Evidence against NeoDarwinism - Nonrandom DNA changes

[bob b]

The title of this thread uses the term "nonrandom DNA changes" instead of mutations, because the term "mutations" is a loaded word.

The changes being observed in experiments that show lifeforms adapting rapidly to a changed environment happen too repeatedly and too rapidly to be due to errors coming in a random manner. It is far more likely that these adaptations are the result of designed mechanisms not yet discovered.

Here are several cases that point in this direction. I will first discuss the experiment reported by Barry Hall in 1982, reported in Evolutionary Biology, vol 15, pp 85-150, "Evolution In A Petri Dish: The evolved Bgalactosidase system etc."

(This experimental effect was called "evolution" even though it violated the NeoDarwinism assumption of random mutations, i.e. it happened much too rapidly and was repeatable)

If someone has a rebuttal ("just-so story" no doubt) please tell us about it. In the meantime I will search myself to see how this apparent falsification of neoDarwinism was explained away by evolutionists.

 

[SUTG]

The title of this thread uses the term "nonrandom DNA changes" instead of mutations, because the term "mutations" is a loaded word.

The changes being observed in experiments that show lifeforms adapting rapidly to a changed environment happen too repeatedly and too rapidly to be due to errors coming in a random manner. It is far more likely that these adaptations are the result of designed mechanisms not yet discovered.

Here are several cases that point in this direction. I will first discuss the experiment reported by Barry Hall in 1982, reported in Evolutionary Biology, vol 15, pp 85-150, "Evolution In A Petri Dish: The evolved Bgalactosidase system etc."

(This experimental effect was called "evolution" even though it violated the NeoDarwinism assumption of random mutations, i.e. it happened much too rapidly and was repeatable)

If someone has a rebuttal ("just-so story" no doubt) please tell us about it. In the meantime I will search myself to see how this apparent falsification of neoDarwinism was explained away by evolutionists.

I think you forgot to include the evidence.

 

[PlastikBuddha]

I did stumble across this article:
http://jb.asm.org/cgi/content/full/182/11/2993
As discussed above, background mutations are sequence directed and not random in the sense that they occur in bases made vulnerable by virtue of their particular location within specific DNA sequences, such as tandem repeats, or the unpaired and mispaired bases of stem-loop structures. Dobzhansky's statement (22) enlarges upon this point: "The structure of a gene is a distillate of its history, and the mutations that may occur in a gene are determined by the succession of environments in which that gene and its ancestors existed since the beginnings of life. The environment prevailing at the time mutation takes place is only a component of the environmental complex that determines the mutation." The definitions of directed and random that are appropriate in the above context are neither relevant nor useful, however, when discussing mechanisms of evolution. By the neo-Darwinian definition, a mutation is random if it is unrelated to the metabolic function of the gene and if it occurs at a rate that is undirected by specific selective conditions of the environment. For example, mutagenic DNA-destabilizing events associated with cell division are random, as they are dependent upon growth rate and selective conditions of the environment only insofar as those conditions affect the rate of cell division. However, the focus of this minireview concerns the consequences of environmental stress on evolution. What are the DNA-destabilizing processes operative in stressed, nongrowing organisms forced to mutate before they can continue to multiply? Mechanisms must have evolved in starving cells to stimulate metabolic changes and mutations that facilitate adaptation to new circumstances.

With the above neo-Darwinian definition of random in mind, an impressive array of circumstances that enhance background mutation rates in response to environmental stress may be examined with respect to whether or not they are random (undirected). Examples of conditions that result in undirected, genomewide hypermutation include those caused by UV irradiation, reactive oxygen species, mismatch repair-deficient mutator phenotypes (35, 98), horizontal gene transfer by transduction with a viral particle, and mobile genetic elements that increase mutation rates by inserting at particular regions or at target sequences within the genome (73, 76). Such mechanisms are undirected because, for example, a mismatch repair deficiency will result in failure to repair a particular kind of lesion regardless of whether or not it confers a selective advantage upon its host.

In higher organisms, environmental conditions of stress do not have direct access to the cells involved in reproduction, and different mechanisms resulting in hypervariation have evolved. For example, localized DNA rearrangements and shuffling produce extensive beneficial variation (82, 96), and hypervariable sequences provide continual changes in the composition of venoms produced by snakes (29) or snails (78) to overcome resistance developed by their predators or prey. These mechanisms are also random. The threat of predators does not result in hypermutation; there is no evidence that the circumstances selecting such hypermutable genes bear any metabolic relationship to the mechanisms by which they originally arose. A gene may be hypermutable because it contains a hot spot due to a particular DNA sequence, and if a high mutation rate is advantageous to its host, that gene will be selected during evolution. However, its hypermutability per se is undirected, since it is unrelated to those selective conditions and to the function of the gene. These random mechanisms resulting in hypermutation are in essence serendipitous relationships; in contrast, hypermutation resulting from derepression is localized as a direct consequence of a specific response to environmental challenge.

