in our small intestine. However, these too acquired the same function as the original enzymes. Why? Aren’t mutations supposed to change the basic function of these? Can we call this an increase of information, or simply an adaptation (preservation of the species)? You decide.

Thank you for the clarification on "serendipity." However, how is something you stumble into by accident supposed to be "teleological" (purposeful/goal-directed)?

Cheers!

What you have here is a silent mutation that reverts back to it original function. This happens all of the time, and always before the mutations confer selectable properties. No. This is not an increase of information.

Well, information cannot simply be measured by the increase of alleles in a genome. There must be novel functions, if we are to get the sort of gradations that Darwin envisioned in the history of life.

Think of it this way: If you have "duplicates" acquiring the same function as the original, how is that helping to bring about "successions" of biological form?

The reason I asked these questions is because, depending of the ID supporter, vastly different types of evidence is required. Some will not accept any form of bioinformatics, whereas perhaps you will (judging by your example of hemoglobin/myoglobin)??? In that case, would examples of what looks like genes having swapped domains with eachother suffice? I know of at least a few people who would say that this is not an increase in information, simply because there has just been a rearrangement of existing information, even though the resulting gene product has novel functionality.

I have encountered several people saying that the the direct observation of a new function occuring is an absolute must; some even claim that simple point mutations are not even an example of evolution but rather is a sign of fore-sight of the organism in question (meaning that the organims already possessed the information somehow anyway(?)). In these cases, showing evidence would be VERY difficult and impossible respectively.

So, when I wasking asking what you would consider evidence, what I really meant was what lines of evidence you would consider valid. Bioinformatic? Direct observation? Others?

As for serendipity - I´ve had myself thouroughly confused more than once! I think I know what you meant...

I will try to respond to the last three posts here.

TRoutMac wrote:

we just might find that precise correlation… that the more complex the organism, the more genetic information required.

Kind of thinking out loud here. Would someone care to expand on that?

Yes. More complexity requires larger genomes. To be sure, metazoans require more information to control all of the biochemical processes of multicelularity, while protozoans need only to worry about one cell, namely, itself.

Hawks wrote:

So, when I wasking asking what you would consider evidence, what I really meant was what lines of evidence you would consider valid. Bioinformatic? Direct observation? Others?

Direct observation is not necessary since duplicates can be easily spotted. Like I said, functional divergence is a must!

As for "bioinformatics." I am not sure how they can help unless you have an empirical factor to attribute the data to. It's all great in print, but can it be extrapolated from reality? Probably not.

Patrick wrote:

There is actually a bacteria that has a genome several times larger than a human's genome (I forget the name at this moment). Problem is, based upon research on those pesky voles we know we still have a lot to learn about this vastly interconnected system.

That may be the case, but a larger genome must be characterized by additional functions, otherwise you're probably just talking about polyploidy.

Many blessings--

Hello Kelloseppa,

Actually, frameshifts always cause a fitness cost on the bacteria. The focus of the article is on the advantage it aquired, but missed to say anything about the effect on the original code. The framshift could have caused the bacteria to have difficulty metabolizing other things, and yet acquire the ability to break down nylon. The fitness cost IS a loss of information, even when it acquires new information. Moreover, remember my example above. It is no different from what the nylon bug is doing. I said:

"There is another example that comes to mind. That is, there are some enzymes produced through gene duplication that are capable of breaking down dietary RNA within higher acidity levels in our small intestine"

Does this lead to larger morphological change? Like turning this bug into a metazoan? Well, No.
cheers!

The protest appears to be identical to this line of reasoning:

Since sealiving creatures evolved to live on land, but lost the ability to live in the sea, no evolution has happened.

Or

Since bird's wings give it the ability to fly, but they lost their ability to grasp with their fingers, no evolution has happened.

Or

Humans may have evolved from ancient ape-like creatures but they are still primates, therefore no new information has arisen.

Just to be clear.

And:
"Does this lead to larger morphological change? Like turning this bug into a metazoan? Well, No."

I wasn't aware morphological change was necessary. You talked about novel functions. If you originally meant also morphological changes then, my bad.

