Questions for Sean Pitman

[LiveFreeOrDie]

Please answer the questions below. For each answer, please indicate the objective evidence and reasoning that supports your answer.

1. How old is the Earth?

2. Where did all the species we observe today come from?

 

[Sean Pitman]

Originally posted by LiveFreeOrDie
Please answer the questions below. For each answer, please indicate the objective evidence and reasoning that supports your answer.

1. How old is the Earth?

2. Where did all the species we observe today come from?

Really, I'm not all that concerned with the age of the Earth per se, but more with the age of the geologic column. The earth itself may in fact be about 4.5 billion years old, but that really is a non-issue with me. I take issue with the idea that the geologic column was formed over the past several hundred million years. It seems to me that the geologic column was formed relatively rapidly as well as recently. For details as to why I think this visit:

"http://naturalselection.0catch.com/Files/The%20Geologic%20Column.html"


As far as the species on earth, many times various forms are given different species names based on phenotypic variations that are not necessarily outside the range for creatures that do in fact share a common gene pool.

For example, if the bulldog phenotype where found only in the fossil record and the German Shepherd were living today, would they be classed in the same species or even genus groups when compared side-by-side? I doubt it.

Since a single gene pool can produce "drastic" differences in phenotypic forms, how are scientists so sure of their fossil classification models? Often only slight phenotypic differences are enough to place a fossil creature in a different species, genus or even family group than its modern-day counterpart or than its counterpart found elsewhere in the geologic column. The problem is that differences, even fairly significant differences are known to exist between members of the same gene pool. Because of this fact, taxonomic classification models can be quite subjective and even misleading.

For example, scientists from Berkeley have noted that, "the planktonic larvae of many marine invertebrates are commonly described as separate species when they are first discovered in the ocean. Only later when they can be reared in the laboratory can the link to their adult form be recognized. Similarly, the different life stages of many fungi are given different names because they have different physical forms and hosts. Only through detailed inoculation studies can mycologists work out which forms are members of the same life cycle. Since some fungi may have more than five discrete life cycle stages, this can be a long process. Similar problems exist for some marine algae and multiple-host parasitic organisms of many kinds. Even among well-studied vertebrates, some tropical birds have been described as separate species until they are observed to mate and rear young together."

"http://www.ucmp.berkeley.edu/IB181/VPL/Pres/Pres1.html"

Also, a "Detailed study of large sympatric populations and fossil assemblages of the highly variable species Elphidium excavatum (Terquem) [Benthic foraminifera] collected from 20 widely spaced locations indicates that a variety of morphotypes of Elphidium can be linked to one another in a number of interlocking intergradational series. Ten morphotypes are recognized and grouped as formae (ecophenotypes) of Elphidium excavatum (Terquem); these morphotypes were previously considered as 22 independent taxa by various authors. Although all of these formae belong to the same species, it is suggested [by the authors] that the distinction among them should be retained because of their potential as a valuable interpretive tool in paleo-ecological and biostratigraphic studies of Holocene and Pleistocene sediments."

"http://www.dal.ca/~es/abstract/ab_th_83.htm"

Likewise, the classifications of plants is classically prone to give different names to very similar plants or even parts of the same plant. Bill DiMichele, a paleobotanist, notes, "The problem of organ association is one of the reasons why paleobotanists insist on so many different names for isolated parts of the same whole plant. Furthermore, there are phenotypic convergences that can cause great confusion, such leaves of virtually identical morphology borne on ferns and seed plants. Separate names for each fossil plant organ can be carried to extremes, however, and not all paleobotanists, myself included, favor the attribution of separate names to organs otherwise known in attachment (yes, this is still done routinely, no kidding)."

"http://www.ngdc.noaa.gov/mgg/sepm/palaios/9810/dimichele.html"


The Mazon Creek flora is incredibly diverse. Over 400 species from at least 130 genera have been identified from Mazon Creek nodules. However, the number of different kinds of plants represented is very difficult to determine. There are at least two reasons for this difficulty. The first reason is the convention among paleobotanists that separate plant parts receive different names. This procedure tends to inflate the number of plant names. The second reason is that paleobotanists are still trying to determine which taxa are valid.

"http://www.museum.state.il.us/exhibits/mazon_creek/about_mazon_creek.html"

The point is that many of the different "species" that we observe today could have descended from a smaller group of relatively static gene pools. Relatively static gene pools can and do give rise to a huge variety of forms or phenotypes. Each one of these different forms is simply an expression of part of a larger gene pool of phenotypic options. The gene pool itself need not have evolved to give rise to the variations. For example, the various breeds of dogs cover a very large range of different phenotypic forms, and yet such variations are not based on the acquisition of new genetic information into the gene pool. In other words, a non-evolving gene pool can rapidly give rise to a huge variety of different forms via some selection process that is not dependent upon allelic mutations or the gain of new information.

It seems to me that various gene pools are isolated by neutral gaps in genetic functions that cannot be crossed with the aid of natural selection in what anyone would consider to be a reasonable amount of time. Of course, studies done with galactosidase and nylonase evolution in bacteria have been hailed as clear example of evolution in action. To a point, I would agree. However, a closer look at what is actually involved with these cases also shows a clear limit to what functions such evolution can evolve. The gaps that are crossed by such mutations are one or at most two point mutations wide. Many might argue that the evolution of nylonase arose via a frame-shift mutation that involved changing hundreds of amino acids. This is true, but it was a change in only one amino acid that caused the frame shift. Thus, the gap between what was already there, and the new nylonase function, was crossed by a single mutation of one base pair position. Such a gap is not much a problem for random mutations like this to cross. It is only one random mutational step wide. The problem for evolution comes when new functions cannot be realized in just one or two steps, but are separated from all current functions by gaps of neutral mutations that are wider than two or three of these neutral steps.

For example, in an experiment with colonies of E. coli bacteria B.G. Hall deleted the lacZ genes. Of course, the lacZ genes are the genes responsible for the production the lactase enzyme. Hall then grew these mutated bacteria on selective lactose enriched media. In a very short time, they "evolved" the ability to utilize lactose for energy again. What happened is that another gene with an unknown function evolved to produce a brand new enzyme with the lactase function after experiencing a single point mutation (ebgA – evolved beta galactosidase). Hall was happy for the success of his experiment, but disappointed that only a single point mutation was all that was needed to evolve the new lactase enzyme. What is especially interesting is that he then proceeded to delete both the lacZ genes and the newly evolved ebgA gene in some of his E. coli to see if these double mutants would evolve the lactase enzyme if placed on lactose media. They didn't and they haven't despite observation for over 20 years now. Hall described these bacteria as having, "limited evolutionary potential."

So, what is it that limits the evolutionary potential of a living organism? I propose that the blockade to evolution can be found in gaps of neutral function that are simply too wide to cross without the aid of natural selection in what anyone would consider a reasonable amount of time... even given an evolutionary time scale of billions of years.

For a more detailed discussion of this topic see:

"http://naturalselection.0catch.com/Files/Galactosidase%20Evolution.html"


Anyway, I hope this helps you understand my position better.

