Discussions concerning the concept of irreducible complexity (IC) are quite common and usually involve some confusion about the definition of IC. The following question posed by "sds" sparked my interest.
"sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message <news:bbcj98$t4d$1@slb6.atl.mindspring.net>... > Do you believe is it possible to show that an object or mechanism has an > intelligent origin? Take the mousetrap again (for which I understand you > *don't* find "irreducibly complex" to be a meaningful characterization). > Can we show that a mousetrap probably could not exist without some > intelligence to design it?
It seems to me that the concept of IC is quite helpful indeed. The problem is that many, even Behe himself, seem to try to limit the definition of IC to "very complex" systems of function in order to show that IC systems cannot evolve.
As I see it all systems of function are IC. It is just that some systems are more simple than other systems of function. There is a spectrum of complexity, but all systems along this spectrum from simple to more and more complex are all IC. In other words, not all setups of a given number of parts or part types will be able to perform a given function. The parts in any system of function can in fact be altered, removed, or ordered in a different manner so that the function of the system is completely destroyed. In fact, there are vastly more non-functional potential arrangements of parts than there are beneficially functional arrangements of parts in a particular scenario.
Take, for example, Behe's famous mousetrap IC illustration. Many try to argue that a mousetrap is not IC since parts can be removed or changed and it still can catch mice. That is not the issue. If you change the mousetrap, it may still catch mice, but not in the same way. The changed mousetrap is a different mousetrap that catches mice in a different way. Certainly there are many different kinds of mousetraps that can catch mice, some more effectively than others. However, all of these mousetraps are dependent upon a certain number of parts that are all arranged in a very specific way in order for these parts to work together to catch mice (i.e., To perform their function). Clearly there are a lot more arrangements of mousetrap parts for any given type of mousetrap that would not catch mice at all. All mousetraps can in fact be reduced or changed in a way that would destroy their function completely. And, these potential non-functional mousetraps are far more numerous than those comparatively few arrangements than can actually perform the mouse catching function.
Of course, it is theoretically possible to arrange several of these working mousetraps in sequential order so that very small steps seem to exist as one moves from one type of trap to the other. Obviously then, it is NOT impossible for IC systems to evolve via function-based selection mechanisms since such an evolutionary path need not necessarily cross wide neutral gaps in function or non-function. The problem is that these gaps are often wider than one might initially think.
Even functions that are based on the workings of single proteins, such as the enzymatic functions of lactase or nylonase, are IC in that there are a limited number of parts that are required to give rise to that particular type of function. For more simple functions, such as these single-protein-based functions, there might be a much higher ratio of sequences of a given length or smaller that would be able to perform a given function, like the lactase or nylonase function. For example, given a sequence of amino acids 1,000aa in size, there are about 1 x 10e1300 different possible protein sequences. This is an absolutely huge number of different possibilities. It is a 1 with 1,300 zeros following it. Out of all of these possibilities, how many would have the lactase function? Certainly there would be many of these sequences that would have the lactase function, but certainly not all of them or even most of them. Perhaps the ratio would be as high as 1 in a trillion? If the ratio where 1 in a trillion, that means that any given functional lactase AA sequence would be surrounded by an average of 1 trillion non-lactase sequences. If a particular functioning lactase sequence is changed or "reduced" beyond a certain point, it will no longer function at all, not even a little bit. This is the definition of IC. The lactase function, even though based in the AA sequence of a single protein, is IC. Of course, compared to other systems of function, the lactase and nylonase single protein enzymes are not all that complex since there are is a relatively high percentage of potential lactase sequences as compared with the total number of possible sequences out there. Because of this, these functions are relatively simple, requiring a relatively short stretch of DNA to code for their function. Other systems of function require multiple proteins all working together simultaneously. Much more DNA real estate is necessary.
Before thinking about more complex systems function, such as bacterial motility, consider that even the evolution of the relatively simple lactase function is quite difficult. Barry Hall demonstrated this in several experiments where he deleted the lacZ genes in E. coli bacteria to see if they would evolve the lactase function back again using some other genetic sequence. And, they did evolve the lactase function in just one or two generations. As it turned out, a single point mutation to a completely different DNA sequence was able to produce a selectively advantageous lactase function in a lactose environment. Hall called this "evolved" sequence the ebg gene (evolved beta galactosidase gene). But, he started wondering, "If this worked for the deletion of the lacZ gene, what will happen if I delete the ebg gene too?" So, Hall deleted the ebg and lacZ genes in certain colonies of E. coli. What happened next is very interesting. These double mutant E. coli colonies never evolved the lactase function back again despite high population numbers, high mutation rates, 4 million base pairs of DNA each, positive selection pressure, and tens of thousands of generations.
Now, why didn't Hall's double mutant E. coli colonies evolve the relatively simple lactase function back again? Hall himself described this colonies as having, "limited evolutionary potential." What was it that limited their ability to evolve the relatively simple lactase function despite very positive benefits if they were to ever evolve this helpful function?
It seems that neutral gaps existed between what was there and what was needed. The genetic real estate of this huge population of E. coli simply was not large enough to undergo the random walk across this neutral gap in beneficial function despite being given thousands of generations.
Obviously then, even such simple functions as the function of single proteins are IC and this can and often does create difficulties for mindless evolutionary processes. The problems only increase (exponentially) as one moves up the spectrum of complex systems.
Discussions concerning the concept of irreducible complexity (IC) are quite common and usually involve some confusion about the definition of IC. The following question posed by "sds" sparked my interest.
"sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message <news:bbcj98$t4d$1@slb6.atl.mindspring.net>... > Do you believe is it possible to show that an object or mechanism has an > intelligent origin? Take the mousetrap again (for which I understand you > *don't* find "irreducibly complex" to be a meaningful characterization). > Can we show that a mousetrap probably could not exist without some > intelligence to design it?
It seems to me that the concept of IC is quite helpful indeed. The problem is that many, even Behe himself, seem to try to limit the definition of IC to "very complex" systems of function in order to show that IC systems cannot evolve.
As I see it all systems of function are IC. It is just that some systems are more simple than other systems of function. There is a spectrum of complexity, but all systems along this spectrum from simple to more and more complex are all IC. In other words, not all setups of a given number of parts or part types will be able to perform a given function. The parts in any system of function can in fact be altered, removed, or ordered in a different manner so that the function of the system is completely destroyed. In fact, there are vastly more non-functional potential arrangements of parts than there are beneficially functional arrangements of parts in a particular scenario.
Take, for example, Behe's famous mousetrap IC illustration. Many try to argue that a mousetrap is not IC since parts can be removed or changed and it still can catch mice. That is not the issue. If you change the mousetrap, it may still catch mice, but not in the same way. The changed mousetrap is a different mousetrap that catches mice in a different way. Certainly there are many different kinds of mousetraps that can catch mice, some more effectively than others. However, all of these mousetraps are dependent upon a certain number of parts that are all arranged in a very specific way in order for these parts to work together to catch mice (i.e., To perform their function). Clearly there are a lot more arrangements of mousetrap parts for any given type of mousetrap that would not catch mice at all. All mousetraps can in fact be reduced or changed in a way that would destroy their function completely. And, these potential non-functional mousetraps are far more numerous than those comparatively few arrangements than can actually perform the mouse catching function.
Of course, it is theoretically possible to arrange several of these working mousetraps in sequential order so that very small steps seem to exist as one moves from one type of trap to the other. Obviously then, it is NOT impossible for IC systems to evolve via function-based selection mechanisms since such an evolutionary path need not necessarily cross wide neutral gaps in function or non-function. The problem is that these gaps are often wider than one might initially think.
Even functions that are based on the workings of single proteins, such as the enzymatic functions of lactase or nylonase, are IC in that there are a limited number of parts that are required to give rise to that particular type of function. For more simple functions, such as these single-protein-based functions, there might be a much higher ratio of sequences of a given length or smaller that would be able to perform a given function, like the lactase or nylonase function. For example, given a sequence of amino acids 1,000aa in size, there are about 1 x 10e1300 different possible protein sequences. This is an absolutely huge number of different possibilities. It is a 1 with 1,300 zeros following it. Out of all of these possibilities, how many would have the lactase function? Certainly there would be many of these sequences that would have the lactase function, but certainly not all of them or even most of them. Perhaps the ratio would be as high as 1 in a trillion? If the ratio where 1 in a trillion, that means that any given functional lactase AA sequence would be surrounded by an average of 1 trillion non-lactase sequences. If a particular functioning lactase sequence is changed or "reduced" beyond a certain point, it will no longer function at all, not even a little bit. This is the definition of IC. The lactase function, even though based in the AA sequence of a single protein, is IC. Of course, compared to other systems of function, the lactase and nylonase single protein enzymes are not all that complex since there are is a relatively high percentage of potential lactase sequences as compared with the total number of possible sequences out there. Because of this, these functions are relatively simple, requiring a relatively short stretch of DNA to code for their function. Other systems of function require multiple proteins all working together simultaneously. Much more DNA real estate is necessary.
Before thinking about more complex systems function, such as bacterial motility, consider that even the evolution of the relatively simple lactase function is quite difficult. Barry Hall demonstrated this in several experiments where he deleted the lacZ genes in E. coli bacteria to see if they would evolve the lactase function back again using some other genetic sequence. And, they did evolve the lactase function in just one or two generations. As it turned out, a single point mutation to a completely different DNA sequence was able to produce a selectively advantageous lactase function in a lactose environment. Hall called this "evolved" sequence the ebg gene (evolved beta galactosidase gene). But, he started wondering, "If this worked for the deletion of the lacZ gene, what will happen if I delete the ebg gene too?" So, Hall deleted the ebg and lacZ genes in certain colonies of E. coli. What happened next is very interesting. These double mutant E. coli colonies never evolved the lactase function back again despite high population numbers, high mutation rates, 4 million base pairs of DNA each, positive selection pressure, and tens of thousands of generations.
Now, why didn't Hall's double mutant E. coli colonies evolve the relatively simple lactase function back again? Hall himself described this colonies as having, "limited evolutionary potential." What was it that limited their ability to evolve the relatively simple lactase function despite very positive benefits if they were to ever evolve this helpful function?
It seems that neutral gaps existed between what was there and what was needed. The genetic real estate of this huge population of E. coli simply was not large enough to undergo the random walk across this neutral gap in beneficial function despite being given thousands of generations.
Obviously then, even such simple functions as the function of single proteins are IC and this can and often does create difficulties for mindless evolutionary processes. The problems only increase (exponentially) as one moves up the spectrum of complex systems.
>Discussions concerning the concept of irreducible complexity (IC) are >quite common and usually involve some confusion about the definition >of IC. The following question posed by "sds" sparked my interest.
>> Do you believe is it possible to show that an object or mechanism has an >> intelligent origin? Take the mousetrap again (for which I understand you >> *don't* find "irreducibly complex" to be a meaningful characterization). >> Can we show that a mousetrap probably could not exist without some >> intelligence to design it?
>It seems to me that the concept of IC is quite helpful indeed. The >problem is that many, even Behe himself, seem to try to limit the >definition of IC to "very complex" systems of function in order to >show that IC systems cannot evolve.
>As I see it all systems of function are IC.