Mario:
As for "bioinformatics." I am not sure how they can help unless you have an empirical factor to attribute the data to. It's all great in print, but can it be extrapolated from reality? Probably not.

I'm not sure I understand exactly what you mean by empirical factor. Care to elaborate?

Functional divergence requires more than going from breaking down one type of material to another, and losing robustness in the process. The basic function of metabolism remains unchanged, and the original function suffered a fitness cost.

The article on the Nylon bug acknowledges this much:

This is a fitness cost and degradation of information; even when acquiring a selective advantage.

Why would a new metabolic function not be considered a new function? What I am missing here? Also, there is hardly a fitness cost if there is a selective advantage. By definition, selective advantage=higher fitness.

First of all, my apologies for taking so long to respond. High work load and a forgetful mind are the main contributors responsible.

Mario: Sure thing. Bioinformatics deals with a lot of things. What I am concerned with here is with algorithms to come up with some evolutionary mechanism that increases genomic information. If you can produce such computation, you are going to have to show how it can be reproduced in a lab.

When I was talking about bioinformatics I was more thinking along the lines of comparative genetics. I.e. would the comparison of published sequence data from different organisms count as evidence?

Me: Why would a new metabolic function not be considered a new function? What I am missing here? Also, there is hardly a fitness cost if there is a selective advantage. By definition, selective advantage=higher fitness.

Mario: A metabolic function is a metabolic function, not a "new" function. Therefore, no functional "divergence."

You've lost me here. Are you saying that a new metabolic function is not a new function?

The fitness cost is that the organism loses most of its metabolic function simply to acquire the ability to breakdown one type of material, nylon. Furthermore, it is very unlikely that it could survive in its original environment (i.e. one without nylon). The selective advantage is simply an advanatage selected for within that particular environment. Its fitness is--therefore--limited and null.

Either I'm misunderstanding your writing, or you're misunderstanding certain concepts.

If an organism has a selective advantage in a certain environment then it has higher fitness in that environment. The fitness might be limited to that environment but it is still an increase in fitness since it now does better in that environment than it used to (i.e. NOT null).

Please also note that when a micro-organism gains a new metabolic function, it does not follow that the only organisms that will be able to take advantage of it are the organism itself or it's descendants. Horizontal gene transfer is rife among prokaryotes. So, even if an organism should loose some functionality to gain a new one, this new trait can transfer to other organisms (the donor and recipient don't even have to be closely related).

Mario: We cannot simply assume that random mutations increased genomic information.

So, back to the original question. What would you consider to be evidence of "mutations that actually increase the informational content in such a way that it produces novel biological functions"? You brought up hemoglobin and myoglobin as an example of gene duplication, but like sequence data from divergent organisms, YOU should not simply assume that mutations created these from a common gene ancestor (this is your reasoning, I take it?). So, apart from direct observation, is there any other line of evidence?

Me: You've lost me here. Are you saying that a new metabolic function is not a new function?
Mario: Indeed. It was a metabolic function to begin with.

Eeeeer? So, let's for arguments sake say that we have an ancestral population of organisms that could only metabolise substance x as a food source, and whose descendants can metabolise x, y and z. Are you saying that the descendants have not acquired any new functions? What is your definition of function?

It simply aquired the ability to break down nylon, while losing 50% of its original function to break down other things. Again, this is a fitness cost. Not gain. It is adapted to the nylon environment, but with a 50% loss of metabolic function. It's sort of like trading a dollar for two quarters.

No it's not necessarily a fitness cost. If it gains fitness in one environment that it has gained fitness. Instead of just being able to live in environment x, some of the bugs can now live in environment y. I.e. we started with one population of bugs that could only live in x. After a mutation, we have two populations. One can live in x. One can live in y. That is NOT a cost.

You are missing the point. Yes, it can break down nylon, but "loses" 50% fitness. Its like humans aquiring the ability to eat a bar of soap, but losing the ability to eat anything else. It loses fitness because now it is limited to that ecological niche, while before it was not.