Sean

 

[sulphur]

AS to your answer about the geolgic column,have you any knowledge about pre cambrian or cambrian rocks. If not then that part of your answer is a load of rubbish

 

[LiveFreeOrDie]

Originally posted by Sean Pitman
Really, I'm not all that concerned with the age of the Earth per se, but more with the age of the geologic column. The earth itself may in fact be about 4.5 billion years old, but that really is a non-issue with me. I take issue with the idea that the geologic column was formed over the past several hundred million years. It seems to me that the geologic column was formed relatively rapidly as well as recently. For details as to why I think this visit:

"http://naturalselection.0catch.com/Files/The%20Geologic%20Column.html"

Wow. That's a regular Gish Gallop of a web page if I ever saw one. It's nothing more than the usual creationist quote mining, selective misuse of data, and scientific misunderstanding. Underlying the whole affair is the presumption that scientists were too stupid to consider any of this stuff before.

The big problem for you is that you've done absolutely nothing to prove your hypothesis. So you think the geologic column was formed relatively recently due to a global catastrophe? When exactly did it happen? What kind of catastrophe was it? Where is the geologic evidence? How does your theory account for the geological, paleontological, and chemical evidence that seem to indicate a very old age?

Until you offer a concrete hypothesis and evidence to back it up, your Chicken Little strategy with regard to mainstream science will get you exactly nowhere.

As far as the species on earth, many times various forms are given different species names based on phenotypic variations that are not necessarily outside the range for creatures that do in fact share a common gene pool.

For example, if the bulldog phenotype where found only in the fossil record and the German Shepherd were living today, would they be classed in the same species or even genus groups when compared side-by-side? I doubt it.

Since a single gene pool can produce "drastic" differences in phenotypic forms, how are scientists so sure of their fossil classification models? Often only slight phenotypic differences are enough to place a fossil creature in a different species, genus or even family group than its modern-day counterpart or than its counterpart found elsewhere in the geologic column. The problem is that differences, even fairly significant differences are known to exist between members of the same gene pool. Because of this fact, taxonomic classification models can be quite subjective and even misleading.

I don't understand why you are bringing up this line of reasoning as it would seem to argue against your point. If a single gene pool can produce drastic differences, and species differences are in some cases very insignificant, then doesn't it follow that evolution could easily be responsible for the origin of new species?

"http://www.ucmp.berkeley.edu/IB181/VPL/Pres/Pres1.html"

"http://www.dal.ca/~es/abstract/ab_th_83.htm"

"http://www.ngdc.noaa.gov/mgg/sepm/palaios/9810/dimichele.html"

"http://www.museum.state.il.us/exhibits/mazon_creek/about_mazon_creek.html"

All these web pages do is highlight the fact that it can often be difficult to precisely determine species boundaries. Isn't this exactly what we would expect if evolution were in fact occurring?

The point is that many of the different "species" that we observe today could have descended from a smaller group of relatively static gene pools. Relatively static gene pools can and do give rise to a huge variety of forms or phenotypes. Each one of these different forms is simply an expression of part of a larger gene pool of phenotypic options.

If you're comfortable with all current species having evolved from a few "static" gene pools (whatever that is), then it shouldn't be a very big leap for you to get comfortable with them evolving from ONE gene pool of common ancestors. After all, if you have no problem with the idea of 100 species coming from 10, then it should be equally acceptable for those 10 to have arisen from 1.

The gene pool itself need not have evolved to give rise to the variations. For example, the various breeds of dogs cover a very large range of different phenotypic forms, and yet such variations are not based on the acquisition of new genetic information into the gene pool. In other words, a non-evolving gene pool can rapidly give rise to a huge variety of different forms via some selection process that is not dependent upon allelic mutations or the gain of new information.

I'm sorry, a gene pool can't be both "non-evolving" and "give rise to a huge variety of forms", as that would be a contradiction.

And where did you get the idea that dog breeding doesn't require mutations? What magical armor protects dog DNA against mutations?

It seems to me that various gene pools are isolated by neutral gaps in genetic functions that cannot be crossed with the aid of natural selection in what anyone would consider to be a reasonable amount of time.

Argument from incredulity. Big deal.

Of course, studies done with galactosidase and nylonase evolution in bacteria have been hailed as clear example of evolution in action. To a point, I would agree. However, a closer look at what is actually involved with these cases also shows a clear limit to what functions such evolution can evolve. The gaps that are crossed by such mutations are one or at most two point mutations wide. Many might argue that the evolution of nylonase arose via a frame-shift mutation that involved changing hundreds of amino acids. This is true, but it was a change in only one amino acid that caused the frame shift. Thus, the gap between what was already there, and the new nylonase function, was crossed by a single mutation of one base pair position.

Again, I can't see why you are bringing this up as it harms your case. These experiments show just how powerful random mutation can be as an engine to produce novelty. A single mutation allowed these bacteria to develop a whole new function. A SINGLE MUTATION. Just think how much novelty could be produced by stringing together multiple mutations in a row. Why, I bet you could climb Mount Improbable if you waited long enough.

Such a gap is not much a problem for random mutations like this to cross. It is only one random mutational step wide. The problem for evolution comes when new functions cannot be realized in just one or two steps, but are separated from all current functions by gaps of neutral mutations that are wider than two or three of these neutral steps.

Talking about "gaps of neutral mutations" is begging the question. How do you know the intermediate mutations were neutral? In fact we have every reason to suspect that they wouldn't be.

For example, in an experiment with colonies of E. coli bacteria B.G. Hall deleted the lacZ genes. Of course, the lacZ genes are the genes responsible for the production the lactase enzyme. Hall then grew these mutated bacteria on selective lactose enriched media. In a very short time, they "evolved" the ability to utilize lactose for energy again. What happened is that another gene with an unknown function evolved to produce a brand new enzyme with the lactase function after experiencing a single point mutation (ebgA – evolved beta galactosidase). Hall was happy for the success of his experiment, but disappointed that only a single point mutation was all that was needed to evolve the new lactase enzyme. What is especially interesting is that he then proceeded to delete both the lacZ genes and the newly evolved ebgA gene in some of his E. coli to see if these double mutants would evolve the lactase enzyme if placed on lactose media. They didn't and they haven't despite observation for over 20 years now. Hall described these bacteria as having, "limited evolutionary potential."

This is a fine example of creationist selective quotation. Hall's own analysis adds far more qualifications to his findings:

The present study shows that ... the existing sequence of the wild-type ebgA gene, together with the genetic code, impose an evolutionary constraint against that particular solution under these experimental conditions. (emphasis mine)

You are making a completely unwarranted extrapolation of Hall's results.

So, what is it that limits the evolutionary potential of a living organism? I propose that the blockade to evolution can be found in gaps of neutral function that are simply too wide to cross without the aid of natural selection in what anyone would consider a reasonable amount of time... even given an evolutionary time scale of billions of years.

That's a nice hypothesis. Unfortunately for you, the problems are twofold:

1. There is no evidence that the gaps between species are SOLELY the result of changes that are neutral in function. In fact, the opposite is probably true. Fossil evidence, like the evolutionary sequence for whales, illustrates this quite nicely. Each whale intermediate is fully functional yet slightly better adapted to the marine environment than its predecessor.

2. Strong experimental evidence indicates that rates of evolution in the wild are more than enough to produce the observed genetic differences between species.


So it appears your position on the age of the Earth and the origin of species is based on some rather faulty premises and logic. If you'd like to better understand the mainstream scientific position on those issues, I'm sure the participants on this board would be happy to direct you to the proper resources.