And, as such, there is no possibility of change in the world. Thank you very much Zeno.
> It is just that some >systems are more simple than other systems of function. There is a >spectrum of complexity, but all systems along this spectrum from >simple to more and more complex are all IC. In other words, not all >setups of a given number of parts or part types will be able to >perform a given function.
In actual words, each set of things in the world are different from other sets of things. BFD.
>The parts in any system of function can in >fact be altered, removed, or ordered in a different manner so that the >function of the system is completely destroyed. In fact, there are >vastly more non-functional potential arrangements of parts than there >are beneficially functional arrangements of parts in a particular >scenario.
Whatever you do, don't breath. You will alter your function.
>Take, for example, Behe's famous mousetrap IC illustration. Many try >to argue that a mousetrap is not IC since parts can be removed or >changed and it still can catch mice. That is not the issue. If you >change the mousetrap, it may still catch mice, but not in the same >way. The changed mousetrap is a different mousetrap that catches mice >in a different way. Certainly there are many different kinds of >mousetraps that can catch mice, some more effectively than others. >However, all of these mousetraps are dependent upon a certain number >of parts that are all arranged in a very specific way in order for >these parts to work together to catch mice (i.e., To perform their >function). Clearly there are a lot more arrangements of mousetrap >parts for any given type of mousetrap that would not catch mice at >all. All mousetraps can in fact be reduced or changed in a way that >would destroy their function completely. And, these potential >non-functional mousetraps are far more numerous than those >comparatively few arrangements than can actually perform the mouse >catching function.
Now all you have to do is show that there is some connection between IC and evolution.
>Of course, it is theoretically possible to arrange several of these >working mousetraps in sequential order so that very small steps seem >to exist as one moves from one type of trap to the other. Obviously >then, it is NOT impossible for IC systems to evolve via function-based >selection mechanisms since such an evolutionary path need not >necessarily cross wide neutral gaps in function or non-function. The >problem is that these gaps are often wider than one might initially >think.
And the problem for the ID/IC people is to make an actual case that some actual gap is a problem. You make the assertion, you provide the evidence.
[snip]
--
Matt Silberstein TBC HRL OMM
We are not here to judge other people, we are just here to be better than they are.
> Discussions concerning the concept of irreducible complexity (IC) are > quite common and usually involve some confusion about the definition > of IC. The following question posed by "sds" sparked my interest.
> "sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message
> > Do you believe is it possible to show that an object or mechanism has an > > intelligent origin? Take the mousetrap again (for which I understand you > > *don't* find "irreducibly complex" to be a meaningful characterization). > > Can we show that a mousetrap probably could not exist without some > > intelligence to design it?
> It seems to me that the concept of IC is quite helpful indeed. The > problem is that many, even Behe himself, seem to try to limit the > definition of IC to "very complex" systems of function in order to > show that IC systems cannot evolve.
> As I see it all systems of function are IC. It is just that some > systems are more simple than other systems of function. There is a > spectrum of complexity, but all systems along this spectrum from > simple to more and more complex are all IC. In other words, not all > setups of a given number of parts or part types will be able to > perform a given function. The parts in any system of function can in > fact be altered, removed, or ordered in a different manner so that the > function of the system is completely destroyed. In fact, there are > vastly more non-functional potential arrangements of parts than there > are beneficially functional arrangements of parts in a particular > scenario.
> Take, for example, Behe's famous mousetrap IC illustration. Many try > to argue that a mousetrap is not IC since parts can be removed or > changed and it still can catch mice. That is not the issue. If you > change the mousetrap, it may still catch mice, but not in the same > way. The changed mousetrap is a different mousetrap that catches mice > in a different way. Certainly there are many different kinds of > mousetraps that can catch mice, some more effectively than others. > However, all of these mousetraps are dependent upon a certain number > of parts that are all arranged in a very specific way in order for > these parts to work together to catch mice (i.e., To perform their > function). Clearly there are a lot more arrangements of mousetrap > parts for any given type of mousetrap that would not catch mice at > all. All mousetraps can in fact be reduced or changed in a way that > would destroy their function completely. And, these potential > non-functional mousetraps are far more numerous than those > comparatively few arrangements than can actually perform the mouse > catching function.
> Of course, it is theoretically possible to arrange several of these > working mousetraps in sequential order so that very small steps seem > to exist as one moves from one type of trap to the other. Obviously > then, it is NOT impossible for IC systems to evolve via function-based > selection mechanisms since such an evolutionary path need not > necessarily cross wide neutral gaps in function or non-function. The > problem is that these gaps are often wider than one might initially > think.
> Even functions that are based on the workings of single proteins, such > as the enzymatic functions of lactase or nylonase, are IC in that > there are a limited number of parts that are required to give rise to > that particular type of function. For more simple functions, such as > these single-protein-based functions, there might be a much higher > ratio of sequences of a given length or smaller that would be able to > perform a given function, like the lactase or nylonase function. For > example, given a sequence of amino acids 1,000aa in size, there are > about 1 x 10e1300 different possible protein sequences. This is an > absolutely huge number of different possibilities. It is a 1 with > 1,300 zeros following it. Out of all of these possibilities, how many > would have the lactase function? Certainly there would be many of > these sequences that would have the lactase function, but certainly > not all of them or even most of them. Perhaps the ratio would be as > high as 1 in a trillion? If the ratio where 1 in a trillion, that > means that any given functional lactase AA sequence would be > surrounded by an average of 1 trillion non-lactase sequences. If a > particular functioning lactase sequence is changed or "reduced" beyond > a certain point, it will no longer function at all, not even a little > bit. This is the definition of IC. The lactase function, even though > based in the AA sequence of a single protein, is IC. Of course, > compared to other systems of function, the lactase and nylonase single > protein enzymes are not all that complex since there are is a > relatively high percentage of potential lactase sequences as compared > with the total number of possible sequences out there. Because of > this, these functions are relatively simple, requiring a relatively > short stretch of DNA to code for their function. Other systems of > function require multiple proteins all working together > simultaneously. Much more DNA real estate is necessary.
> Before thinking about more complex systems function, such as bacterial > motility, consider that even the evolution of the relatively simple > lactase function is quite difficult. Barry Hall demonstrated this in > several experiments where he deleted the lacZ genes in E. coli > bacteria to see if they would evolve the lactase function back again > using some other genetic sequence. And, they did evolve the lactase > function in just one or two generations. As it turned out, a single > point mutation to a completely different DNA sequence was able to > produce a selectively advantageous lactase function in a lactose > environment. Hall called this "evolved" sequence the ebg gene > (evolved beta galactosidase gene). But, he started wondering, "If > this worked for the deletion of the lacZ gene, what will happen if I > delete the ebg gene too?" So, Hall deleted the ebg and lacZ genes in > certain colonies of E. coli. What happened next is very interesting. > These double mutant E. coli colonies never evolved the lactase > function back again despite high population numbers, high mutation > rates, 4 million base pairs of DNA each, positive selection pressure, > and tens of thousands of generations.
> Now, why didn't Hall's double mutant E. coli colonies evolve the > relatively simple lactase function back again? Hall himself described > this colonies as having, "limited evolutionary potential." What was > it that limited their ability to evolve the relatively simple lactase > function despite very positive benefits if they were to ever evolve > this helpful function?
> It seems that neutral gaps existed between what was there and what was > needed. The genetic real estate of this huge population of E. coli > simply was not large enough to undergo the random walk across this > neutral gap in beneficial function despite being given thousands of > generations.
> Obviously then, even such simple functions as the function of single > proteins are IC and this can and often does create difficulties for > mindless evolutionary processes. The problems only increase > (exponentially) as one moves up the spectrum of complex systems.
> Discussions concerning the concept of irreducible complexity (IC) are > quite common and usually involve some confusion about the definition > of IC. The following question posed by "sds" sparked my interest.
> "sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message
> > Do you believe is it possible to show that an object or mechanism has an > > intelligent origin? Take the mousetrap again (for which I understand you > > *don't* find "irreducibly complex" to be a meaningful characterization). > > Can we show that a mousetrap probably could not exist without some > > intelligence to design it?
> It seems to me that the concept of IC is quite helpful indeed. The > problem is that many, even Behe himself, seem to try to limit the > definition of IC to "very complex" systems of function in order to > show that IC systems cannot evolve.
> As I see it all systems of function are IC.
As soon as you change the definition then there is no way to continue the argument. You are calling a duck a dog and want to know why we don't see the wings.
Nobody cares if the base of the mousetrap is pure gold or cheap wood. It is the design that he claims is irreducible.
seanpitnos...@naturalselection.0catch.com (Sean Pitman) wrote: >It seems to me that the concept of IC is quite helpful indeed. The >problem is that many, even Behe himself, seem to try to limit the >definition of IC to "very complex" systems of function in order to >show that IC systems cannot evolve.
>As I see it all systems of function are IC. [...]
So? We know very well that IC is not the least bit of an obstacle to evolution.
-- Mark Isaak a...@earthlink.net "Voice or no voice, the people can always be brought to the bidding of the leaders. That is easy. All you have to do is tell them they are being attacked, and denounce the pacifists for lack of patriotism and exposing the country to danger." -- Hermann Goering
seanpitnos...@naturalselection.0catch.com (Sean Pitman) wrote in message <news:80d0c26f.0306010803.5ff5cbfd@posting.google.com>... > Discussions concerning the concept of irreducible complexity (IC) are > quite common and usually involve some confusion about the definition > of IC. The following question posed by "sds" sparked my interest.
> > Do you believe is it possible to show that an object or mechanism has an > > intelligent origin? Take the mousetrap again (for which I understand you > > *don't* find "irreducibly complex" to be a meaningful characterization). > > Can we show that a mousetrap probably could not exist without some > > intelligence to design it?
> It seems to me that the concept of IC is quite helpful indeed. The > problem is that many, even Behe himself, seem to try to limit the > definition of IC to "very complex" systems of function in order to > show that IC systems cannot evolve.
Behe relies on very complex systems because he realizes that an argument as you use in the following paragraphs is too weak to hold up under criticism.
As I see it, your argument depends on an unspoken assumption that context (selective environment) stays fixed, but that is an assumption that is not valid. In nature, there are few contexts so stable that opportunities for improvement do not present themselves, and indeed in those few cases, we can find ancient organisms who have been able to sustain form and function as long as that context has been sustained. Without selective context, evolution will happen only slowly in the form of individual genetic arrangements and optimization.
But in an organism who has a great deal of "evolvability" --that is, a systemic toolbox that is able to allow that organism entry into other contexts, we should see appearence of function from existing parts that are easily seen to be a result of co-option of existing pieces of existing systems, OUT of their original context. In the case of a mousetrap, the first step could only require a block of wood in a completely different context. Then, nature sequentially rummages through the vast "kitchen drawer" of biological tools and eventually comes up with a mousetrap, as you've noted, in sequential steps.
At each step of parts generation, a new and different context (ie, selective environment) was being answered to. A mousetrap was not necessarily the item needed in predecessor contexts -- however, the majority of the parts, from the spring to the board -- should have existed in some early form before optimization. The predecessor parts of the mousetrap, appeared not because of a need for a mousetrap, and indeed if the mousetrap pieces were not already in existence, the mousetrap would have never been assembled when the context for "need mousetrap" arose.