If an population of organisms can sustain themselves in a "niche" better than their ancestors could (which in this instance was NOT AT ALL) then it has definitely gained fitness - BY DEFINITION.

It does not aquire a "higher" function.

Care to give your defintion of function?

I agree. However, an increase of information requires that no information is lost. In the case of the nylon bug, information was lost, making the minor advantage null.

Might be that the ONE organism "lost information". But you now have TWO functionally divergent populations instead of one. On a grand total, no information was lost. It was a gain in the ability for a new metabolic function. And as I said, prokaryotes (especially) are very prone to exchange genetic information, so it is not a stretch of the imagination to state as a possibility that organisms will arise that can do both old and new functions.

Thank you TRoutMac,

Good illustration.

Hawks in bold:

So, back to the original question. What would you consider to be evidence of "mutations" that actually increase the informational content in such a way that it produces novel biological functions"? You brought up hemoglobin and myoglobin as an example of gene duplication, but like sequence data from divergent organisms, YOU should not simply assume that mutations created these from a common gene ancestor (this is your reasoning, I take it?). So, apart from direct observation, is there any other line of evidence?

Sure. Like I said, if you can provide a sequence that has a duplicate that has diveged from its original function (and acquiring a new one, of course) without interrupting the original code, then you have more info.

Eeeeer? So, let's for arguments sake say that we have an ancestral population of organisms that could only metabolise substance x as a food source, and whose descendants can metabolise x, y and z. Are you saying that the descendants have not acquired any new functions? What is your definition of function?

Well, I guess the easiest way to put is that a function is really a "role." In this case, the role of the enzymes are to metabolize. The enzymes did not acquire a novel role, they assumed the same role "having only 2% of the efficiency of the regular enzymes" and "don't work at all on the bacterium's original food" (i.e. carbohydrates). Moreover, it did not go from metabolizing x to metabolizing x, y, and z. Quite the contrary, it went from metabolizing x, y, and z to metabolizing x (=fitness cost).

No it's not necessarily a fitness cost. If it gains fitness in one environment that it has gained fitness. Instead of just being able to live in environment x, some of the bugs can now live in environment y. I.e. we started with one population of bugs that could only live in x. After a mutation, we have two populations. One can live in x. One can live in y. That is NOT a cost.

Indeed it is. If you want to get more complexity, you cannot go backward in fitness. The bug went from 100% efficiency to 2%. How can this not be a "cost?" The fact that one moved out of town (ecological niche) does not necessarily mean it is a story of fortune or success.

If an population of organisms can sustain themselves in a "niche" better than their ancestors could (which in this instance was NOT AT ALL) then it has definitely gained fitness - BY DEFINITION.

Who's definition? (Analogy) Would you trade a dollar for 50 cents?

Care to give your defintion of function?

I like "role."

Might be that the ONE organism "lost information". But you now have TWO functionally divergent populations instead of one. On a grand total, no information was lost. It was a gain in the ability for a new metabolic function. And as I said, prokaryotes (especially) are very prone to exchange genetic information, so it is not a stretch of the imagination to state as a possibility that organisms will arise that can do both old and new functions.

Sure, but you still need additional information to get both functional divergence and morphological divergence, otherwise you will have bugs no matter how many populations adapt to new environments. This is precisely why natural selection is excellent to explain the preservation of species.

Sure. Like I said, if you can provide a sequence that has a duplicate that has diveged from its original function (and acquiring a new one, of course) without interrupting the original code, then you have more info.

Well, here's the problem. I still don't know what kind of sequence you would accept as evidence. Would a comparative genetic approach do it (for perhaps organisms that are not closely related)? Would the creation of the sequence have to have been observed in a lab?

Well, I guess the easiest way to put is that a function is really a "role." In this case, the role of the enzymes are to metabolize. The enzymes did not acquire a novel role, they assumed the same role "having only 2% of the efficiency of the regular enzymes" and "don't work at all on the bacterium's original food" (i.e. carbohydrates). Moreover, it did not go from metabolizing x to metabolizing x, y, and z. Quite the contrary, it went from metabolizing x, y, and z to metabolizing x (=fitness cost).