 

[Jerry Smith]

To a point, I would agree. However, a closer look at what is actually involved with these cases also shows a clear limit to what functions such evolution can evolve. The gaps that are crossed by such mutations are one or at most two point mutations wide. Many might argue that the evolution of nylonase arose via a frame-shift mutation that involved changing hundreds of amino acids. This is true, but it was a change in only one amino acid that caused the frame shift.

You've made it clear that you don't understand much about how DNA is structured and transcribed here. It was a change in one "nucleotide" that caused the frame shift (rather than in one amino acid), but that frame shift carries far-reaching results. Consider:

gcc gaa tag agt agt gat tcg ctt gac acg ...
Now, frame shifted:
cgg aat aga gta gtg att cgc ttg aca cg...
Here we have 9 codons (each designating one amino acid) affected by a single mutation (a frameshift on one nucleotide).

This just scratches the surface. There are many types of mutation that can have far-reaching consequences for the pheontype.

 

[Sean Pitman]

Originally posted by Jerry Smith
You've made it clear that you don't understand much about how DNA is structured and transcribed here. It was a change in one "nucleotide" that caused the frame shift (rather than in one amino acid), but that frame shift carries far-reaching results. Consider:

gcc gaa tag agt agt gat tcg ctt gac acg ...
Now, frame shifted:
cgg aat aga gta gtg att cgc ttg aca cg...
Here we have 9 codons (each designating one amino acid) affected by a single mutation (a frameshift on one nucleotide).

This just scratches the surface. There are many types of mutation that can have far-reaching consequences for the pheontype.

Certainly frame-shift mutations do involve a change or changes in DNA or nucleotides.  I never meant to indicate otherwise. Mutations themselves are changes in nucleotides, not amino acids.  However, these changes result in amino acid changes.  That is what makes them functionally/phenotypically different.  The frame-shift that resulted from a single nucleotide mutation resulted in the production of a brand new protein composed of a completely different sequence of amino acids.  This is what gave this new enzyme its new nylonase function.

Certainly there are a great many different types of mutations that can and do have far-reaching consequences for the resulting phenotype.  Most of these functional (non-neutral) mutations are harmful to the phenotype.  Rarely, one of them will be beneficial, such as the one that produced the nylonase enzyme in a nylon rich environment.  However, the problem is that there are certain phenotypic functions that are separated from existing genotypic sequences by gaps of neutral mutations that are wider than one or two point mutations.  It was statistically easy to cross the gap to the nylonase function because only one mutation was required to achieve the nylonase function for that bacterium.  However, what if several neutral mutations were required before the nylonase function could be realized?  It might take a lot longer for the evolution of such a function to be achieved. It seems to me that with each neutral mutation that is required to achieve a particular function, the amount of time that is needed increases so dramatically that its evolution becomes statistically impossible for that creature's descendants.

 

Sean

 

[Jerry Smith]

Sean,

Scientists are debating the relative impact on selectively-neutral mutations on the course evolution. Obviously, they do have some impact. Sometimes it is a neutral mutation that changes the genotype in a way that one adaptive solution to an environmental problem becomes more probable than other possible solutions.

One problem with the approach you seem to be taking is that you cannot statistically account for all of the possible adaptive solutions to any given evolutionary problem. You look at the individual probability of the mutations that lead from phenotype A to phenotype B (where there is possibly no selective advantage found in the genetic midway mark between the two), and conclude that the change is too improbable. It may be the case that there was very little selectively neutral mutation between the two steps after all (do you have research on any particular adaptions and the number of selectively neutral mutations required to bring them about??)... On the other hand, it may have been that there were thousands of genetic paths to the same phenotypic adaptation, and/or thousands of phenotypic adaptations that would have equally well satisfied the evolutionary need. This would greatly affect, and most likely obviate any probability calculation based on the particular genetic route that was ultimately responsible for the adaptation found in nature.

 

[Sean Pitman]

Rufus,

I'm sorry, a gene pool can't be both "non-evolving" and "give rise to a huge variety of forms", as that would be a contradiction.

As I understand it, a non-evolving gene pool can give rise to many different phentypic forms.  The same unchanging gene pool can give rise to a huge number of different forms.  Creatures that arise from a given gene pool are but partial reflections of a larger gene pool of phenotypic options. Gregor Mendel was the first one to describe this phenomenon.  His beautifully designed experiments with pea plants were the first to focus on the numerical relationships among traits appearing in the progeny of hybrids.  His interpretation for this phenomenon was that material and unchanging hereditary “elements” undergo segregation and independent assortment.  These elements are then passed on unchanged (except in arrangement) to offspring thus yielding a very large, but finite number of possible variations.


"http://naturalselection.0catch.com/Files/Gregor%20Mendel.html"


A given gene pool contains many trait options or "elements" that are not all expressed in any one creature.  Different creatures that arise from a common gene pool express different elements or traits that are contained by the same static (unchanging) gene pool. 

This is not to say that gene pools do not mutate and change, but many observed variations that we see between different creatures from the same gene pool need not be dependent upon such mutations.  Drastic changes in morphology can be realized without relying on any new mutations or the evolution of even one novel function. 

For example, breeding is not generally based on the establishment of new functions via mutations and natural selection, but on the selection of pre-established functions from a common gene pool of options.  Breeding can produce dramatic changes in a very rapid manner because no evolution is required.  All the various options for these drastic changes were already pre-programmed into the gene pool of options.  When Mendel bred two pea plants together that each produced purple flowers, and 25% of their offspring produced white flowers . . .  was this startling change an example of "evolution in action"?  No, it wasn't. . . at least not in that particular generation.  It certainly was a startling phenotypic change in one generation, but the change was made possible, not because of a new mutation or the evolution of a new allelic function, but because the option was already there, waiting, preformed, in the pea gene pool of options.

So, many phenotypic changes, significant changes, can often be explained without reliance on mutation and natural selection.  These are therefore not examples of genotypic evolution in action.  Phenotypic change is not always based on genotypic mutation/evolution. Also, such phenotypic variations, that do not involve the evolution of new genetic information, are often classed in different taxonomic groups.  These creatures may in fact have arisen from the same gene pool and be based on the same genotypic blueprint, and yet, based on phenotypic differences, they are classed as different species or even higher taxonomic groups.  But, where is the genotypic evolution here?


Sean

 

[Jerry Smith]

So, many phenotypic changes, significant changes, can often be explained without reliance on mutation and natural selection. These are therefore not examples of genotypic evolution in action. Phenotypic change is not always based on genotypic mutation/evolution. Also, such phenotypic variations, that do not involve the evolution of new genetic information, are often classed in different taxonomic groups. These creatures may in fact have arisen from the same gene pool and be based on the same genotypic blueprint, and yet, based on phenotypic differences, they are classed as different species or even higher taxonomic groups. But, where is the genotypic evolution here?