From predecessor states of other existing systems (a pair of scissors, a pen with a spring, a wire hanger), a mousetrap eventually is able to be generated as the system's "kitchen drawer" became more and more populated with evolved tools generated from other contexts. The main driving force for such experimentation and shuffling is not only born out of the "messy" assembly experiments that we find in nature, but also the need FOR the appearence of the context demanding "mouse trap". This isn't mere supposition, but is born out of observed instance.
Nylonase, as you pointed out, is one such example of an utilization of existing systems to process a substance in a new context (that of man-made nylon abundance). Yet, we hear about the successes. There are plenty of examples of life NOT being able to adapt. For instance, these bacteria that generated nylonase were probably not able to quickly generate an enzymatic system that can feed off of granite. In order to evolve a function, an organism must have predecessor units from other contexts. Additionally, the right context must be present. Contexts and opportunities (such as a rich diet in nylon fiber) must exist in which to allow selection.
Therefore, the problem for Intelligent Design is NOT trying to show "irreducible complexity" because, despite what Behe says, "IC" can be generated easily by adaptation and refinement of an already not-IC system.
The true problem for ID is to show that any biological system is unable to adapt to new contexts utilizing existing parts (except there are already instances of this occuring in nature). Beyond denying existing evidence, ID could show a certain "neatness" of biological function. Except we find that biological systems are full of noise and re-arrangements, as if these systems were constantly attempting to produce a large playing field of adaptations in order for something to select for advantage.
ID'ers must show that biological systems are perfect machines that cannot move from one context to another context simply by adapting -- by evolutionary process as outlined -- their existing systems to other contexts. Arguing that yeast cannot adapt to space conditions (as an hypothetical example) is no argument, however, since evolution does not require such great leaps. Evolution only requires reasonable context jumps -- nylon instead of granite. The largest problem for ID is, however, that they'd be arguing against observation.
G'Day All Address altered to avoid spam, delete RemoveInsert
On Sun, 1 Jun 2003 17:01:23 +0000 (UTC),
seanpitnos...@naturalselection.0catch.com (Sean Pitman) wrote: >Discussions concerning the concept of irreducible complexity (IC) are >quite common and usually involve some confusion about the definition >of IC. The following question posed by "sds" sparked my interest.
Partially relevant to this, I've posted some replies to our last exchange in the Ken Miller thread. It's over a weeklate, but circumstances beyond my control and all that.
>>Discussions concerning the concept of irreducible complexity (IC) are >>quite common and usually involve some confusion about the definition >>of IC. The following question posed by "sds" sparked my interest.
>>>Do you believe is it possible to show that an object or mechanism has an >>>intelligent origin? Take the mousetrap again (for which I understand you >>>*don't* find "irreducibly complex" to be a meaningful characterization). >>>Can we show that a mousetrap probably could not exist without some >>>intelligence to design it?
>>It seems to me that the concept of IC is quite helpful indeed. The >>problem is that many, even Behe himself, seem to try to limit the >>definition of IC to "very complex" systems of function in order to >>show that IC systems cannot evolve.
> Behe relies on very complex systems because he realizes that an > argument as you use in the following paragraphs is too weak to hold up > under criticism.
> As I see it, your argument depends on an unspoken assumption that > context (selective environment) stays fixed, but that is an assumption > that is not valid. In nature, there are few contexts so stable that > opportunities for improvement do not present themselves, and indeed in > those few cases, we can find ancient organisms who have been able to > sustain form and function as long as that context has been sustained. > Without selective context, evolution will happen only slowly in the > form of individual genetic arrangements and optimization.
> But in an organism who has a great deal of "evolvability" --that is, a > systemic toolbox that is able to allow that organism entry into other > contexts, we should see appearence of function from existing parts > that are easily seen to be a result of co-option of existing pieces of > existing systems, OUT of their original context. In the case of a > mousetrap, the first step could only require a block of wood in a > completely different context. Then, nature sequentially rummages > through the vast "kitchen drawer" of biological tools and eventually > comes up with a mousetrap, as you've noted, in sequential steps.
> At each step of parts generation, a new and different context (ie, > selective environment) was being answered to. A mousetrap was not > necessarily the item needed in predecessor contexts -- however, the > majority of the parts, from the spring to the board -- should have > existed in some early form before optimization. The predecessor parts > of the mousetrap, appeared not because of a need for a mousetrap, and > indeed if the mousetrap pieces were not already in existence, the > mousetrap would have never been assembled when the context for "need > mousetrap" arose.
> From predecessor states of other existing systems (a pair of scissors, > a pen with a spring, a wire hanger), a mousetrap eventually is able to > be generated as the system's "kitchen drawer" became more and more > populated with evolved tools generated from other contexts. The main > driving force for such experimentation and shuffling is not only born > out of the "messy" assembly experiments that we find in nature, but > also the need FOR the appearence of the context demanding "mouse > trap". This isn't mere supposition, but is born out of observed > instance.
> Nylonase, as you pointed out, is one such example of an utilization of > existing systems to process a substance in a new context (that of > man-made nylon abundance). Yet, we hear about the successes. There are > plenty of examples of life NOT being able to adapt. For instance, > these bacteria that generated nylonase were probably not able to > quickly generate an enzymatic system that can feed off of granite. In > order to evolve a function, an organism must have predecessor units > from other contexts. Additionally, the right context must be present. > Contexts and opportunities (such as a rich diet in nylon fiber) must > exist in which to allow selection.
> Therefore, the problem for Intelligent Design is NOT trying to show > "irreducible complexity" because, despite what Behe says, "IC" can be > generated easily by adaptation and refinement of an already not-IC > system.
> The true problem for ID is to show that any biological system is > unable to adapt to new contexts utilizing existing parts (except there > are already instances of this occuring in nature). Beyond denying > existing evidence, ID could show a certain "neatness" of biological > function. Except we find that biological systems are full of noise and > re-arrangements, as if these systems were constantly attempting to > produce a large playing field of adaptations in order for something to > select for advantage.
> ID'ers must show that biological systems are perfect machines that > cannot move from one context to another context simply by adapting -- > by evolutionary process as outlined -- their existing systems to other > contexts. Arguing that yeast cannot adapt to space conditions (as an > hypothetical example) is no argument, however, since evolution does > not require such great leaps. Evolution only requires reasonable > context jumps -- nylon instead of granite. The largest problem for ID > is, however, that they'd be arguing against observation.
It is the evolutionists, not the ID'ers who are faced with insurmountable difficulties. Evolutionists (especially darwinists) must demonstrate that these functional adaptations can be discovered by random, non-directed processes in spite of the fact that mathematical analysis has shown a random search strategy to be highly inefficient. For every functional system, the number of non-functional alternatives is nearly infinite. To find these isolated "islands of function" from within a "sea of noise" would be truly miraculous. Intelligent guidance reduces the number of non-functional alternatives and directs the system to optimum function is a much shorter time. To say that natural selection is the operative equivalent of intelligent guidance and accomplishes this task is blindly optimistic and not grounded in reality.
In article <3EDB7443.4020...@charliewagner.com>, Charlie Wagner wrote: > It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties. Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient.
What does random search have to do with evolution, Charlie?
> For every functional system, the number of non-functional alternatives > is nearly infinite. To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous.
Not miraculous at all, as genetic algorithms clearly and reliably demonstrate.
> Intelligent guidance reduces the number of non-functional > alternatives and directs the system to optimum function is a much > shorter time.
There is that "intelligent guidance" phrase you like so much. It's a pity that you don't know what it is. Why not just call it "obfuscatonium"?
> To say that natural selection is the operative equivalent of > intelligent guidance and accomplishes this task is blindly optimistic > and not grounded in reality.
> >>Discussions concerning the concept of irreducible complexity (IC) are > >>quite common and usually involve some confusion about the definition > >>of IC. The following question posed by "sds" sparked my interest.
> >>"sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message
> >>>Do you believe is it possible to show that an object or mechanism has an > >>>intelligent origin? Take the mousetrap again (for which I understand you > >>>*don't* find "irreducibly complex" to be a meaningful characterization). > >>>Can we show that a mousetrap probably could not exist without some > >>>intelligence to design it?
> >>It seems to me that the concept of IC is quite helpful indeed. The > >>problem is that many, even Behe himself, seem to try to limit the > >>definition of IC to "very complex" systems of function in order to > >>show that IC systems cannot evolve.
> > Behe relies on very complex systems because he realizes that an > > argument as you use in the following paragraphs is too weak to hold up > > under criticism.
> > As I see it, your argument depends on an unspoken assumption that > > context (selective environment) stays fixed, but that is an assumption > > that is not valid. In nature, there are few contexts so stable that > > opportunities for improvement do not present themselves, and indeed in > > those few cases, we can find ancient organisms who have been able to > > sustain form and function as long as that context has been sustained. > > Without selective context, evolution will happen only slowly in the > > form of individual genetic arrangements and optimization.
> > But in an organism who has a great deal of "evolvability" --that is, a > > systemic toolbox that is able to allow that organism entry into other > > contexts, we should see appearence of function from existing parts > > that are easily seen to be a result of co-option of existing pieces of > > existing systems, OUT of their original context. In the case of a > > mousetrap, the first step could only require a block of wood in a > > completely different context. Then, nature sequentially rummages > > through the vast "kitchen drawer" of biological tools and eventually > > comes up with a mousetrap, as you've noted, in sequential steps.
> > At each step of parts generation, a new and different context (ie, > > selective environment) was being answered to. A mousetrap was not > > necessarily the item needed in predecessor contexts -- however, the > > majority of the parts, from the spring to the board -- should have > > existed in some early form before optimization. The predecessor parts > > of the mousetrap, appeared not because of a need for a mousetrap, and > > indeed if the mousetrap pieces were not already in existence, the > > mousetrap would have never been assembled when the context for "need > > mousetrap" arose.
> > From predecessor states of other existing systems (a pair of scissors, > > a pen with a spring, a wire hanger), a mousetrap eventually is able to > > be generated as the system's "kitchen drawer" became more and more > > populated with evolved tools generated from other contexts. The main > > driving force for such experimentation and shuffling is not only born > > out of the "messy" assembly experiments that we find in nature, but > > also the need FOR the appearence of the context demanding "mouse > > trap". This isn't mere supposition, but is born out of observed > > instance.
> > Nylonase, as you pointed out, is one such example of an utilization of > > existing systems to process a substance in a new context (that of > > man-made nylon abundance). Yet, we hear about the successes. There are > > plenty of examples of life NOT being able to adapt. For instance, > > these bacteria that generated nylonase were probably not able to > > quickly generate an enzymatic system that can feed off of granite. In > > order to evolve a function, an organism must have predecessor units > > from other contexts. Additionally, the right context must be present. > > Contexts and opportunities (such as a rich diet in nylon fiber) must > > exist in which to allow selection.
> > Therefore, the problem for Intelligent Design is NOT trying to show > > "irreducible complexity" because, despite what Behe says, "IC" can be > > generated easily by adaptation and refinement of an already not-IC > > system.