I wasn't talking about any specific examples here. I'm trying to find out what you mean specifically when you say new information and function. So, hypothetically, if a population of organisms that could only metabolize x creates descendants that 1) still only can metabolize x, 2) can metabolize x and y and 3) can only metabolise y and z, would the now three populations not have more information and functions?

Who's definition?

Fitness is all about reproductive capability. For a new environment, an organism has gone from zero to more-than-zero fitness. That is an increase in fitness.

Sure, but you still need additional information to get both functional divergence and morphological divergence, otherwise you will have bugs no matter how many populations adapt to new environments. This is precisely why natural selection is excellent to explain the preservation of species.

When did the morphological divergence come into play?

Hawks, the thrust of my point with the mutation generator was to illustrate what we mean by an "increase" in information, and what that would look like in a more familiar language system.

It may not be a good example in the sense that you remain convinced, it would seem, that information can arise by chance and you persist in viewing natural selection as a mechanism which makes macro-evolution possible, rather than seeing that natural selection is actually an obstacle to macro-evolution… it preserves and confines the form and function of species.

In this sense, ID advocates have more respect for the reality of natural selection than even Darwinists do. Ironic, isn't it?

I believe most if not all ID proponents would never have any problem accepting any instance of micro-evolution. So I could be wrong but everyone is probably assuming macro-evolution is under discussion here. I'm also assuming that everyone is equating macro-evolution to significant "increases in information and function" that would contradict ID. The argument is over what constitutes "significant".

While information might be created by chance, it is the non-chance mechanism of selection that preserves it.

You do understand why selection isn't an issue when it comes to a Direct Darwinian Pathway creating IC? (Or at least it's not an issue until the IC structure is functional and provides selection benefit.)

You guys might find this statement by professor Allen Macneill interesting:

Q: "Do the "engines of variation" (EvoDevo, etc) provide sufficient variation to move beyond microevolution to macroevolution."

A: This is indeed the central question. One of the central tenets of the "modern synthesis of evolutionary biology" as celebrated in 1959 was the idea that macroevolution and microevolution were essentially the same process. That is, macroevolution was simply microevolution extrapolated over deep evolutionary time, using the same mechanisms and with essentially the same effects. A half century of research into macroevolution has shown that this is probably not the case.

Allen then went onto explain the different mechanisms or "engines" he thinks "might" provide the answer but at the same time he admits "we know surprisingly little [about these mechanisms]...[but] we are learning an immense amount at present." In short his hopes lie in the unknown. Allen is not only a Darwinist but an atheist or an agnostic. This new line of research may or may not support his beliefs, but he's hopeful.

I believe most if not all ID proponents would never have any problem accepting any instance of micro-evolution. So I could be wrong but everyone is probably assuming macro-evolution is under discussion here. I'm also assuming that everyone is equating macro-evolution to significant "increases in information and function" that would contradict ID. The argument is over what constitutes "significant".

It MIGHT be true that macro-evolution requires increases in information and function. But from there, it does in no way follow that increases in information and function must lead to macro-evolution. Your assumption is wrong - so the one doing goalpost-shifting here is not me.

You do understand why selection isn't an issue when it comes to a Direct Darwinian Pathway creating IC? (Or at least it's not an issue until the IC structure is functional and provides selection benefit.)

Since when did irreducible complexity come into the discussion. Moving the goalposts again, are we?

I'm a bit confused here. When I preview my posts, other peoples comments that I've copied (and put in cite tags) appear italizised. They obviously don't when I post them. Why?

It MIGHT be true that macro-evolution requires increases in information and function. But from there, it does in no way follow that increases in information and function must lead to macro-evolution. Your assumption is wrong - so the one doing goalpost-shifting here is not me.

My response (borrowing heavily from Eugenio Darbesio in order to save time):

Macro-evolution is the creation of novel cell types, tissue types, organs, and body plans. The boundary point between micro and macro evolution is that microevolution doesn't need new CSI and instead macro evolution does need new CSI. ID theory was developed exactly to clarify this basic distinction. The fundamental concept of ID is indeed CSI and CSI is what serves us to do the micro-macro distinguishing.