A static gene pool would quickly reach a kind of equilibrium under a given set of environmental circumstances, with only selectively neutral phenotypic traits being varied. This never happens for two reasons: 1) no gene pool is static. Mutations are inevitable and constant, and 2) no environmental circumstances are static over the very long run. For these two reasons, evolution is unavoidable. Dogs evolved from wolves, yet they learn to understand and accept signalled communication from humans far above any other canine species, including wolves. This may or may not represent genotypic evolution (it is extremely unlikely that wolves had a genetic program for learning to accept human instruction in their oldest ancestral gene pool). One way or the other, it does represent the evolution of new information in the dog. Chances are that the ancestral wolf population did have a genetic program for learning canine signalling conventions, and that it was only a small change on this program, early in the evolution of dogs that was strongly selected for in an environment where canines and humans lived in proximity. Thus, we most likely have an increase in both genotypic and phenotypic information. Of course, the gene pool must be enriched by mutations that are usually selectively neutral at the time they occur before the genetic diversity that selection acts upon can produce novel changes in a population that will result in a new taxonomic group.

 

[LiveFreeOrDie]

Originally posted by Sean Pitman
Rufus

Um, I'm not Rufus.

These elements are then passed on unchanged (except in arrangement) to offspring thus yielding a very large, but finite number of possible variations.

Not true. If you accept that mutations occur, then occasionally new "elements" (alleles is probably the more correct term) will be added to the gene pool making the number of variations theoretically infinite.

A given gene pool contains many trait options or "elements" that are not all expressed in any one creature.  Different creatures that arise from a common gene pool express different elements or traits that are contained by the same static (unchanging) gene pool.

No. Some creatures have a random new thing added now and then.

This is not to say that gene pools do not mutate and change,

I believe you just conceded my point.

...but many observed variations that we see between different creatures from the same gene pool need not be dependent upon such mutations.  Drastic changes in morphology can be realized without relying on any new mutations or the evolution of even one novel function. 

Just because morphological changes CAN be realized without new mutations doesn't mean that they MUST.

For example, breeding is not generally based on the establishment of new functions via mutations and natural selection, but on the selection of pre-established functions from a common gene pool of options.  Breeding can produce dramatic changes in a very rapid manner because no evolution is required.  All the various options for these drastic changes were already pre-programmed into the gene pool of options.

Breeding doesn't rely on random mutations because then it would be a pretty unproductive activity. Starting with one good-tasting tomato plant and waiting for its offspring to randomly evolve disease resistance is clearly going to take longer than trying to cross-breed it with stock from existing disease-resistant varieties. People aren't stupid.

And contrary to your statement, breeding IS a form of evolution. Any time the distribution of alleles in a population changes, it has evolved. The reason breeding can produce results faster than natural evolution is because the selection criteria are very tightly controlled.

So, many phenotypic changes, significant changes, can often be explained without reliance on mutation and natural selection.  These are therefore not examples of genotypic evolution in action.  Phenotypic change is not always based on genotypic mutation/evolution. Also, such phenotypic variations, that do not involve the evolution of new genetic information, are often classed in different taxonomic groups.

You're committing the same fallacy again. Just because SOME changes can be explained without reliance on mutation, does not mean that they ALL can.

These creatures may in fact have arisen from the same gene pool and be based on the same genotypic blueprint, and yet, based on phenotypic differences, they are classed as different species or even higher taxonomic groups.  But, where is the genotypic evolution here?

The genotypic evolution is in the change of the distribution of the traits within the gene pool. Take a gene pool that starts out with a normal bell curve distribution. Then, over time, say two somewhat distinct populations develop clustered around the ends of the distribution. Now your distribution looks sort of like a suspension bridge, with peaks near the ends and a dip in the middle. In fact it starts to look like two bell curves stuck together. Now the important part is that, over time, random mutations will keep extending the ends of the curve. If these mutations provide an advantage, the two populations may grow further and further apart until, eventually, the “bridge” snaps and the gene pools become completely isolated.

That whole process, from change in distribution, to divergence, to isolation, IS evolution. Since you conceded that mutations within gene pools do occur, I do not see how you can deny the facts of evolution as stated above.

 

[LiveFreeOrDie]

By the way, I see you've dropped the age of the Earth issue. Another typical Gatling Gish tactic -- when the temperature gets too hot, move on to something else.

 

[LiveFreeOrDie]

Hello? Dr. Pitman?

 

[RufusAtticus]

I need Pitman to come back and show me how "incompetent" I am in Genetics.

 

[lucaspa]

Originally posted by Sean Pitman
The problem for evolution comes when new functions cannot be realized in just one or two steps, but are separated from all current functions by gaps of neutral mutations that are wider than two or three of these neutral steps.

For example, in an experiment with colonies of E. coli bacteria B.G. Hall deleted the lacZ genes. Of course, the lacZ genes are the genes responsible for the production the lactase enzyme. Hall then grew these mutated bacteria on selective lactose enriched media. In a very short time, they "evolved" the ability to utilize lactose for energy again. What happened is that another gene with an unknown function evolved to produce a brand new enzyme with the lactase function after experiencing a single point mutation (ebgA – evolved beta galactosidase). Hall was happy for the success of his experiment, but disappointed that only a single point mutation was all that was needed to evolve the new lactase enzyme. What is especially interesting is that he then proceeded to delete both the lacZ genes and the newly evolved ebgA gene in some of his E. coli to see if these double mutants would evolve the lactase enzyme if placed on lactose media. They didn't and they haven't despite observation for over 20 years now. ...
So, what is it that limits the evolutionary potential of a living organism? I propose that the blockade to evolution can be found in gaps of neutral function that are simply too wide to cross without the aid of natural selection in what anyone would consider a reasonable amount of time... even given an evolutionary time scale of billions of years.

For a more detailed discussion of this topic see:

"http://naturalselection.0catch.com/Files/Galactosidase%20Evolution.html" 

You've brought this up several times, so let's look at it and the website in detail.

First, Miller uses the Hall experiment as an example of the evolution of an irreducibly complex system. 

Second, the comment of "now for 20 years" is misleading, since Hall hasn't been running the experiment for 20 years.  The original paper was written in 1982, but there is no indication Hall continued to run the experiment after the paper was published. In fact, experience with other researchers would indicate that the experiment was terminated.

Now, Hall deleted the lac Z gene and, it turned out, that one bacteria had a variation of the egbA protein that had some galactosidase activity. This ability was conferred by a single point mutation in the gene. Because the selection criteria were so stringent, pretty soon all the bacteria were descended from this clone.

"One must also note that <I style="mso-bidi-font-style: normal">only</I> a mutation of this particular gene gave the needed lactase activity.<SPAN style="mso-spacerun: yes">&nbsp; </SPAN>No mutations in any other gene ended up giving a bacterial colony lactase ability.<SPAN style="mso-spacerun: yes">&nbsp; </SPAN>Therefore, without this spare tire gene, it can be assumed that the “evolution” of lactase ability might be quite a bit more difficult.

As you can see, this is a bit misleading. Within the time span of the experiment, this is the only mutation seen in this population.&nbsp; It is not the only possible one, but the one seen within the limits.

Now, other strains of bacteria (from other clones), didn't have this variation:

"In fact, several of Hall’s mutant strains of <I>E. coli</I> could not evolve lactase ability at all.<SPAN style="mso-spacerun: yes">&nbsp; </SPAN>He described these strains as having “limited evolutionary potential.”<SUP> "</SUP>

IOW, they didn't have the variation in the population and the favorable mutation didn't appear in the time frame.&nbsp; This would lead to extinction of these strains if only galactosidase was present as an energy source.&nbsp; Plain and simple.