> > The true problem for ID is to show that any biological system is > > unable to adapt to new contexts utilizing existing parts (except there > > are already instances of this occuring in nature). Beyond denying > > existing evidence, ID could show a certain "neatness" of biological > > function. Except we find that biological systems are full of noise and > > re-arrangements, as if these systems were constantly attempting to > > produce a large playing field of adaptations in order for something to > > select for advantage.
> > ID'ers must show that biological systems are perfect machines that > > cannot move from one context to another context simply by adapting -- > > by evolutionary process as outlined -- their existing systems to other > > contexts. Arguing that yeast cannot adapt to space conditions (as an > > hypothetical example) is no argument, however, since evolution does > > not require such great leaps. Evolution only requires reasonable > > context jumps -- nylon instead of granite. The largest problem for ID > > is, however, that they'd be arguing against observation.
> It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties. Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient.
How come? The question is not one that would apply to the theory of evolution. Natural selection is not random, in fact, it is decidedly non-random. I am afraid your mathematical analysis was unnecessary.
> For every functional system, the number of non-functional alternatives > is nearly infinite. To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous. Intelligent guidance > reduces the number of non-functional alternatives and directs the system > to optimum function is a much shorter time. To say that natural > selection is the operative equivalent of intelligent guidance and > accomplishes this task is blindly optimistic and not grounded in reality.
Demolish that strawman Charlie! Just whack at it. Hope it makes you feel better.
> Take, for example, Behe's famous mousetrap IC illustration. Many try > to argue that a mousetrap is not IC since parts can be removed or > changed and it still can catch mice. That is not the issue. If you > change the mousetrap, it may still catch mice, but not in the same > way.
Mousetraps are not living organisms, and mousetrap parts are not proteins. This analogy is a very poor one. In fact, I have yet to see a GOOD analogy between living organisms, and any practical invention which was intelligently designed by humans. I'm therefore puzzled why the "appearance of design" argument is viewed as a compelling arguement by so many creationists.
> Even functions that are based on the workings of single proteins, such > as the enzymatic functions of lactase or nylonase, are IC in that > there are a limited number of parts that are required to give rise to > that particular type of function.
Then how has it been possible for scientists to demonstrate the evolution of similar enzyme functions in vitro, applying a variety of selection strategies, and using random pools of protein, RNA, antibodies or even DNA as the starting material?
On Mon, 02 Jun 2003 15:58:48 +0000, Charlie Wagner wrote: > It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties. Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient.
Who says evolution is anything other than highly inefficient?
How many pounds of ancestry have died to make your short life possible?
> For every functional system, the number of non-functional alternatives > is nearly infinite. To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous.
Actually, "island" solutions can be found even by dull-witted hill-climbing algorithms, for some kinds of fitness landscapes.
Are you going to demonstrate that the fitness landscape provided by the biosphere is not amenable to optimization by evolution?
> Intelligent guidance reduces the number of non-functional alternatives > and directs the system to optimum function is a much shorter time.
Sure, our descendents will probably be able to do in a day what took evolution billions of years. That's hardly an argument that evolution didn't happen.
> To say that natural selection is the operative equivalent of intelligent > guidance and accomplishes this task is blindly optimistic and not > grounded in reality.
> >>Discussions concerning the concept of irreducible complexity (IC) are > >>quite common and usually involve some confusion about the definition > >>of IC. The following question posed by "sds" sparked my interest.
> >>>Do you believe is it possible to show that an object or mechanism has an > >>>intelligent origin? Take the mousetrap again (for which I understand you > >>>*don't* find "irreducibly complex" to be a meaningful characterization). > >>>Can we show that a mousetrap probably could not exist without some > >>>intelligence to design it?
> >>It seems to me that the concept of IC is quite helpful indeed. The > >>problem is that many, even Behe himself, seem to try to limit the > >>definition of IC to "very complex" systems of function in order to > >>show that IC systems cannot evolve.
> > Behe relies on very complex systems because he realizes that an > > argument as you use in the following paragraphs is too weak to hold up > > under criticism.
> > As I see it, your argument depends on an unspoken assumption that > > context (selective environment) stays fixed, but that is an assumption > > that is not valid. In nature, there are few contexts so stable that > > opportunities for improvement do not present themselves, and indeed in > > those few cases, we can find ancient organisms who have been able to > > sustain form and function as long as that context has been sustained. > > Without selective context, evolution will happen only slowly in the > > form of individual genetic arrangements and optimization.
> > But in an organism who has a great deal of "evolvability" --that is, a > > systemic toolbox that is able to allow that organism entry into other > > contexts, we should see appearence of function from existing parts > > that are easily seen to be a result of co-option of existing pieces of > > existing systems, OUT of their original context. In the case of a > > mousetrap, the first step could only require a block of wood in a > > completely different context. Then, nature sequentially rummages > > through the vast "kitchen drawer" of biological tools and eventually > > comes up with a mousetrap, as you've noted, in sequential steps.
> > At each step of parts generation, a new and different context (ie, > > selective environment) was being answered to. A mousetrap was not > > necessarily the item needed in predecessor contexts -- however, the > > majority of the parts, from the spring to the board -- should have > > existed in some early form before optimization. The predecessor parts > > of the mousetrap, appeared not because of a need for a mousetrap, and > > indeed if the mousetrap pieces were not already in existence, the > > mousetrap would have never been assembled when the context for "need > > mousetrap" arose.
> > From predecessor states of other existing systems (a pair of scissors, > > a pen with a spring, a wire hanger), a mousetrap eventually is able to > > be generated as the system's "kitchen drawer" became more and more > > populated with evolved tools generated from other contexts. The main > > driving force for such experimentation and shuffling is not only born > > out of the "messy" assembly experiments that we find in nature, but > > also the need FOR the appearence of the context demanding "mouse > > trap". This isn't mere supposition, but is born out of observed > > instance.
> > Nylonase, as you pointed out, is one such example of an utilization of > > existing systems to process a substance in a new context (that of > > man-made nylon abundance). Yet, we hear about the successes. There are > > plenty of examples of life NOT being able to adapt. For instance, > > these bacteria that generated nylonase were probably not able to > > quickly generate an enzymatic system that can feed off of granite. In > > order to evolve a function, an organism must have predecessor units > > from other contexts. Additionally, the right context must be present. > > Contexts and opportunities (such as a rich diet in nylon fiber) must > > exist in which to allow selection.
> > Therefore, the problem for Intelligent Design is NOT trying to show > > "irreducible complexity" because, despite what Behe says, "IC" can be > > generated easily by adaptation and refinement of an already not-IC > > system.
> > The true problem for ID is to show that any biological system is > > unable to adapt to new contexts utilizing existing parts (except there > > are already instances of this occuring in nature). Beyond denying > > existing evidence, ID could show a certain "neatness" of biological > > function. Except we find that biological systems are full of noise and > > re-arrangements, as if these systems were constantly attempting to > > produce a large playing field of adaptations in order for something to > > select for advantage.
> > ID'ers must show that biological systems are perfect machines that > > cannot move from one context to another context simply by adapting -- > > by evolutionary process as outlined -- their existing systems to other > > contexts. Arguing that yeast cannot adapt to space conditions (as an > > hypothetical example) is no argument, however, since evolution does > > not require such great leaps. Evolution only requires reasonable > > context jumps -- nylon instead of granite. The largest problem for ID > > is, however, that they'd be arguing against observation.
> It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties. Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient. > For every functional system, the number of non-functional alternatives > is nearly infinite. To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous. Intelligent guidance > reduces the number of non-functional alternatives and directs the system > to optimum function is a much shorter time. To say that natural > selection is the operative equivalent of intelligent guidance and > accomplishes this task is blindly optimistic and not grounded in reality.
Natural selection is not a random search strategy, and it has been found to be an efficient search strategy.
> >>Discussions concerning the concept of irreducible complexity (IC) are > >>quite common and usually involve some confusion about the definition > >>of IC. The following question posed by "sds" sparked my interest.
> >>"sds" <bcnorw...@mindspring.com.leavethispartoff> wrote in message
> >>>Do you believe is it possible to show that an object or mechanism has an > >>>intelligent origin? Take the mousetrap again (for which I understand you > >>>*don't* find "irreducibly complex" to be a meaningful characterization). > >>>Can we show that a mousetrap probably could not exist without some > >>>intelligence to design it?
> >>It seems to me that the concept of IC is quite helpful indeed. The > >>problem is that many, even Behe himself, seem to try to limit the > >>definition of IC to "very complex" systems of function in order to > >>show that IC systems cannot evolve.
> > Behe relies on very complex systems because he realizes that an > > argument as you use in the following paragraphs is too weak to hold up > > under criticism.
> > As I see it, your argument depends on an unspoken assumption that > > context (selective environment) stays fixed, but that is an assumption > > that is not valid. In nature, there are few contexts so stable that > > opportunities for improvement do not present themselves, and indeed in > > those few cases, we can find ancient organisms who have been able to > > sustain form and function as long as that context has been sustained. > > Without selective context, evolution will happen only slowly in the > > form of individual genetic arrangements and optimization.
> > But in an organism who has a great deal of "evolvability" --that is, a > > systemic toolbox that is able to allow that organism entry into other > > contexts, we should see appearence of function from existing parts > > that are easily seen to be a result of co-option of existing pieces of > > existing systems, OUT of their original context. In the case of a > > mousetrap, the first step could only require a block of wood in a > > completely different context. Then, nature sequentially rummages > > through the vast "kitchen drawer" of biological tools and eventually > > comes up with a mousetrap, as you've noted, in sequential steps.
> > At each step of parts generation, a new and different context (ie, > > selective environment) was being answered to. A mousetrap was not > > necessarily the item needed in predecessor contexts -- however, the > > majority of the parts, from the spring to the board -- should have > > existed in some early form before optimization. The predecessor parts > > of the mousetrap, appeared not because of a need for a mousetrap, and > > indeed if the mousetrap pieces were not already in existence, the > > mousetrap would have never been assembled when the context for "need > > mousetrap" arose.
> > From predecessor states of other existing systems (a pair of scissors, > > a pen with a spring, a wire hanger), a mousetrap eventually is able to > > be generated as the system's "kitchen drawer" became more and more > > populated with evolved tools generated from other contexts. The main > > driving force for such experimentation and shuffling is not only born > > out of the "messy" assembly experiments that we find in nature, but > > also the need FOR the appearence of the context demanding "mouse > > trap". This isn't mere supposition, but is born out of observed > > instance.
> > Nylonase, as you pointed out, is one such example of an utilization of > > existing systems to process a substance in a new context (that of > > man-made nylon abundance). Yet, we hear about the successes. There are > > plenty of examples of life NOT being able to adapt. For instance, > > these bacteria that generated nylonase were probably not able to > > quickly generate an enzymatic system that can feed off of granite. In > > order to evolve a function, an organism must have predecessor units > > from other contexts. Additionally, the right context must be present. > > Contexts and opportunities (such as a rich diet in nylon fiber) must > > exist in which to allow selection.
> > Therefore, the problem for Intelligent Design is NOT trying to show > > "irreducible complexity" because, despite what Behe says, "IC" can be > > generated easily by adaptation and refinement of an already not-IC > > system.