Microevolution implies only the tuning or trigger of some pre-existing parameter or function of pre-existing systems. Instead macroevolution implies the arise of entire new biological systems. In engineering it is very easy to understand the difference between tuning a parameter and to design (and construct) an entire new system. If you ask me to change the background color or the size of the tables of the DNA Random Mutation Simulator that's a one-minute job. If you ask me to develop a new Matlab that's a many year-man job. Darwinists don't see the difference because they haven't to design the biological systems but to look at them only. To look is easier than to design.

The transitions from fish to amphibian to reptile to mammal involve new CSI because, for instance, an arm or a leg are apparatuses fully different from fin.

Conceptually the CSI necessary for new systems MUST come from somewhere. If this CSI pre-exists in the ancestor then we speak of "front-loading".

If this CSI doesn't exist in the ancestor then it must be injected
top-down by an intelligent cause. There's always the possibility of a self-modifying system that takes core components and monitors changes but that doesn't have much evidence at this moment... There are no other rational choices. In fact the Darwinian "third way" (RM + NS) is a nonsense insofar as knowledgeable Darwinists rightly say that random "mutations are virtually always deleterious". Fusion events such as those posited by Margulis are interesting and so is EvoDevo as a whole but we're still looking for a plausible mechanism which hasn't been found. Hence the choice is between front-loading and top-down separated design.

Now you could attempt to argue that an indirect Darwinian pathway could take pre-existing mechanisms and recombine them into a new novel whole with a different function (like if you were to take a bunch of spare parts from a car and make something used in an airplane). But even that would require the rise of some new information in the information regulating construction and would be considered macroevolution. Your attempt at redefining the core point of disagreement is precisely why you are the one doing the goalpost-shifting.

Since when did irreducible complexity come into the discussion. Moving the goalposts again, are we?

We're discussing ID and the rise of new information in biology. IC is part of ID. You stated that the mutation generator was a bad example and I clarified. Your response indicated you didn't comprehend my clarification. Selection isn't some magical wand you wave around to make the problem go away.

You appear to want to win this argument via semantics wrangling and by force-fitting everything into a little logical bubble that rejects related subject matter.

I'm a bit confused here. When I preview my posts, other peoples comments that I've copied (and put in cite tags) appear italizised. They obviously don't when I post them. Why?

Block quotes don't work either. I don't know if or when they'll be fixed. In the meantime I've been editing your comments to bold people you're quoting.

You do understand that the bug needed to be exposed to the new "niche" before it needed to adapt to it, right? That is referred to as an environmental pressure.

Yes. That is what I wrote.

Now, regarding fitness and functions:
The only reason that we are talking about fitness (that makes any sense) is whether or not a certain trait can be sustained through selection. If the trait gives sustainable reproductive success then it will be maintained in a poulation. So, even though the loss of trait x gives a loss of fitness in environment z1, the acquisition of trait y gives a gain in fitness in environment z2. Trait y is then maintained in z2. Futhermore, trait y is a new metabolic function, ie it can metabolize something which it's ancestor could not. Since you are trying to tell me that a new function is not a new function, you are going to have to tell me what a new function actually is. Role says nothing more than function. My example where an organism effectively gains y on top of x obviously doesn't cut it. What will?

Comparing sequences is not enough, remember that similar sequences can derive from entirely unrelated organisms, and furthermore, may confer entirely different functions.

That is a very interesting point coming from an ID proponent, especially from you in this discussion. You have been claiming all along that new functions can't arise, and yet you maintain that even similar sequences that have entirely different functions. Wouldn't that make it easy for mutations and selection to acquire new functions?

Yes. That is what I wrote.

No. Here is what you wrote:

"I never claimed that the novel information arose because of divergence to a new niche. I claimed that a mutation caused new functionality which allowed for adaptation to a new niche. This led to two populations, each having different functions - one of them having a new one. Again, I was not talking about any specific examples. This was a hypothetical, so the talk about frameshift is largely irrelevant."