Now, let's look at some of the other&nbsp; statements:

"The mutational change was unguided by natural selection since full function was achieved in a single point mutation without any functional intermediaries.<SPAN style="mso-spacerun: yes">&nbsp; "</SPAN>

Red herring. All mutation are unguided by natural selection.&nbsp; Mutations are variations and provide the raw material for natural selection to work upon.

"We also know that only an extremely small fraction of the total number of possible different proteins of this length (or smaller) could even theoretically cleave lactose."

Excuse me? How do we know this? The article doesn't give any data on this. It's a bare assertion critical to the argument but just given without any support.

What Pitman then proposes is that not one, but 5 mutations are needed in a 1,000 amino acid protein to confer lactase activity.&nbsp; He also supposes that these mutations cannot start until the necessity of having a lactase activity is required.&nbsp; Then Pitman calculates that there is not enough time.

&nbsp;He also ignores that several of the mutations could have been accumulating for 40,000 years before the environment changed.&nbsp; So, there really could have been 5 point mutations needed, but 4 had already been done and were present in the gene.

Pitman also assumes that none of the 4 point mutations has any selective value for a function other than lactase activity.&nbsp; IOW, exaptation.

"By Hall's own calculations, the true mutation rate would be closer to one mutation per 4,200,000 base pairs in 1,000 generations"

That's way too low.&nbsp; Just copying errors by polymerase are 1 per 1,000,000 base pairs per cell division, or generation.&nbsp; Never mind radiation and chemicals. This quoted mutation rate is 10^9 lower than anyone else has seen.&nbsp; We really need to look at the original paper. I'll get it.

Pitman's article then becomes very confused, mixing in IC with all this. Perhaps you can help explain this.

However, the basic flaw is the assumption that you must have neutral mutations.&nbsp; That the mutations can't possibly be selective for other functions and neutral for the one under study. Furthermore, studies since Hall have shown hypermutant strains and sequential evolution of systems.

3.&nbsp; D. Grady, Quick-change pathogens gain an evolutionary advantage.Science, vol.274: 1081, 1996 (November 15).&nbsp; The primary research articleis JE LeClerc, B Li, WL Payne, TA Cebula, High mutation frequencies among Eschericia coli and Salmonella pathogens. Science, 274: 1208-1211, 1996 (Nov.15).
3a.&nbsp; PB rainey and ER Moxon, When being hyper keeps you fit.&nbsp; Science 288: 1186-1187, May 19, 2000.

3. Science issue on evolution&nbsp; http://www.sciencemag.org/content/vol284/issue5423/index.shtml

&nbsp;

<SPAN style="mso-spacerun: yes">&nbsp;</SPAN>

 

[LiveFreeOrDie]

Hello, Sean?

I've seen you lurking here. Any response?

 

[Sean Pitman]

Part One Reply

Originally posted by lucaspa
You've brought this up several times, so let's look at it and the website in detail.

First, Miller uses the Hall experiment as an example of the evolution of an irreducibly complex system.

The problem&nbsp;here is that every genetic function is irreducibly complex to one degree or another. Behe's particular problem is that he does not detail the degree to which the evolution of an irreducibly complex system becomes "impossible." Clearly, irreducibly complex functions can evolve. The lactase function, for example, is "irreducibly complex". This can be proven without a doubt by simply reducing the molecular structure of any lactase enzyme until it no longer works. Since not every protein can hydrolyze lactose, the ones that can are clearly irreducibly complex in their specialized function. If some series of amino acids that does not have lactase activity can be changed via mutation and natural selection into one that does have lactase activity, evolution of an irreducibly complex function has occurred. Behe makes the mistake of trying to define irreducible complexity as something more than it really is. He tries to raise the bar too high by describing systems of function that involve many uniquely functional proteins. He seems to overlook the fact that a single protein is itself irreducibly complex. Miller doesn't need to work so hard to disprove Behe's primary contention. Behe has a great idea, but fails to recognize the fact that all functions are irreducibly complex, not just the more complex functions.

Second, the comment of "now for 20 years" is misleading, since Hall hasn't been running the experiment for 20 years. The original paper was written in 1982, but there is no indication Hall continued to run the experiment after the paper was published. In fact, experience with other researchers would indicate that the experiment was terminated.

In Hall's paper he noted, "We thus tentatively concluded that in E. coli K12 there is only one locus, the ebg locus, which can evolve a lactose-hydrolyzing enzyme under our selective conditions. That tentative hypothesis has been borne out over several years. A strain deleted for both the ebg gene and the lacZ gene has repeatedly been subjected to the standard selective regimen on Lac-TET plates, and has additionally been mutagenized with a variety of chemical mutagens before being subjected to selection. All of those experiments failed to yield any lactose-utilizing mutants. Thus, E. coli has a clearly limited evolutionary potential for this particular new function."

If Hall kept a strain deleted for LacZ and ebg genes around for several years by the time this paper was published, I am betting he still keeps a colony on hand. You don't just throw away colonies of genetically altered bacteria. If you need them again, you don't want to have to go through the laborious process of deleting genes again. Even so, I will alter the paper to reflect the fact that I know of no specific experiment has been carried out over the course of 20+ years with these bacteria.

Also, note that these bacteria where subjected to mutagenic chemicals that dramatically increase mutation rates . . . and they still failed to evolve the lactase function.

"One must also note that only a mutation of this particular gene gave the needed lactase activity. No mutations in any other gene ended up giving a bacterial colony lactase ability. Therefore, without this spare tire gene, it can be assumed that the "evolution" of lactase ability might be quite a bit more difficult."

As you can see, this is a bit misleading. Within the time span of the experiment, this is the only mutation seen in this population. It is not the only possible one, but the one seen within the limits.

Obviously there were many other mutations, possibly with many other functions gained or lost. The fact remains however that the only gene that was capable of evolving the lactase function in particular was the ebg gene. No other mutation or series of mutations to any other gene or sections of genetic real estate gave rise to the lactase function despite heavy selection pressures over a prolonged course of time (at least "several years" by the time this paper was published). If "several years" means at least 3 years, this translates into around 75,000 generations with a steady state population of 10 billion organisms per colony.

"In fact, several of Hall’s mutant strains of E. coli could not evolve lactase ability at all. He described these strains as having "limited evolutionary potential."<SUP> </SUP>

IOW, they didn't have the variation in the population and the favorable mutation didn't appear in the time frame. This would lead to extinction of these strains if only galactosidase was present as an energy source. Plain and simple.

You evidently do not understand the experiment. The E. coli strains that had both the ebg and the lacZ genes deleted were grown on lactose selective media (Lac-TET plates). These strains did not die out because lactose selective media is not limited to lactose as the only source of energy. These colonies can be and were in fact grown on such selective media over an extended course of time, and yet they failed to evolve the lactase function despite heavy selection and mutagenic pressures. Variations in the population would obviously add up over time via neutral mutations and genetic drift. And yet, none of these variations were able to produce the lactase function despite huge populations and tens of thousands of generations.

For further validation of this concept, go to any hospital laboratory and ask to see their records on bacterial enzymatic capabilities over the past 40 or 50 years. You will note that many types of bacteria have been lactase negative over this entire time (ie: Salmonella, Proteus, and Pseudomonas etc) despite the benefits that would come if they were to ever evolve a lactase enzyme.

"The mutational change was unguided by natural selection since full function was achieved in a single point mutation without any functional intermediaries."