> > The true problem for ID is to show that any biological system is > > unable to adapt to new contexts utilizing existing parts (except there > > are already instances of this occuring in nature). Beyond denying > > existing evidence, ID could show a certain "neatness" of biological > > function. Except we find that biological systems are full of noise and > > re-arrangements, as if these systems were constantly attempting to > > produce a large playing field of adaptations in order for something to > > select for advantage.
> > ID'ers must show that biological systems are perfect machines that > > cannot move from one context to another context simply by adapting -- > > by evolutionary process as outlined -- their existing systems to other > > contexts. Arguing that yeast cannot adapt to space conditions (as an > > hypothetical example) is no argument, however, since evolution does > > not require such great leaps. Evolution only requires reasonable > > context jumps -- nylon instead of granite. The largest problem for ID > > is, however, that they'd be arguing against observation.
> It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties.
1) How do you know they are "insurmountable"? Just because there is no handy answer *now*? That is argument from ignorance/incredulity.
2) It is the very nature of science to attempt to answer these "dificulties".
3) But I suppose you prefer the IDer's "Well, that's a complex process, and since I can't figure itout, let's just close the lab, say some intelligent designer (wink, wink, nudge, nudge) didit!"
> Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient.
Nobody ever claimed that biological evolution or it's component theories was highly effiecient (aside form the context of what you mena by "effiicient") Viewed one way, it is mercylessly effieient, while viewed another it is clumsy, time consuming and "hit or miss".
> For every functional system, the number of non-functional alternatives > is nearly infinite.
And the "failures" never live long enough to reproduce in any numbers large enough to make an impact on the population as a hole. That would be the "mercylessly efficient" part.
> To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous.
That would be the "clumsy, time consuming and "hit or miss" part.
> Intelligent guidance > reduces the number of non-functional alternatives and directs the system > to optimum function is a much shorter time.
The time could also be trimmed if there are large numbers of individuals in the population too. It seems to me that the IDer's that follow your line of reasoning think that there is only one "trial" going on at a time, when in fact, every individual of a popultation is "on trial".
> To say that natural > selection is the operative equivalent of intelligent guidance and > accomplishes this task is blindly optimistic and not grounded in reality.
Actually, "optimistic" is relative (just like in an election year, the Republicans are optimistic that their candidate will win, and eht Democrats are just as optimistic that their candidate will win), and reality is where the observed little bits of evidence that you ignore came from in the first place. Or did you think that, as far as NS goes, Darwin just dreamed it up out of the blue?
Get a grip chuckles. Just because you *want* there to be some alien guiding force involved, does not mean that the modern synthysis of the ToE is wrong, or that your desires are the answer.
Besides, *if* there were an alien designer (or whatever entity you are pushing for) involved, how do you know it didn't design it's basic "starter life's" genome to mutate at random in order to generate variations within the population of the original "seed" of life on Earth?
But of course, any answer you can give to that question would be nothing more than baseless speculation....
-- Boikat
"Hokey religions and ancient weapons are no match for a good blaster at your side, kid." Han Solo, Star Wars, Episode IV
"I find your lack of faith disturbing" Darth Vader, Star Wars, Episode IV
>>> Discussions concerning the concept of irreducible complexity (IC) are >>> quite common and usually involve some confusion about the definition >>> of IC. The following question posed by "sds" sparked my interest.
>>>> Do you believe is it possible to show that an object or mechanism has an >>>> intelligent origin? Take the mousetrap again (for which I understand you >>>> *don't* find "irreducibly complex" to be a meaningful characterization). >>>> Can we show that a mousetrap probably could not exist without some >>>> intelligence to design it?
>>> It seems to me that the concept of IC is quite helpful indeed. The >>> problem is that many, even Behe himself, seem to try to limit the >>> definition of IC to "very complex" systems of function in order to >>> show that IC systems cannot evolve.
>> Behe relies on very complex systems because he realizes that an >> argument as you use in the following paragraphs is too weak to hold up >> under criticism.
>> As I see it, your argument depends on an unspoken assumption that >> context (selective environment) stays fixed, but that is an assumption >> that is not valid. In nature, there are few contexts so stable that >> opportunities for improvement do not present themselves, and indeed in >> those few cases, we can find ancient organisms who have been able to >> sustain form and function as long as that context has been sustained. >> Without selective context, evolution will happen only slowly in the >> form of individual genetic arrangements and optimization.
>> But in an organism who has a great deal of "evolvability" --that is, a >> systemic toolbox that is able to allow that organism entry into other >> contexts, we should see appearence of function from existing parts >> that are easily seen to be a result of co-option of existing pieces of >> existing systems, OUT of their original context. In the case of a >> mousetrap, the first step could only require a block of wood in a >> completely different context. Then, nature sequentially rummages >> through the vast "kitchen drawer" of biological tools and eventually >> comes up with a mousetrap, as you've noted, in sequential steps.
>> At each step of parts generation, a new and different context (ie, >> selective environment) was being answered to. A mousetrap was not >> necessarily the item needed in predecessor contexts -- however, the >> majority of the parts, from the spring to the board -- should have >> existed in some early form before optimization. The predecessor parts >> of the mousetrap, appeared not because of a need for a mousetrap, and >> indeed if the mousetrap pieces were not already in existence, the >> mousetrap would have never been assembled when the context for "need >> mousetrap" arose.
>> From predecessor states of other existing systems (a pair of scissors, >> a pen with a spring, a wire hanger), a mousetrap eventually is able to >> be generated as the system's "kitchen drawer" became more and more >> populated with evolved tools generated from other contexts. The main >> driving force for such experimentation and shuffling is not only born >> out of the "messy" assembly experiments that we find in nature, but >> also the need FOR the appearence of the context demanding "mouse >> trap". This isn't mere supposition, but is born out of observed >> instance.
>> Nylonase, as you pointed out, is one such example of an utilization of >> existing systems to process a substance in a new context (that of >> man-made nylon abundance). Yet, we hear about the successes. There are >> plenty of examples of life NOT being able to adapt. For instance, >> these bacteria that generated nylonase were probably not able to >> quickly generate an enzymatic system that can feed off of granite. In >> order to evolve a function, an organism must have predecessor units >> from other contexts. Additionally, the right context must be present. >> Contexts and opportunities (such as a rich diet in nylon fiber) must >> exist in which to allow selection.
>> Therefore, the problem for Intelligent Design is NOT trying to show >> "irreducible complexity" because, despite what Behe says, "IC" can be >> generated easily by adaptation and refinement of an already not-IC >> system.
>> The true problem for ID is to show that any biological system is >> unable to adapt to new contexts utilizing existing parts (except there >> are already instances of this occuring in nature). Beyond denying >> existing evidence, ID could show a certain "neatness" of biological >> function. Except we find that biological systems are full of noise and >> re-arrangements, as if these systems were constantly attempting to >> produce a large playing field of adaptations in order for something to >> select for advantage.
>> ID'ers must show that biological systems are perfect machines that >> cannot move from one context to another context simply by adapting -- >> by evolutionary process as outlined -- their existing systems to other >> contexts. Arguing that yeast cannot adapt to space conditions (as an >> hypothetical example) is no argument, however, since evolution does >> not require such great leaps. Evolution only requires reasonable >> context jumps -- nylon instead of granite. The largest problem for ID >> is, however, that they'd be arguing against observation.
> It is the evolutionists, not the ID'ers who are faced with > insurmountable difficulties. Evolutionists (especially darwinists) must > demonstrate that these functional adaptations can be discovered by > random, non-directed processes in spite of the fact that mathematical > analysis has shown a random search strategy to be highly inefficient. > For every functional system, the number of non-functional alternatives > is nearly infinite. To find these isolated "islands of function" from > within a "sea of noise" would be truly miraculous. Intelligent guidance > reduces the number of non-functional alternatives and directs the system > to optimum function is a much shorter time. To say that natural > selection is the operative equivalent of intelligent guidance and > accomplishes this task is blindly optimistic and not grounded in reality.
You know, humans are intelligent designers. They have designed many things and even manufactured some of them. Including living organisms. It is instructive to ask how (what mechanisms were used) humans designed living organisms to better suit human needs. Did they build a "dachshund" factory and construct "dachsunds" from scratch using a blueprint? Did they build domestic chicken breeds from scratch? Did they build dairy cattle by starting with horns and intestines and udders and randomly plugging them together? Did they intelligently build maize?
Or did they use "selection" starting with previously existing organisms that had some desired features? Did they take advantage of random mutations that produced desired effects? Did they cull out thousands of individuals to get breeding stock? What has been the mechanism by which humans have intelligently designed 'living organisms' to suit their needs?
"Frank Reichenbacher" <fr...@bio-con.com> wrote in message <news:6z6dnRTnMO7Z4UajXTWcqA@speakeasy.net>... > > It is the evolutionists, not the ID'ers who are faced with > > insurmountable difficulties. Evolutionists (especially darwinists) must > > demonstrate that these functional adaptations can be discovered by > > random, non-directed processes in spite of the fact that mathematical > > analysis has shown a random search strategy to be highly inefficient.
> How come? The question is not one that would apply to the theory of > evolution. Natural selection is not random, in fact, it is decidedly > non-random. I am afraid your mathematical analysis was unnecessary. > Demolish that strawman Charlie! Just whack at it. Hope it makes you feel > better.
It seems to me, Frank, that you don't have a clue as to how natural selection works. You are correct in saying that natural selection is "not random". However, what you do not seem to realize is that there are times when natural selection cannot selection between various genetic changes that do in fact occur on a very regular basis. These changes are called "neutral mutations". These neutral mutations are purely *random* genetic mutations that do not result in phenotypic changes. Natural selection cannot select between two *equally* functional or nonfunctional genetic sequences. If such neutral sequence gaps do exist between the genetic real estate that is currently available and certain sequences that would in fact code for certain complex beneficial functions, natural selection would not be able to help in the crossing of such neutral gaps. Neutral gaps are the death knell of natural selection. The only thing left as a force for change is the force of purely *random* mutations. So you see, neutral gaps make mindless processes of evolutionary change entirely random. Charlie is right. This is no straw man here. This is reality.
Now, your job would be to explain one of two things. Explain either how these gaps are crossed without natural selection OR explain how these gaps do not really exist. That is your job if you are thinking to rescue the theory of mindless naturalistic evolution from this neutral gap problem.
Perhaps a good place to start your explanations would be to explain why Hall's mutant E. coli colonies were incapable of evolving a relatively simple lactase function despite being given large populations sizes, high mutation rates, adequate selection pressures, and many thousands of generations of time? This is a very curious finding. How is it explained? What, exactly, was the limiting factor that prevented these bacteria from evolving a relatively simple function that would in fact have been quite beneficial to them if they ever were to evolve it?
> ID'ers must show that biological systems are perfect machines that > cannot move from one context to another context simply by adapting -- > by evolutionary process as outlined -- their existing systems to other > contexts. Arguing that yeast cannot adapt to space conditions (as an > hypothetical example) is no argument, however, since evolution does > not require such great leaps. Evolution only requires reasonable > context jumps -- nylon instead of granite. The largest problem for ID > is, however, that they'd be arguing against observation.