In the bolded sentence, it appears as though you are saying that the mutation "caused new functionality" which then "allowed for adaptation to a new niche." What I am saying is that an organism must first be exposed to the ecological niche where it will (from that point) reside. In other words, the mutation resulted from exposure to the new environment, not the other way around.

Now, regarding fitness and functions:
The only reason that we are talking about fitness (that makes any sense) is whether or not a certain trait can be sustained through selection. If the trait gives sustainable reproductive success then it will be maintained in a poulation. So, even though the loss of trait x gives a loss of fitness in environment z1, the acquisition of trait y gives a gain in fitness in environment z2. Trait y is then maintained in z2. Futhermore, trait y is a new metabolic function, ie it can metabolize something which it's ancestor could not. Since you are trying to tell me that a new function is not a new function, you are going to have to tell me what a new function actually is. Role says nothing more than function. My example where an organism effectively gains y on top of x obviously doesn't cut it. What will?

Again, I am not negating the fact that the organism can live in its new environment. But "fitness" can only be measured in comparison to the reproduction rates and efficiency of the parent species. If the rate and efficiency is diminished, it is considered a "cost." If by "fitness" you mean "the ability to survive and reproduce in a different environment," then you are talking about a different mechanism of evolution (i.e. speciation).

I have already explained what I mean by functional divergence here:

"...some contend that hemoglobin is an ancient paralog of myoglobin, but even if it were true, why doesn't the new sequence diverge from its basic function (i.e. oxygen transport)?"

and here:

"...I guess the easiest way to put is that a function is really a "role." In this case, the role of the enzymes are to metabolize. The enzymes did not acquire a novel role, they assumed the same role "having only 2% of the efficiency of the regular enzymes" and "don't work at all on the bacterium's original food" (i.e. carbohydrates). Moreover, it did not go from metabolizing x to metabolizing x, y, and z. Quite the contrary, it went from metabolizing x, y, and z to metabolizing x (=fitness cost)."

In other words, The "role" to metabolize did not change into a different biochemical reaction.

Enzymes can be classified by the kind of chemical reaction catalyzed.

Addition or removal of water

1. Hydrolases - these include esterases, carbohydrases, nucleases, deaminases, amidases, and proteases
2. Hydrases such as fumarase, enolase, aconitase and carbonic anhydrase

Transfer of electrons

1. Oxidases
2. Dehydrogenases

Transfer of a radical

1. Transglycosidases - of monosaccharides
2. Transphosphorylases and phosphomutases - of a phosphate group
3. Transaminases - of amino group
4. Transmethylases - of a methyl group
5. Transacetylases - of an acetyl group

Splitting or forming a C-C bond

1. Desmolases

Changing geometry or structure of a molecule

1. Isomerases

or

Joining two molecules through hydrolysis of pyrophosphate bond in ATP or other tri-phosphate

1. Ligases

What I contend is that there is no functional divergence from the ability of the enzyme to break down material through a hydrase catalyctic reaction, to say, the transferring of a radical.

I hope this is clear now.

So far we have learned that:

1. The bug went from 100% efficiency to 2% effciency to metabolize.
2. The bug lost genetic info. as a result of a frameshift.
3. The bug has a lower reproductive rate and efficiency.
4. The bug cannot survive amongst the parent species.
5. The bug acquired no functional divergence.

I am not sure how much further we can push this discussion, but I think you may need to perform some serious semantic acrobatics to contend for an "increase" of information.

That is a very interesting point coming from an ID proponent, especially from you in this discussion. You have been claiming all along that new functions can't arise, and yet you maintain that even similar sequences that have entirely different functions. Wouldn't that make it easy for mutations and selection to acquire new functions?

That is the point of this discussion. Can natural mechanisms produce new information and novel biological functions?

That is not a problem for ID. Quite the contrary. When you see large amounts of information appear in the history of life (such as the emergence of single-celled organisms, and then the sudden appearance of multi-cellularity), you must assume a mechanism that represents the effects of chance and natural law, or the effects of teleology. It seems to me that nature is recalcitrant in organizing into complex and specified patterns, unless acted upon by an external force (i.e. intelligence).