Red herring. All mutation are unguided by natural selection. Mutations are variations and provide the raw material for natural selection to work upon.

Natural selection can only work upon sequence differences if they are functionally different from each other. If they are beneficially different, they are protected or maintained by natural selection. More beneficial mutations can then be added onto this first beneficial change. This was in fact demonstrated by Hall in his experiments with E. coli. Certain of the functions that evolved via selective guidance required a series of 2 or 3 point mutations before they were realized. Of course, each point mutation was selectively advantageous in a functional way over that which came before. Thus, the evolution of such a function that took 2 or 3 point mutations was "guided" along the evolutionary path by natural selection . . . each step of the way. Without natural selection, there is no "guidance" down any path. Without the selection of particular mutations, all mutations are allowed to drift in a completely random way. Of course, a purely random process leads to homogeny, not toward increasing complexity (ie: primordial soup turning into humans).

A single point mutation either does or does not result in a beneficial function. If it does result in a beneficial function, it does so instantly. There is no path that must be traversed that requires time or the "guidance" of natural selection. The function is achieved by purely random chance. Natural selection is not needed to achieve this new function. It might help to maintain the function once it is achieved, but the arrival of the function itself was purely random and sudden. A series of beneficial mutations is a guided and gradual process, but the individual mutations are not.

"We also know that only an extremely small fraction of the total number of possible different proteins of this length (or smaller) could even theoretically cleave lactose."

Excuse me? How do we know this? The article doesn't give any data on this. It's a bare assertion critical to the argument but just given without any support.

&nbsp;

There is plenty of support for this assertion. True, Hall does not directly address this issue in his paper, but the support for this assertion is fairly obviously.

Consider that the protein produced by the lacZ gene is a tetramer totaling about 4,000 amino acids. Considering one unit of the tetramer (~1,000 AA), how many possible proteins of this length are there? There are 1 x 10e1301 different sequences of this length.

Now, an E. coli bacterium has around 4.1 million base pairs in its genetic real estate. Out of all this genetic real estate, only one other gene, the ebg gene, is close enough to anything that can produce the lactase function. What does this mean? It means that relatively few genetic sequences of a given length can produce the lactase function. Out of all that real estate in the E. coli genome, only two genes could do it, and one of them had to get mutated first. Also, despite a great deal of mutagenic and selective pressures on a sizable population over an extended course of time involving at least 50,000+ generations, no other genetic sequence in the E. coli bacteria was able to achieve the lactase function. Obviously then, the fraction of potential lactase proteins compared to the total number of possible proteins is most likely . . . miniscule.

End of Part One Reply

 

[Sean Pitman]

Part Two Response

What Pitman then proposes is that not one, but 5 mutations are needed in a 1,000 amino acid protein to confer lactase activity. He also supposes that these mutations cannot start until the necessity of having a lactase activity is required. Then Pitman calculates that there is not enough time.

He also ignores that several of the mutations could have been accumulating for 40,000 years before the environment changed. So, there really could have been 5 point mutations needed, but 4 had already been done and were present in the gene.

You do understand that I set up a hypothetical situation here to think about the average time involved to cross certain neutral gaps in genetic function . . . right? The hypothetical situation that assumes a starting point of 5 neutral mutations from the lactase function would require and average time of greater than 40,000 years to cross. Of course, this is based on a large steady state population (one trillion), an extremely high mutation rate (10e-4 mutations per base pair per generation), and a fairly rapid generation time of 20 minutes.

I do not "suppose that mutations cannot start until the necessity of having lactase activity is required." What I do is propose that if such a starting point is known, that the average time needed for lactase function increases significantly with each neutral step that must be crossed.

You suggest that there might only be one mutation needed for lactase function in a particular colony since such a sequence might have drifted along randomly over the course of the past "40,000 years" or so. You are most certainly correct. However, if such a sequence did happen to drift along to this place where only one more mutation was needed to achieve lactase function, this mutation would be realized in short order (only one generation for an average bacterial colony of 10 billion organisms).

But, how often does such a sequence drift so close to one of the relatively few lactase sequences in a particular bacterial colony that could benefit from such a sequence? The fact that lacZ and ebg negative E. coli never evolved the lactase enzyme should tell us that something is blocking lactase evolution in these creatures. Other types of bacteria have always been lactase negative as long as we have known about them. Why don’t they ever evolve this enzyme when it would be to their benefit if they did? What is it, exactly, that is "limiting" their "evolutionary potential"?

&nbsp;

Certainly neutral mutations could accumulate that just so happen to provide lactase function before it is actually needed, as you suggest. Of course, if they did this, natural selection would not select to maintain such enzymes. It might even be detrimental to maintain such an enzyme since protein production uses energy resources. If the protein is not beneficial, natural selection will select to get rid of it. So, at best, such mutations would come and go randomly. So, in estimating the probability of such a beneficial sequence just happening to be there when needed via previous neutral mutations, one must consider the number of times such a sequence would come along in a certain span of time. If the number of sequences that could produce a particular function is relatively rare, one might then figure that the number of times such sequences would drift through a particular genomic pool of 10 billion individuals in say, a million years, might be very few times indeed.

In any case, given a known starting point, a calculation of the average time required to achieve a particular function can be estimated. If the particular function is more than one or two mutations away from anything currently in the genetic real estate, the average time required to realize this desired function increases dramatically with each additional neutral step that must be crossed without the aid of natural selection. Such steps, of course, must be crossed with random chance alone.

Pitman also assumes that none of the 4 point mutations has any selective value for a function other than lactase activity. IOW, exaptation.

I figured that eventually you would suggest that evolution is not required to travel in any one particular direction. Evolution can go in any number of directions to achieve diversity of function. Any number of different functions might be beneficial for a given organism in a given environment.

I do understand your position here. It is a common argument. You are suggesting that although it might be difficult to evolve the lactase function in particular, other functions might not be so hard to evolve. After all, evolution can travel down any one of an infinite number of paths . . . right? With this concept in mind, one might expect that the evolution of at least one of a practically infinite number of potential functions would evolve in relatively short order. In reality though, such evolution might be more limited than one might think at first glance.

The genetics of living things functions very much like any other language system . . . such as the English language or "code". Symbolic sequences are translated into other symbolic sequences much like the Morse Code is translated into the letters of another alphabet system, such as the letters used in the English alphabet. The Morse Code is based on a series of dots and dashes. DNA is based on a series of four chemicals labeled A, T, C and G. A certain number and sequence of dots and dashes represents a letter in the Morse Code. Likewise, a certain number of chemicals in DNA (three) represents an amino acid. Both coded systems are arbitrary. There is no inherent reason why a particular sequence must code for anything in particular. Likewise, various series of letters in the English language are also given arbitrary meaning or "function". Not every series of letters has meaning in the English language or "code". The same is true for proteins in living things. Not every series of amino acids caries meaning for a particular living system. In fact, as with the English language, the vast majority of potential protein "words" are not defined by a given cell. They have no function at all for that cell. Each protein word is in fact surrounded like an island by a sea of non-defined/non-functional proteins.

For example, consider the word "evolve". This word is made up of 6 letters. How many defined 6-letter words are there in the English dictionary? I’d be willing to bet that there are not anywhere near the 308,915,776 different words that could be made using just six letters. Just for argument’s sake, let’s say that there are around 100,000 defined six-letter words in the English dictionary. If true, this would mean that each defined word is surrounded by 3,089 other words that are not defined.