Nylon instead of granite? Granite? Do you know of anything that can eat granite? I was not aware that granite was such a potential energy source for biological organisms. But hey, that isn't really the point now is it?
I offered a simple example where certain E. coli colonies (lacking the lacZ and ebgA genes) had been grown on a lactose rich media/environment. They failed to evolve the lactase function despite the obvious benefit to them if they ever did evolve this relatively simple single protein based enzyme. These particular bacteria were grown on this lactose rich media for tens of thousands of generations with high mutation rates and large population sizes, and they still never evolved this relatively simple lactase function. Really, we are not talking about a dramatic shift in environment here. We aren't talking about a lethal "outer space" environment either. The E. coli bacteria grew just fine without the lactase function, but they would have done much better in the lactose rich environment if they did have this function. So, why didn't they evolve this function?
These very same bacteria would quickly evolve resistance to penicillin if it were added to their environment. No more than a handful of generations would be required. Why then is antibiotic resistance so much easier for them to evolve than the lactase function? What is it about the evolution of relatively simple enzymes that is so much more difficult than the evolution of antibiotic resistance?
Also, we have actually seen a few relatively rare real time demonstrations of enzyme evolution, to include the evolution of the lactase function in some types of E. coli, but never in other types of mutant E. coli and never in many other types of bacteria over the course of 50+ years. However, we have never seen a bacterial function evolve that requires multiple proteins working together at the same time, such as would be required for the function of bacterial motility. Why is this type of multi-protein function so difficult to evolve in real time? Hmmmmm?
I look forward to finally hearing from someone in the know as to why antibiotic resistance evolves so much faster than the functions of enzymes and why enzymes evolve at least on some rare occasions, but functions with multiple proteins working together at the same time, never seem to evolve in real time. I mean, if it is so easy, as you seem to be saying, then evolution should proceed rapidly, should it not? If there were no neutral gaps to slow the process of evolution down, then given the proper environment, the evolution of beneficial functions, such as the lactase function in a lactose rich environment, should proceed very quickly. This lactose environment ain't outer space and it ain't granite you know. One little enzyme is all that is needed to use this new environment in a more advantageous way. And yet, many different types of bacteria seem unable to evolve the lactase enzyme despite hundreds of thousands and even millions of generations of time. What then, exactly, is slowing this process down? Please, you seem so knowledgeable . . . what is the answer?
> snip > > ID'ers must show that biological systems are perfect machines that > > cannot move from one context to another context simply by adapting -- > > by evolutionary process as outlined -- their existing systems to other > > contexts. Arguing that yeast cannot adapt to space conditions (as an > > hypothetical example) is no argument, however, since evolution does > > not require such great leaps. Evolution only requires reasonable > > context jumps -- nylon instead of granite. The largest problem for ID > > is, however, that they'd be arguing against observation.
> Nylon instead of granite? Granite? Do you know of anything that can > eat granite? I was not aware that granite was such a potential energy > source for biological organisms. But hey, that isn't really the point > now is it?
> I offered a simple example where certain E. coli colonies (lacking the > lacZ and ebgA genes) had been grown on a lactose rich > media/environment. They failed to evolve the lactase function despite > the obvious benefit to them if they ever did evolve this relatively > simple single protein based enzyme. These particular bacteria were > grown on this lactose rich media for tens of thousands of generations > with high mutation rates and large population sizes, and they still > never evolved this relatively simple lactase function. Really, we are > not talking about a dramatic shift in environment here. We aren't > talking about a lethal "outer space" environment either. The E. coli > bacteria grew just fine without the lactase function, but they would > have done much better in the lactose rich environment if they did have > this function. So, why didn't they evolve this function?
You are contrasting the ease with which a single mutation can lead to gain of function (starting on the right background) with the problem of evolving a new enzyme from scratch (or from an enzyme with unrelated function). Yes. It is much faster if there is a gene already there which needs just a single mutation to develop a new, useful activity.
Here is a similar contrast from drug resistant malaria. Mefloquine is a new anti-malarial drug that has been on the market for about 15 years. Mefloquine resistance began to appear in malaria parasites within a few years of the release of the drug to the market and is now a significant problem in treating malaria in southeast asia and the amazon. One can start a culture of mefloquine-sensitive malaria parasites in the lab (beginning with a single, cloned parasite) and, by adding progressively higher concentrations of mefloquine select for a mefloquine resistant population. A single mutation in a single gene does the trick.
On the other hand, chloroquine resistance is diffferent. Chloroquine resitance in malaria parasites appeared in the wild in the 60's and spread throughout the world-wide malaria population over the following 30 years. However, no one has succeeded in starting with a chloroquine sensitive parasite clone and selecting a chloroquine resistant population in in vitro culture. Based on sequencing data from chloroquine sensitive and chloroquine resistant strains it looks like the problem is that chloroquine resistance requires the acquisition of a series of 6 or 7 mutations in a particular order. No one has been able to get this to happen in cultured parasites in the lab. But it clearly happened in "real time" in nature as a result of widespread use of chloroquine against malaria.
So... Both resistances evolved in nature in years to decades; evolution of mefloquine resistance has been reproduced in the lab; evolution of chloroquine resistance has not. Does this mean that the "Designer" let P. falciparum handle mefloquine on its own, but intervened to help P. falciparum deal with chloroquine?
> These very same bacteria would quickly evolve resistance to penicillin > if it were added to their environment. No more than a handful of > generations would be required. Why then is antibiotic resistance so > much easier for them to evolve than the lactase function? What is it > about the evolution of relatively simple enzymes that is so much more > difficult than the evolution of antibiotic resistance?
Enzymes are really complicated. You are right. It almost certainly takes more time than you have to watch to evolve a new enzyme from scratch (or even from an unrelated enzyme). We all agree that evolution takes a long time. Building enzymes from scratch is actually more a part of abiogenesis than evolution, but most scientists would agree, I think, that abiogenesis took a billion years or so, not a few months, even with artificially boosted mutation rates.
It is possible to select for enzymatic activity in antibody molecules (not originally enzymes at all) in the lab by cycles of mutation and selection. That works pretty quickly. You can search in Medline under Richard Lerner and/or Angray Kang to read about that system.
> Also, we have actually seen a few relatively rare real time > demonstrations of enzyme evolution, to include the evolution of the > lactase function in some types of E. coli, but never in other types of > mutant E. coli and never in many other types of bacteria over the > course of 50+ years. However, we have never seen a bacterial function > evolve that requires multiple proteins working together at the same > time, such as would be required for the function of bacterial > motility. Why is this type of multi-protein function so difficult to > evolve in real time? Hmmmmm?
> I look forward to finally hearing from someone in the know as to why > antibiotic resistance evolves so much faster than the functions of > enzymes and why enzymes evolve at least on some rare occasions, but > functions with multiple proteins working together at the same time, > never seem to evolve in real time.
Antiobiotic resistance is often easy because
(1) The gene already exists on plasmids in wild populations of the bacterium in question and the plasmid is exchanged in the bacterial populations (that is the case for some forms of penicillin resistance). Remember, we've only been using penicillin for 60 or 70 years, but fungi have been using it for millions, so the bacteria have had plenty of time to develop a suite of resistance genes.
or
(2) The action of the drug requires binding to some bacterial protein and a simple mutation in the gene encoding the bacterial protein destroys the binding site. This happens with other forms of penecillin resistance, and with resistance to several antibiotic that bind to bacterial ribosomes, like tetracycline.
So, yes, that's a lot easier than getting to a complex multi-enzyme complex from scratch. No doubts.
I mean, if it is so easy, as you
> seem to be saying, then evolution should proceed rapidly, should it > not?
Depends on what you mean by rapidly? It will not proceed rapidly if by that you mean "right before my eyes."
>If there were no neutral gaps to slow the process of evolution > down, then given the proper environment, the evolution of beneficial > functions, such as the lactase function in a lactose rich environment, > should proceed very quickly. This lactose environment ain't outer > space and it ain't granite you know. One little enzyme is all that is > needed to use this new environment in a more advantageous way. And > yet, many different types of bacteria seem unable to evolve the > lactase enzyme despite hundreds of thousands and even millions of > generations of time. What then, exactly, is slowing this process > down? Please, you seem so knowledgeable . . . what is the answer?
> Nylon instead of granite? Granite? Do you know of anything that can > eat granite? I was not aware that granite was such a potential energy > source for biological organisms. But hey, that isn't really the point > now is it?
<snip>
Speaking of "the point", Dr, you seem to have not answered my simple question. So I'll ask again.
As a medical dorctor, do you advise your patients to reject their materialistic naturalistic atheistic biases when they get sick? Do you advise them to seek non-naturalistic cures for the non-naturalistic causes of their diseases -- such as evil spirits or curses or The Evil Eye from local witches? Or do you use materialistic naturalistic antibiotics to treat their materialistic naturalistic diseases by killing their materialistic naturalistic germs.
Are you just a materialistic natuiralisic atheist at heart, Dr?
=============================================== "There are no loose threads in the web of life"
brog...@noguchi.mimcom.net (Bill Rogers) wrote in message <news:8984713a.0306120103.5e7edabb@posting.google.com>... > You are contrasting the ease with which a single mutation can lead to > gain of function (starting on the right background) with the problem > of evolving a new enzyme from scratch (or from an enzyme with > unrelated function). Yes. It is much faster if there is a gene > already there which needs just a single mutation to develop a new, > useful activity.
Finally, someone who actually seems to understand what I am talking about. There are clearly different levels of functional complexity. The function of bacterial antibiotic resistance is extremely simple, even in comparison to the most simple enzymatic functions. The reason for this is that there is a dramatically higher ratio of functional mutations as compared to neutral mutations in the development of antibiotic resistance as compared to the evolution of a certain enzymatic activities.
> Here is a similar contrast from drug resistant malaria. Mefloquine is > a new anti-malarial drug that has been on the market for about 15 > years. Mefloquine resistance began to appear in malaria parasites > within a few years of the release of the drug to the market and is now > a significant problem in treating malaria in southeast asia and the > amazon. One can start a culture of mefloquine-sensitive malaria > parasites in the lab (beginning with a single, cloned parasite) and, > by adding progressively higher concentrations of mefloquine select for > a mefloquine resistant population. A single mutation in a single gene > does the trick.
Exactly . . .
> On the other hand, chloroquine resistance is diffferent. Chloroquine > resitance in malaria parasites appeared in the wild in the 60's and > spread throughout the world-wide malaria population over the following > 30 years. However, no one has succeeded in starting with a chloroquine > sensitive parasite clone and selecting a chloroquine resistant > population in in vitro culture. Based on sequencing data from > chloroquine sensitive and chloroquine resistant strains it looks like > the problem is that chloroquine resistance requires the acquisition of > a series of 6 or 7 mutations in a particular order. No one has been > able to get this to happen in cultured parasites in the lab. But it > clearly happened in "real time" in nature as a result of widespread > use of chloroquine against malaria.
The most likely reason why this has not been observed in the lab is because the lab didn't use a large enough population size to overcome the neutral gap created by 6 or 7 neutral mutations. A series of 7 neutral mutations in DNA would create a neutral gap or sea of 16,384 possibilities. In this case, only one of these possibilities is "correct." In order to find this correct sequence out of all the other possibilities, the given population of malaria parasites would have to undergo random walk. This random walk takes time and this time is dependent upon several factors. Lets see if we can figure out a rough estimate based on these factors.