 

[Johnny]

Talks of this have fizzled out in recent years because of ongoing research.

Rosche WA, and Foster PL. The role of transient hypermutators in adaptive mutation in Escherichia coli. Proc Natl Acad Sci USA, 6862-7.

Basically the lack of a metabolic substrate leads to double-stranded breaks in the DNA. DNA pol III then has to kick in, with the help of some primers, to rejoin the DNA. Thus, more errors are made than in a normal population of dividing bacteria.

So the whole thing turned out to be random mutations -- just more of them occur in times of stress -- so it looks like the "required" genes are rapidly evolving because although the whole genome is rapidly mutating, only the metabolic genes are under high selectional pressures.

This "just-so" story brought to you by empirical, testable science. Spetner forgot to tell you about that, didn't he?

(Edit: PlastikBuddha beat me to it.)

 

[bob b]

I did stumble across this article:
http://jb.asm.org/cgi/content/full/182/11/2993
As discussed above, background mutations are sequence directed and not random in the sense that they occur in bases made vulnerable by virtue of their particular location within specific DNA sequences, such as tandem repeats, or the unpaired and mispaired bases of stem-loop structures. Dobzhansky's statement (22) enlarges upon this point: "The structure of a gene is a distillate of its history, and the mutations that may occur in a gene are determined by the succession of environments in which that gene and its ancestors existed since the beginnings of life. The environment prevailing at the time mutation takes place is only a component of the environmental complex that determines the mutation." The definitions of directed and random that are appropriate in the above context are neither relevant nor useful, however, when discussing mechanisms of evolution. By the neo-Darwinian definition, a mutation is random if it is unrelated to the metabolic function of the gene and if it occurs at a rate that is undirected by specific selective conditions of the environment. For example, mutagenic DNA-destabilizing events associated with cell division are random, as they are dependent upon growth rate and selective conditions of the environment only insofar as those conditions affect the rate of cell division. However, the focus of this minireview concerns the consequences of environmental stress on evolution. What are the DNA-destabilizing processes operative in stressed, nongrowing organisms forced to mutate before they can continue to multiply? Mechanisms must have evolved in starving cells to stimulate metabolic changes and mutations that facilitate adaptation to new circumstances.

With the above neo-Darwinian definition of random in mind, an impressive array of circumstances that enhance background mutation rates in response to environmental stress may be examined with respect to whether or not they are random (undirected). Examples of conditions that result in undirected, genomewide hypermutation include those caused by UV irradiation, reactive oxygen species, mismatch repair-deficient mutator phenotypes (35, 98), horizontal gene transfer by transduction with a viral particle, and mobile genetic elements that increase mutation rates by inserting at particular regions or at target sequences within the genome (73, 76). Such mechanisms are undirected because, for example, a mismatch repair deficiency will result in failure to repair a particular kind of lesion regardless of whether or not it confers a selective advantage upon its host.

In higher organisms, environmental conditions of stress do not have direct access to the cells involved in reproduction, and different mechanisms resulting in hypervariation have evolved. For example, localized DNA rearrangements and shuffling produce extensive beneficial variation (82, 96), and hypervariable sequences provide continual changes in the composition of venoms produced by snakes (29) or snails (78) to overcome resistance developed by their predators or prey. These mechanisms are also random. The threat of predators does not result in hypermutation; there is no evidence that the circumstances selecting such hypermutable genes bear any metabolic relationship to the mechanisms by which they originally arose. A gene may be hypermutable because it contains a hot spot due to a particular DNA sequence, and if a high mutation rate is advantageous to its host, that gene will be selected during evolution. However, its hypermutability per se is undirected, since it is unrelated to those selective conditions and to the function of the gene. These random mechanisms resulting in hypermutation are in essence serendipitous relationships; in contrast, hypermutation resulting from derepression is localized as a direct consequence of a specific response to environmental challenge.

Nice job of searching. I knew they could come up with a good "story". They always do.

Chapter 5 of Ken Miller's book, Finding Darwin's God, talks about the Hall case, but Miller just chalks the results up to "evolution" and conveniently omits any discussion of why the results always turn out the same and happen millions of times faster than people usually assume that evolution happens.

The text you posted does a much better job of seeming to explain nothing except to assert that somehow it converts randomness into certainty and takes no time at all to be effective.

I have taken the liberty of highlighting some of the key steps in the above "miracle".

 

[Johnny]

HIGH STRESS > HIGH MUTATIONS > FASTER EVOLUTION (> SOME REALLY CONFUSED CREATIONISTS THINKING MUTATIONS ARE NOW DIRECTED)

Did I lose you?