The same situation is true for proteins. Not all proteins are defined by a given cell. In fact, as far as the total number of potential sequences of average length, only the tiniest of fractions is defined. For example, let’s say that the average protein in a given organism is somewhere around 100 amino acids in length. Without considering tertiary structures, how many different proteins could be made that are 100 amino acids in length? The answer is on the order of 1 x 10e130. Ok, ok, but proteins can change somewhat without loosing function. They can also undergo neutral changes where the amino acids change but the function does not change at all. In other words, there is a fair amount of protein plasticity as far as function is concerned. However, there is a point beyond which proteins cannot change without a complete loss of function. Many amino acids cannot change at all and are called "invariant". Some can only change within the same class of amino acids (polar, non-polar, etc). So, in a given cell, about how many different proteins that average 100 amino acids in length will be recognized?

To begin looking into this question, let’s consider an average E. coli bacterium. How many different proteins will an E. coli bacterium recognize as functional? With a genome of 4.1 million base pairs and with 3 nucleotides coding for each amino acid, the E. coli genome could theoretically code for around 13,000 different proteins averaging 100 AA in length. Of course, each of these proteins might be fairly plastic with a potential for many different sequence variations to code for the same function. If each protein had an average of 50% sequence plasticity, a given protein of 100AA could have up to 1 x 10e65 different sequence variations that would still do the same function to one degree or another. It would be kinda like changing the letters in a sentence and still being able to figure out what the sentence says. With all 13,000 proteins having such variation potential, the total number of different protein sequences that our bacterium could recognize would be on the order of 1 x 10e70. Certainly, this a huge number of proteins that could be recognized, but it is still a tiny fraction compared to those amino acid sequences that cannot be recognized. Subtracting the sequences that can be recognized out of the potential pool of protein sequences leaves the pool barely touched. In the pool there are still 1 x 10e130 protein sequences that have no unique function given them by the E. coli dictionary of protein words. The number of proteins that a given cell might recognize is still nothing compared with the total number of potential proteins that it does not recognize. In our hypothetical example, each recognized protein is surrounded by an average of 1 x 10e60 non-recognized or non-functional proteins.<B> </B>So, each functional protein is in fact an island. Each genetic sequence is if fact isolated from any one of these potentially functional proteins by a sea of non-functional proteins that is vast indeed. Evolution simply cannot take off in any direction that it wants to if it plans on each mutation being functionally different from the one before. Odds are that very soon the functional chain will dry up no matter which direction it starts off in. At this point, further evolution will be required to resort to drifting along without the guidance of natural selection. Such random drifting on such a large open sea of non-function or neutral function requires ages upon ages to come across the tiny islands of new function that are scattered throughout that sea. And this is only the average time required to achieve the relatively simple functions that need only a single protein to perform them . . . such as the enzymatic lactase function. The problem gets unimaginably worse when more complex functions (such as cellular motility or light recognition) are considered.

"By Hall's own calculations, the true mutation rate would be closer to one mutation per 4,200,000 base pairs in 1,000 generations."

That's way too low. Just copying errors by polymerase are 1 per 1,000,000 base pairs per cell division, or generation. Never mind radiation and chemicals. This quoted mutation rate is 10^9 lower than anyone else has seen. We really need to look at the original paper. I'll get it.

The mutation rate for bacterial genomes is on the order of 1 x 10e-9 mutations per base pair per generation. With a genome of 4.1 million base pairs, one might expect an ancestral inheritance rate of 1 mutation every 238 generations or so. I will edit my paper to reflect this more accurate number. But really, it makes little difference to the argument since I used a very high mutation rate (1 x 10e-4 mutations per base pair per generation) in my hypothetical ponderings.

"http://genetics.hannam.ac.kr/lecture/Mgen02/Mutation%20Rates.htm"


"http://www.erin.utoronto.ca/~w3bio/bio370/shelley_dna_plasticity_partII/tsld014.htm"
End of Part 2

 

[Sean Pitman]

Part 3 Reply

Pitman's article then becomes very confused, mixing in IC with all this. Perhaps you can help explain this.

However, the basic flaw is the assumption that you must have neutral mutations. That the mutations can't possibly be selective for other functions and neutral for the one under study. Furthermore, studies since Hall have shown hypermutant strains and sequential evolution of systems.

I never said or "assumed" that one "must have neutral mutations". Obviously there are many occasions when a mutation is not "neutral". Also, from the perspective of a given function, those mutations that do not reach that function are not necessarily "neutral", just because they do not result in that particular function. They may have many other non-neutral effects as far as other functions are concerned. When I use the term "neutral mutations" I do so from the perspective of the entire organism, not from the perspective of any one potential function.

Certainly mutations need not produce any one particular function. The question is, given a particular genome, how many functions can it produce or is it close enough to evolve in a given amount of time? The problem is that there is a limited amount of genetic real estate available. If there were an infinite number of genetic sequences available to a given organism or pool of organisms, then the&nbsp;evolution of an infinite number of beneficial functions would be a simple process given the proper environment. The creatures and/or their offspring&nbsp;could quickly "morph" as various environmental needs arose. The problem is that there is simply not enough genetic real estate to cover the potential functions that might be useful should the need arise. Because of the limited nature of the genome (or even pools of genomes - ie: gene pools), certain functions that might be useful to&nbsp;a particular creature and its&nbsp;offspring are&nbsp;simply out of reach. Other functions might just so happen to be close enough to some portion of that&nbsp;gene pool's&nbsp;real estate to be enveloped by random fluctuations in that real estate. However, natural selection limits such fluctuations because it is more concerned with maintaining what is already working that it is with sending portions of its expensive real estate out on voyages across an unknown ocean. Even when such creatures do have extra real estate that can undergo random neutral mutation and "drift" along, what are the odds that they will end up at anything as far as a beneficial function? The odds are that relatively few functions are within quick reach of this relatively limited genetic real estate.

Hypermutation might help somewhat, but only minimally considering the size of the ocean that must be crossed between what is available and what functions are of some potential benefit. The more complex the function, the lower the odds are that these are within reach of what is available. Also, mutation rates have a lethal down side. They can only be increased so far before they wipe out the population.&nbsp;

As an illustration, consider the word "cat". This word has a definition or function in the English language system. How many other words can you get to without loosing function along the way? You can go in any direction by changing one letter at a time or adding or subtracting one letter at a time. For example, we could go from cat to hat to bat to bad to dad to dig to dog. Presto, we have evolved cat into dog without loosing function along the way. We could also go from cat to cap to tap to tip to top to mop. It seems easy doesn’t it? And it is! It just so happens that the functions that are represented by these words are represented by relatively simple sequences. In other words, there are a whole lot of three letter words in the English dictionary as compared with the total number of possible three lettered words. There are only 17,576 possible three-letter words using the 26 letters of the alphabet. If there are 5,000 three-letter words that are actually defined by the English language, almost a third of all the possibilities have been defined. Because of this, the odds that any one particular three-letter word is one mutation away from a different defined and even "beneficial" word are very good.