Let's say that the mutation rate was on the order of 10e-8 mutations per base pair per generation. On average then, it would take around 10e7 generations to get just one mutation to one of our 7 base pairs of interest. If a generation time is one day (I'm not exactly sure what the generation time is for the malaria parasite), a steady state population of 10e3 parasites would experience one mutation in these 7 base pairs every 10,000 days or 27 years on average. Given this relatively small colony of parasites, it would take around 500,000 years to develop resistance to chloroquine. If the colony size were increased to one million parasites, the time required to evolve resistance would drop to around 5,000 years. If the colony size were increased to one billion parasites, the time required would drop to around 5 years.
These rough estimates based, on the time required to cross a known neutral gap, are very much in line with what we have seen in the evolution of chloroquine resistance in the wild and they also explain why this resistance has never been demonstrated in the lab. The lab experiments simply didn't use a large enough population size or didn't carry on the experiments for enough generations.
In any case, it is a great example that demonstrates very nicely the limits that neutral gaps put on the theory of evolution. This only strengthens my theory.
> So... Both resistances evolved in nature in years to decades; > evolution of mefloquine resistance has been reproduced in the lab; > evolution of chloroquine resistance has not. Does this mean that the > "Designer" let P. falciparum handle mefloquine on its own, but > intervened to help P. falciparum deal with chloroquine?
You don't seem to understand the statistics involved here. Obviously, a neutral gap in function of 6 or 7 base pairs can easily be crossed by random walk alone given the much larger population sizes of the malaria parasites (P. falciparum) that exist in the wild as compared to the relatively limited population size that was most likely used in the laboratory experiments. No ID is needed to explain the evolution of chloroquine resistance in either case. The average time required is well within reason.
> > These very same bacteria would quickly evolve resistance to penicillin > > if it were added to their environment. No more than a handful of > > generations would be required. Why then is antibiotic resistance so > > much easier for them to evolve than the lactase function? What is it > > about the evolution of relatively simple enzymes that is so much more > > difficult than the evolution of antibiotic resistance?
> Enzymes are really complicated. You are right. It almost certainly > takes more time than you have to watch to evolve a new enzyme from > scratch (or even from an unrelated enzyme).
I'm glad that you realize this because many people think that the evolution of antibiotic resistance is something very significant and/or complex. What many do not realize or admit is that even the relatively simple function of a single protein based enzyme, is far more complex than the function of antibiotic resistance.
Obviously more time is required to evolve the enzymatic functions than the functions of antibiotic resistance. That question is, "Why?" Why is more time required to evolve functions of increasing complexity? I am proposing that neutral gaps are the reason for this observed phenomenon. What is your explanation?
> We all agree that > evolution takes a long time. Building enzymes from scratch is actually > more a part of abiogenesis than evolution, but most scientists would > agree, I think, that abiogenesis took a billion years or so, not a few > months, even with artificially boosted mutation rates.
Oh, so the evolution of even one little protein sequence is based on "abiogenesis" not on evolution? Really?! This is *most* interesting. This is exactly my whole point. Abiogenesis is based on neutral drift/random walk. Natural selection really is limited when it comes to ideas on abiogenesis since by far most of the changes in abiogenesis are functionally neutral as far as a mindless nature is concerned. This is why scientists think that abiogenesis took billions of years to produce the first self-replicating cell. But why? Why does abiogenesis take so long? Because of the neutral gaps. When you actually start plugging in the numbers and doing some real estimates based on the idea of neutral gaps, you quickly find that the abiogenesis of much of anything would take far longer than a few billion or even many trillions or zillions or googols of years.
> It is possible to select for enzymatic activity in antibody molecules > (not originally enzymes at all) in the lab by cycles of mutation and > selection. That works pretty quickly. You can search in Medline under > Richard Lerner and/or Angray Kang to read about that system.
Yes, this works pretty quickly because it is not based on the needs, mutation rates, or genetic capabilities of any given life form, but on the ability of a human scientist to recognize some sort of specific enzymatic activity from a random pool of proteins. And, even in these experiments, nothing more than the functions of single proteins are demonstrated. These functions are still relatively simple compared to those cellular functions that require multiple proteins all working together at the same time (i.e., bacterial motility systems like the flagellum).
> > Also, we have actually seen a few relatively rare real time > > demonstrations of enzyme evolution, to include the evolution of the > > lactase function in some types of E. coli, but never in other types of > > mutant E. coli and never in many other types of bacteria over the > > course of 50+ years. However, we have never seen a bacterial function > > evolve that requires multiple proteins working together at the same > > time, such as would be required for the function of bacterial > > motility. Why is this type of multi-protein function so difficult to > > evolve in real time? Hmmmmm?
> > I look forward to finally hearing from someone in the know as to why > > antibiotic resistance evolves so much faster than the functions of > > enzymes and why enzymes evolve at least on some rare occasions, but > > functions with multiple proteins working together at the same time, > > never seem to evolve in real time.
> Antiobiotic resistance is often easy because
> (1) The gene already exists on plasmids in wild populations of the > bacterium in question and the plasmid is exchanged in the bacterial > populations (that is the case for some forms of penicillin > resistance). Remember, we've only been using penicillin for 60 or 70 > years, but fungi have been using it for millions, so the bacteria have > had plenty of time to develop a suite of resistance
> snip > > ID'ers must show that biological systems are perfect machines that > > cannot move from one context to another context simply by adapting -- > > by evolutionary process as outlined -- their existing systems to other > > contexts. Arguing that yeast cannot adapt to space conditions (as an > > hypothetical example) is no argument, however, since evolution does > > not require such great leaps. Evolution only requires reasonable > > context jumps -- nylon instead of granite. The largest problem for ID > > is, however, that they'd be arguing against observation.
> Nylon instead of granite? Granite? Do you know of anything that can > eat granite? I was not aware that granite was such a potential energy > source for biological organisms. But hey, that isn't really the point > now is it?
> > We all agree that > > evolution takes a long time. Building enzymes from scratch is actually > > more a part of abiogenesis than evolution, but most scientists would > > agree, I think, that abiogenesis took a billion years or so, not a few > > months, even with artificially boosted mutation rates.
> Oh, so the evolution of even one little protein sequence is based on > "abiogenesis" not on evolution? Really?! This is *most* interesting. > This is exactly my whole point. Abiogenesis is based on neutral > drift/random walk. Natural selection really is limited when it comes > to ideas on abiogenesis since by far most of the changes in > abiogenesis are functionally neutral as far as a mindless nature is > concerned. This is why scientists think that abiogenesis took > billions of years to produce the first self-replicating cell. But > why? Why does abiogenesis take so long? Because of the neutral gaps. > When you actually start plugging in the numbers and doing some real > estimates based on the idea of neutral gaps, you quickly find that the > abiogenesis of much of anything would take far longer than a few > billion or even many trillions or zillions or googols of years.
snip
> Sean
In fact scientist do not believe abiogenesis took billions of years. According to the evidence it took a very short period of time, in the millions at the most.
And again what numbers are you talking about that produce the "trillions or zillions or googols of years" it would take for abiogenesis to happen, you seem to be avoiding supplying these numbers as I have asked you before.
It seems this is the point you are trying to make in all of your post but we have yet to see any of the math supporting your argument. Without the math you are not doing science but instead just PREACHING what is most likely nonsense.
> > You are contrasting the ease with which a single mutation can lead to > > gain of function (starting on the right background) with the problem > > of evolving a new enzyme from scratch (or from an enzyme with > > unrelated function). Yes. It is much faster if there is a gene > > already there which needs just a single mutation to develop a new, > > useful activity.
> Finally, someone who actually seems to understand what I am talking > about. There are clearly different levels of functional complexity.
Really? How is it clear that mefloquine resistance is less complex than chloroquine resistance? Could you have predicted this before the fact based on a description of the function involved, or before an identification of the probable evolutionary pathway? Can you say anything meaningful about their respective complexities without peeking?
> The function of bacterial antibiotic resistance is extremely simple, > even in comparison to the most simple enzymatic functions.
Except of course for the cases in which antibiotic resistance *is* an enzyme function, as in the case of, say vancomycin or cefotaxime resistance.
> The reason > for this is that there is a dramatically higher ratio of functional > mutations as compared to neutral mutations in the development of > antibiotic resistance as compared to the evolution of a certain > enzymatic activities.
So, how do you determine complexity without *first* knowing what evolutionary changes are involved?
> > Here is a similar contrast from drug resistant malaria. Mefloquine is > > a new anti-malarial drug that has been on the market for about 15 > > years. Mefloquine resistance began to appear in malaria parasites > > within a few years of the release of the drug to the market and is now > > a significant problem in treating malaria in southeast asia and the > > amazon. One can start a culture of mefloquine-sensitive malaria > > parasites in the lab (beginning with a single, cloned parasite) and, > > by adding progressively higher concentrations of mefloquine select for > > a mefloquine resistant population. A single mutation in a single gene > > does the trick.
> Exactly . . .
> > On the other hand, chloroquine resistance is diffferent. Chloroquine > > resitance in malaria parasites appeared in the wild in the 60's and > > spread throughout the world-wide malaria population over the following > > 30 years. However, no one has succeeded in starting with a chloroquine > > sensitive parasite clone and selecting a chloroquine resistant > > population in in vitro culture. Based on sequencing data from > > chloroquine sensitive and chloroquine resistant strains it looks like > > the problem is that chloroquine resistance requires the acquisition of > > a series of 6 or 7 mutations in a particular order. No one has been > > able to get this to happen in cultured parasites in the lab. But it > > clearly happened in "real time" in nature as a result of widespread > > use of chloroquine against malaria.
> The most likely reason why this has not been observed in the lab is > because the lab didn't use a large enough population size to overcome > the neutral gap created by 6 or 7 neutral mutations. A series of 7 > neutral mutations in DNA would create a neutral gap or sea of 16,384 > possibilities. In this case, only one of these possibilities is > "correct." In order to find this correct sequence out of all the > other possibilities, the given population of malaria parasites would > have to undergo random walk. This random walk takes time and this > time is dependent upon several factors. Lets see if we can figure out > a rough estimate based on these factors.
> Let's say that the mutation rate was on the order of 10e-8 mutations > per base pair per generation. On average then, it would take around > 10e7 generations to get just one mutation to one of our 7 base pairs > of interest. If a generation time is one day (I'm not exactly sure > what the generation time is for the malaria parasite), a steady state > population of 10e3 parasites would experience one mutation in these 7 > base pairs every 10,000 days or 27 years on average. Given this > relatively small colony of parasites, it would take around 500,000 > years to develop resistance to chloroquine. If the colony size were > increased to one million parasites, the time required to evolve > resistance would drop to around 5,000 years. If the colony size were > increased to one billion parasites, the time required would drop to > around 5 years.
> These rough estimates based, on the time required to cross a known > neutral gap, are very much in line with what we have seen in the > evolution of chloroquine resistance in the wild and they also explain > why this resistance has never been demonstrated in the lab. The lab > experiments simply didn't use a large enough population size or didn't > carry on the experiments for enough generations.