 

[bob b]

Talks of this have fizzled out in recent years because of ongoing research.

Rosche WA, and Foster PL. The role of transient hypermutators in adaptive mutation in Escherichia coli. Proc Natl Acad Sci USA, 6862-7.

Basically the lack of a metabolic substrate leads to double-stranded breaks in the DNA. DNA pol III then has to kick in, with the help of some primers, to rejoin the DNA. Thus, more errors are made than in a normal population of dividing bacteria.

So the whole thing turned out to be random mutations -- just more of them occur in times of stress -- so it looks like the "required" genes are rapidly evolving because although the whole genome is rapidly mutating, only the metabolic genes are under high selectional pressures.

This "just-so" story brought to you by empirical, testable science. Spetner forgot to tell you about that, didn't he?

(Edit: PlastikBuddha beat me to it.)

Nope. He actually mentioned that evolutionists would try increasing the error rate (invoke "hypermutations"), which of course would then run into the dreaded "error catastrophe" problem. In other words increasing the mutation rate contributes to the solution of one problem, but at the cost of introducing a factor whose consequences are not observed: immediate extinction of the entire bacterial culture.

There is no "free" beer.

This is just one more example of slavish adherence to evolutionary dogma inhibiting progress by given the impression that there is no problem, so that nobody is motivated to looking into what is actually going on (their "solution" is a "just-so story").

 

[Johnny]

He actually mentioned that evolutionists would try increasing the error rate (invoke "hypermutations"), which of course would then run into the dreaded "error catastrophe" problem. In other words increasing the mutation rate contributes to the solution of one problem, but at the cost of introducing a factor whose consequences are not observed: immediate extinction of the entire bacterial culture.

Spetner's a moron who is trying to play ball way outside of his home field. He's been smacked down so many times I can hardly believe anyone listens to his inane ramblings at all. Well, to be honest, I'm not at all surpised you do. Remember the archaeopteryx scene he made? Self-infatuation is never good, especially combined with arrogant disregard of one's own ignorance.

But enough about Spetner. So what you're saying is that the mutation rate in the whole genome was NOT increased? Please tell me that's what your saying. Puhlease. Because I can show that it was. And then, as usual, you'd be stuck on the wrong side of reality looking like a complete dunce. Might want to shine your tapdance shoes, you'll be needing them soon enough.

This is just one more example of slavish adherence to evolutionary dogma inhibiting progress by given the impression that there is no problem, so that nobody is motivated to looking into what is actually going on (their "solution" is a "just-so story").

Hah, don't talk to me about not being motivated to look at what's going on, Captain Armchair Biology. Some of us have actually spent years in micro labs doing research on mutagenesis. I've actually been in the labs. I know the techniques. I've done them. I've done research under evolutionary biologists. I spent 4 years of my life learning this stuff. But some people actually spend their whole life researching these subjects. And don't even mention slavish adherence to dogma. Just don't. That would be like a repeat convict lecturing me on staying out of jail.

 

[bob b]

Spetner's a moron who is trying to play ball way outside of his home field. He's been smacked down so many times I can hardly believe anyone listens to his inane ramblings at all. Well, to be honest, I'm not at all surpised you do. Remember the archaeopteryx scene he made? Self-infatuation is never good, especially combined with arrogant disregard of one's own ignorance.

But enough about Spetner. So what you're saying is that the mutation rate in the whole genome was NOT increased? Please tell me that's what your saying. Puhlease. Because I can show that it was. And then, as usual, you'd be stuck on the wrong side of reality looking like a complete dunce. Might want to shine your tapdance shoes, you'll be needing them soon enough.

Hah, don't talk to me about not being motivated to look at what's going on, Captain Armchair Biology. Some of us have actually spent years in micro labs doing research on mutagenesis. I've actually been in the labs. I know the techniques. I've done them. I've done research under evolutionary biologists. I spent 4 years of my life learning this stuff. But some people actually spend their whole life researching these subjects. And don't even mention slavish adherence to dogma. Just don't. That would be like a repeat convict lecturing me on staying out of jail.

I don't doubt that people have their nose to the grindstone doing good experiments. But from my point of view that is the exact problem: they are too focused on one thing and fail to take into consideration other factors that people in other fields also specialize in.

In the case at hand they assume an increase in mutation rate in the genome and forget that experts in other fields claim that the mutation rate can not be too high or one gets "error castastrophe".

A similar situation prevailed in Gould's punc eek, where he assumed that the most rapid evolution would occur in small populations, whereas experts in other fields came to the exact opposite conclusion that evolution proceeds most rapidly in large populations.

I notice these contradictions due to my background in large scale system analysis known as Operations Research, which concentrates on the interactions between smaller subsystems operating within larger systems ("wheels within wheels").