A similar situation is found with the genetic code. The genetic code defines three letter sequences in DNA called codons. Since the genetic alphabet only uses 4 letters, the total number of different sequences are 64. Every single one of these sequences is arbitrarily defined by the genetic code to represent one of 20 amino acids. Obviously this code is redundant since there are fewer definitions than there are sequences giving some amino acids several sequences that code for them. However, every single mutation in a coding region of DNA does in fact have a defined function. Some mutational changes may change the nucleotide sequence for a codon and yet the codon still codes for the same amino acid as the previous codon did. Obviously, In this case, the mutation would be a "neutral" mutation.

But, things do get more complicated. Consider the word "batter". This word is made up of a sequence of 6 letters. The total number of potential words that are six letters long is 308,915,776. If there are 100,000 defined six-letter words in the English dictionary, this would only be about 0.0003% of the total number of possible 6 letter words. In this case, a mutation in a given word would most likely not result in a new defined word since each one of the 100,000 defined six letter words would be surrounded by an average of 300 or so non-defined words. A few clusters of words might be fairly close together, allowing for quick mutation and evolution of function. Batter could mutate to butter or mutter, or bitter to sitter. But soon further mutation runs into walls of non-function.

The situation gets more and more difficult the bigger the word gets. Then sentences come into play. Try evolving a sentence where each new change is functional as well as beneficial in the English language. Consider the Shakespearean phrase "Methinks it is like a weasel" made even more famous by Richard Dawkins. Dawkins illustrated the process of natural selection by starting with a garbled phrase such as "MWR SWTNUZMLDCLEUBXTQHNZVJQF". His computer made random changes in this phrase in each "generation" of phrases and then compared the individual phrases in each generation to the ideal "Methinks it is like a weasel" phrase. Of course, in very short order the "Methinks it is like a weasel" phrase evolved. The problem is; this is not how it works in real life. In real life, there is no selection unless there is a functional difference between the various sequences that are being compared. Dawkins’s illustration fails to explain anything because he starts with a non-functional phrase and then produces many non-functional phrases and then compares these non-functional phrases to see which one of the non-functional phrases is closest to one particular phrase that does actually have function. Of course, if the selection process is based on genotypic comparisons alone then Dawkins’s illustration is a fine way for evolution to proceed. However, if selection is not based on genotypic comparisons, but on phenotypic function, then Dawkins’s illustration is completely worthless.

For example, if we start with a certain portion of genotypic real estate that reads, "MWR SWTNUZMLDCLEUBXTQHNZVJQF", and evolution can proceed in any direction, how long on average would it take to get to something, anything, that has a phenotypic function using random mutation alone? Go ahead and try it. Evolution can go in any direction whatsoever here. Of course, that is the problem. Since neutral evolution can go in any and every direction randomly, it does so. Program a computer with the sequence, "MWR SWTNUZMLDCLEUBXTQHNZVJQF" and have it change one letter at random and see how long it takes to evolve any phrase in English that is actually functional (given any particular steady state population of evolving phrases). Let’s say that there are at least 100 million 28-character phrases that mean something in English. The problem is that there are a lot more 28 character phrases that don’t mean anything in English . . . like 1 x 10e40 of them. You see the problem . . . don’t you? No matter what letter is mutated in "MWR SWTNUZMLDCLEUBXTQHNZVJQF", the resulting sequence will not mean anything. In fact, if several letters in a row are mutated toward any one particular meaningful phrase, the intermediate phrases still will not mean anything until quite a few more mutations have taken place. In each generation a bunch of phrases will exist that don’t mean anything. Natural selection will not be able to select between them since they all have the same non-functional function. All such mutations are therefore selectively neutral.

The problem doesn’t get much better if you start with a functional phrase. Starting with "Methinks it is like a weasel" change one letter at a time and see how many different phrases you can evolve without loosing function in the process. It is very difficult to change this phrase into anything else without loosing function along the way.

The same problem happens with trying to mutate genes that are, comparably, much longer than relatively short phrases like, "Methinks it is like a weasel." The odds are that these genes are separated by gaps of neutral function or even non-function from other uniquely functional sequences that are simply too wide to cross with one or two point mutations. Occasionally, certain sequences might happen to be close to some sequence that produces something functional at just the right time to make it beneficial. Examples of such events can be seen with lactase and nylonase enzymes evolution via point and frame shift mutations as well as with bacterial antibiotic resistance that is universally achieved with single point mutations. Such functions are statistically within the range of what is already in the genome of a given gene pool. The problem is that most potentially beneficial functions are not within range and evolution stalls after traveling down rather short paths that are connected by single point mutations. At the end of these paths are blockades to further evolution that are formed by neutral or even non-functional gaps that prevent further progress.

&nbsp;

Sean

P.S.&nbsp; By the way, unlike many in this forum, I don't have the time to reply to everyone or to post on a regular basis . I'm quite busy these days at work, but I will respond as much as I can because I really do find forums such as this quite interesting.

End of Part 3 Reply

&nbsp;

 

[Jerry Smith]

Sean, I think you are focusing on the "genetic real estate" to the exclusion of the "fitness landscape." The relative improbability of the path to any single functional adaptation is diminished by the large number of potential functional adaptations.

You also have to take into account the diversity of organisms searching on the fitness landscape. E. coli may have been "too far removed" from hydrolyzing lactose (apart from one gene), but (in nature) numerous other organisms also had a shot hydrolyzing lactose. Are all of them too "distant" from a working lactase to evolve one to enable them to occupy that niche?

Is lactose the only possible food source for organisms that are (currently) too far from digesting lactose? Are they not "close" to a protein that will enable them to cleave and digest some other sugar or food source?

How large is the fitness landscape, and how many conceivable solutions are there to any given adaptive problem? Could there be no other protein enzymes that will cleave lactose, or is it just that we haven't stumbled upon any other proteins that will solve the problem. What if there are 15 enzymes (that are not close to one another in chemical structure) that will do the trick? What if each of those 15 enzymes has 10 functional configurations? What if 5 of those enzymes are structurally simlilar to an enzyme that cleaves some other sugar?

How much of the fitness landscape of lactose availability is within reach of the genetic real estate of some microbes now?

How many solutions are there to optimize food sources that will work apart from the evolution of a lactose hyrdolase?

Hall's work shows that I/C systems (a la Behe) can evolve. I don't think that we are learning much more by speculating about what Hall's work did not show.

 

[Jerry Smith]

The fact that lacZ and ebg negative E. coli never evolved the lactase enzyme should tell us that something is blocking lactase evolution in these creatures. Other types of bacteria have always been lactase negative as long as we have known about them. Why don’t they ever evolve this enzyme when it would be to their benefit if they did? What is it, exactly, that is "limiting" their "evolutionary potential"?

To establish that there was a mechanism limiting their evolutionary potential, or that something was actually blocking their evolution of a lactase enzyme, your experiment would have to run somewhat more than 20 years, or even 100 years. I believe that the "limit" Hall mentioned was more a "limit" to what E coli could accomplish over the geological blink of an eye that was his experiment. I don't think it is appropriate to extrapolate a "limiting mechanism" from data that does not cover realistic evolutionary time frames, nor do I think Hall intended for anyone to.

After all - all of the data does prove common descent. It seems almost silly to extrapolate far outside the data to postulate a limiting mechanism exists in order to prove that something couldn't happen when we already have strong evidence that it has happened ubiquitously through history.