> In any case, it is a great example that demonstrates very nicely the > limits that neutral gaps put on the theory of evolution. This only > strengthens my theory.
Not really. No one ever denied that there were evolutionary constraints, nor that the majority of mutations are functionally neutral. Nor did anyone ever suggest that *any* arbitrarily selected function would evolve quickly from *any* given precursor. That is your strawman.
But your theory isn't simply that "neutral gaps" exist. That would be fairly uninteresting, and of no real importance to the theory of common descent at all. Your theory is that they are so pervasive as to preclude evolution of life as we see it today in the available history of the world. The fact that chloroquine resistance may take a large population several years to evolve hardly supports such a generalization.
> > So... Both resistances evolved in nature in years to decades; > > evolution of mefloquine resistance has been reproduced in the lab; > > evolution of chloroquine resistance has not. Does this mean that the > > "Designer" let P. falciparum handle mefloquine on its own, but > > intervened to help P. falciparum deal with chloroquine?
> You don't seem to understand the statistics involved here.
Neither do you, apparently. You have argued that the density of sequences for antibiotic resistance may be as high as 1 in 3; you have suggested elsewhere that the density for functional enzyme sequences is about 1 per 1e12, or is it 1e24? In a different context you argued that the density of functional sequences for a 100aa long protein might be as low as 1 per 1e106 (and the logic you used in that post could be extended to arbitrarily long sequences to get arbitrarily low densities such as ~1e-1277 for a 1000aa sequence). Now here you argue that the density of (genetic) sequences conferring chloroquine resistance may be about 1e-4.
So obviously you have no idea what the sequence density for any given function is ahead of time, although you are good at saying: "See, I knew that!" after the fact. Nor do you know what the available evolutionary pathways were, nor what sort of fitness landscapes they traversed. Nonetheless, you are sure that there are enough neutral gaps around to prevent evolution of many of the functions we observe in life today; you base your confidence on the "statistics involved", which enable you to predict with confidence that the density for functional sequences in a sequence space is somewhere between 1 in 3 and 1 in 1e106 (or perhaps even as low as 1e1277).
> Obviously, > a neutral gap in function of 6 or 7 base pairs can easily be crossed > by random walk alone given the much larger population sizes of the > malaria parasites (P. falciparum) that exist in the wild as compared > to the relatively limited population size that was most likely used in > the laboratory experiments. No ID is needed to explain the evolution > of chloroquine resistance in either case. The average time required > is well within reason.
OK, so at least you are smart enough not to deny the evolvability of something that has been observed to evolve.
> > > These very same bacteria would quickly evolve resistance to penicillin > > > if it were added to their environment. No more than a handful of > > > generations would be required. Why then is antibiotic resistance so > > > much easier for them to evolve than the lactase function? What is it > > > about the evolution of relatively simple enzymes that is so much more > > > difficult than the evolution of antibiotic resistance?
> > Enzymes are really complicated. You are right. It almost certainly > > takes more time than you have to watch to evolve a new enzyme from > > scratch (or even from an unrelated enzyme).
> I'm glad that you realize this because many people think that the > evolution of antibiotic resistance is something very significant > and/or complex. What many do not realize or admit is that even the > relatively simple function of a single protein based enzyme, is far > more complex than the function of antibiotic resistance.
Except, again, when the antibiotic resistance in question *is* an enzyme activity.
> Obviously more time is required to evolve the enzymatic functions than > the functions of antibiotic resistance. That question is, "Why?" Why > is more time required to evolve functions of increasing complexity? I > am proposing that neutral gaps are the reason for this observed > phenomenon. What is your explanation?
My explanation is that you claim with hindsight a level of complexity based on what you already know about the evolutionary pathway, so that your "theory" is basically a circular argument that lacks the predictive value you
...
> > You are contrasting the ease with which a single mutation can lead to > > gain of function (starting on the right background) with the problem > > of evolving a new enzyme from scratch (or from an enzyme with > > unrelated function). Yes. It is much faster if there is a gene > > already there which needs just a single mutation to develop a new, > > useful activity.
> Finally, someone who actually seems to understand what I am talking > about.
That I understand you does not mean that you are correct.
>There are clearly different levels of functional complexity. > The function of bacterial antibiotic resistance is extremely simple, > even in comparison to the most simple enzymatic functions. The reason > for this is that there is a dramatically higher ratio of functional > mutations as compared to neutral mutations in the development of > antibiotic resistance as compared to the evolution of a certain > enzymatic activities.
Why do you say that. Some antibiotic resistance genes encode enzymes. How could you possibly know anything about a "dramatically higher ratio of functional mutations as compared to neutral mutations in the development of antibiotic resistance as compared to the evolution of a certain enzymatic activities" without specifying in a whole lot more detail what genes you are talking about and without doing experiments to determine which changes are or are not functional or neutral? Everything depends on the starting material and the "fitness landscape" around the point you start from. In some cases you pretty clearly even "cannot get there from here," e.g., not many feathered bats, or gilled whales, even though such creatures might be at finess optima if they existed.
> > Here is a similar contrast from drug resistant malaria. Mefloquine is > > a new anti-malarial drug that has been on the market for about 15 > > years. Mefloquine resistance began to appear in malaria parasites > > within a few years of the release of the drug to the market and is now > > a significant problem in treating malaria in southeast asia and the > > amazon. One can start a culture of mefloquine-sensitive malaria > > parasites in the lab (beginning with a single, cloned parasite) and, > > by adding progressively higher concentrations of mefloquine select for > > a mefloquine resistant population. A single mutation in a single gene > > does the trick.
> Exactly . . .
> > On the other hand, chloroquine resistance is diffferent. Chloroquine > > resitance in malaria parasites appeared in the wild in the 60's and > > spread throughout the world-wide malaria population over the following > > 30 years. However, no one has succeeded in starting with a chloroquine > > sensitive parasite clone and selecting a chloroquine resistant > > population in in vitro culture. Based on sequencing data from > > chloroquine sensitive and chloroquine resistant strains it looks like > > the problem is that chloroquine resistance requires the acquisition of > > a series of 6 or 7 mutations in a particular order. No one has been > > able to get this to happen in cultured parasites in the lab. But it > > clearly happened in "real time" in nature as a result of widespread > > use of chloroquine against malaria.
> The most likely reason why this has not been observed in the lab is > because the lab didn't use a large enough population size to overcome > the neutral gap created by 6 or 7 neutral mutations. A series of 7 > neutral mutations in DNA would create a neutral gap or sea of 16,384 > possibilities. In this case, only one of these possibilities is > "correct." In order to find this correct sequence out of all the > other possibilities, the given population of malaria parasites would > have to undergo random walk. This random walk takes time and this > time is dependent upon several factors. Lets see if we can figure out > a rough estimate based on these factors.
> Let's say that the mutation rate was on the order of 10e-8 mutations > per base pair per generation. On average then, it would take around > 10e7 generations to get just one mutation to one of our 7 base pairs > of interest. If a generation time is one day (I'm not exactly sure > what the generation time is for the malaria parasite),
Yeah, that's tricky; in nature when you take into account the likelihood of the parasite actually getting out one host, into a mosquito, and then into another host, the effective generation time is about 6 months, which is completely different than the 48-72 hours it takes for one erythrocytic stage cycle of the parasite.
> a steady state > population of 10e3 parasites would experience one mutation in these 7 > base pairs every 10,000 days or 27 years on average. Given this > relatively small colony of parasites, it would take around 500,000 > years to develop resistance to chloroquine. If the colony size were > increased to one million parasites, the time required to evolve > resistance would drop to around 5,000 years. If the colony size were > increased to one billion parasites, the time required would drop to > around 5 years.
In fact the "colony" sizes people use are on the order of 5,000,000 parasites per culture, though it is possible to grow 10 fold larger amounts easily enough.
> These rough estimates based, on the time required to cross a known > neutral gap, are very much in line with what we have seen in the > evolution of chloroquine resistance in the wild and they also explain > why this resistance has never been demonstrated in the lab. The lab > experiments simply didn't use a large enough population size or didn't > carry on the experiments for enough generations.
> In any case, it is a great example that demonstrates very nicely the > limits that neutral gaps put on the theory of evolution. This only > strengthens my theory.
But how do you know that even these gaps are neutral? Your own example of the evolution of lactase makes it clear that you cannot make ad hoc calculations to tell you how long it will take for something to evolve. Everything depends on the available starting materials, the relative fitness of intermediates, changes in the environment, etc. Multiplying the number of genetic differences between two sequences in related organisms by the estimated population size, mutation rate, and generation time, is pretty irrelevant. No one thinks that evolution works entirely by neutral mutation and random walks.
> > So... Both resistances evolved in nature in years to decades; > > evolution of mefloquine resistance has been reproduced in the lab; > > evolution of chloroquine resistance has not. Does this mean that the > > "Designer" let P. falciparum handle mefloquine on its own, but > > intervened to help P. falciparum deal with chloroquine?
> You don't seem to understand the statistics involved here. Obviously, > a neutral gap in function of 6 or 7 base pairs can easily be crossed > by random walk alone given the much larger population sizes of the > malaria parasites (P. falciparum) that exist in the wild as compared > to the relatively limited population size that was most likely used in > the laboratory experiments. No ID is needed to explain the evolution > of chloroquine resistance in either case. The average time required > is well within reason.
We know what the "average time" is, not because of your post hoc statistics, but because we observed the evolution of chloroquine resistance in nature.
> > > These very same bacteria would quickly evolve resistance to penicillin > > > if it were added to their environment. No more than a handful of > > > generations would be required. Why then is antibiotic resistance so > > > much easier for them to evolve than the lactase function? What is it > > > about the evolution of relatively simple enzymes that is so much more > > > difficult than the evolution of antibiotic resistance?
> > Enzymes are really complicated. You are right. It almost certainly > > takes more time than you have to watch to evolve a new enzyme from > > scratch (or even from an unrelated enzyme).
> I'm glad that you realize this because many people think that the > evolution of antibiotic resistance is something very significant > and/or complex. What many do not realize or admit is that even the > relatively simple function of a single protein based enzyme, is far > more complex than the function of antibiotic resistance.
> Obviously more time is required to evolve the enzymatic functions than > the functions of antibiotic resistance. That question is, "Why?" Why > is more time required to evolve functions of increasing complexity? I > am proposing that neutral gaps are the reason for this observed > phenomenon. What is your explanation?
> > We all agree that > > evolution takes a long time. Building enzymes from scratch is actually > > more a part of abiogenesis than evolution, but most scientists would > > agree, I think, that abiogenesis took a billion years or so, not a few > > months, even with artificially boosted mutation rates.
> Oh, so the evolution of even one little protein sequence is based on > "abiogenesis" not on evolution? Really?! This is *most* interesting. > This is exactly my whole point. >Abiogenesis is based on neutral > drift/random walk. Natural selection really is limited when it comes > to ideas on abiogenesis since by far most of the changes in > abiogenesis are functionally neutral as far as a mindless nature is > concerned.
I have no idea why you think this. Most ideas about abiogenesis (apart from creationist, junkyard to B727, strawmen) are based on selection. We all agree that a random walk through all possible chemical structures
...
