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Theories - Origin of Life

Discussion of everything related to the Theory of Evolution.

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Postby Luxorien » Mon Mar 05, 2012 1:52 am

So the result is that people with this level of immunity from malaria because of carrying the sickle cell mutation are better off are they?
Do they not still have the problem of sickle cell disease?


No. They don't. That's the point: if you are heterozygous, you have no symptoms of sickle cell anemia and you have malaria resistance.

The majority of mutations are neutral, with a few being harmful or beneficial. What this means is that there is a high degree of variation in sexually reproducing populations. This random element provides the fuel for the nonrandom action of natural selection. I guess I'm just confused as to how you can say that mutations are "invariably" harmful when there are copious examples of beneficial mutations, like antibiotic resistance in bacteria and HIV immunity in humans.

The point of bringing up sickle cell anemia is to underscore how relative adaptations are. Whether a mutation is beneficial or neutral is almost entirely dependent on the environment. This means that a mutation which is neutral now may very well turn out to be useful in the future. There's no predicting what might become advantageous later on. That's why the key to species' survival is random genetic variation. No matter what weirdness is going on with your environment, you have at least a chance of capitalizing on some beneficial tweaking of your DNA.
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Re: Theories - Origin of Life

Postby scottie » Mon Mar 05, 2012 11:18 am

No. They don't. That's the point: if you are heterozygous, you have no symptoms of sickle cell anemia and you have malaria resistance.

Actually they do have the symptoms of sickle cell, they just rarely develop the severe life threatening anemia typical of homozygous sicklers.

It would help greatly if you appreciate what the sickle-cell trait actually is.
It is often referred to simply as sickle-cell anemia. 
However, the fact is, its a condition that creates many more medical problems than just anemia. 
Victims of this trait are also likely to experience chronic complications involving their spleen, kidneys, heart, lungs, and immune systems. 
Probably one of the most common symptoms is the persistent and agonizing pain caused by the deflated irregular shaped red blood cells blocking small blood vessels.
So when the whole picture is appreciated it does not portray the rather simple situation you are suggesting.

Additionally we do not know how this sickle trait appeared.
You are just assuming it was a random happening.
If it was it then could not be considered neutral could it? :)

Now do you really want me to respond to all the other examples you have enumerated, because I can if you really wish to extend this periphery point.

However you probably have not appreciated it, but you have just endorsed my entire point when you state
That's why the key to species' survival is random genetic variation.


This is what I said on page 41 Sat Mar 03, 2012 5:23 pm
The reality is that NS has very eloquently described how species may survive but has nothing to say about how they arrived.


So if you are going to debate NS how about addressing the question of arrival, because that is what NS is supposed to have accomplished and what this thread is all about.
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Re: Theories - Origin of Life

Postby Luxorien » Thu Mar 08, 2012 10:21 pm

scottie wrote:It would help greatly if you appreciate what the sickle-cell trait actually is.


Sickle cell anemia is a recessive disorder caused by a point mutation on chromosome 11. The most common disease-causing mutation causes glutamic acid to take the place of valine in hemoglobin's beta chains, which in turn causes a hydrophobic chunk to stick out of the protein, which in turn causes the proteins to clump together. Individuals who are homozygous recessive for the disease-causing variant are quite ill; individuals who are heterozygous, however, rarely experience symptoms. They still make sickle-shaped cells, but those cells generally do not cause them problems.You're right to say that I'm simplifying things a bit. However, I don't think I left out anything which would contradict the main point. The fact remains that most mutations are neutral, and that a mutation's "value" is relative to environmental conditions.

It seems you believe either that most heterozygotes have significant symptoms or that a small number of symptomatic individuals makes the heterozygote advantage irrelevant. As far as I can tell, the former is simply not the case. As for the latter, I don't know what to say other than this: natural selection acts at the population level and only cares about reproduction, so a few individuals experiencing non-lethal symptoms will not outweigh the benefit of being malaria-resistant. If you survive to reproduce, you get to pass on your genes, even if your genes are suboptimal. Evolution doesn't push organisms to be the best that they can be; it pushes them to be good enough. This is why so many people go around talking about "survival of the fitter" instead of "survival of the fittest."

Additionally we do not know how this sickle trait appeared.
You are just assuming it was a random happening.
If it was it then could not be considered neutral could it? :)


We do know how it appeared: a mutation on chromosome 11. There are a couple hundred different ways this gene can get modified. These inadvertent modifications happen during DNA replication at a steady rate. It's a chemical fact of the molecular machinery that runs organisms: mistakes get made. How harmful or beneficial those mistakes are depends largely on the environment.

As for your claim that a random event can't be neutral...I'm utterly perplexed. A random event is one that is not deterministic. A neutral mutation is one that is neither harmful nor beneficial (i.e. does not increase or decrease the organism's chances of survival). There is no causal relationship between these two concepts. I have no clue what you are trying to say.

So if you are going to debate NS how about addressing the question of arrival, because that is what NS is supposed to have accomplished and what this thread is all about.


One of the premises of your argument is that there are no "functional phenotypes that random mutation is supposed to have produced." I take "functional" to mean either beneficial or neutral. It sounds like you are arguing that a random process could not provide the variety and novelty necessary for macroevolution. Therefore, examples of beneficial point mutations are extremely relevant. But perhaps you meant to say something else.
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Re: Theories - Origin of Life

Postby scottie » Fri Mar 09, 2012 11:06 pm

Luxorien
Since you have not disputed my last statement that NS does not explain how species arrive I take it we are both agree in agreement. Is that a correct assumption?

You are right in that sickle cell trait is an abnormality in Chromosome 11.
However it is also brought about by diminished production of one of the two sub units in the hemoglobin molecule. Genic changes that produce this condition are termed thalassemias.

There is a third condition that is brought about by abnormal association of sub units.
The science of how these abnormalities came about is not known, despite your claim that it is.

You will find that there are significant variations in hemoglobins.
Here are some, Hemoglobin S, C, E, H,Constant Spring, and Barts.
All these have different causes.

Your hetrozygous condition that you claimed has no symptoms has in fact several, some of them resulting in conditions as serious as sickle cell disease.

All these changes in the alpha or beta units have a deleterious effect, it is just that in one area the sickle trait provides a survival advantage over people with normal hemoglobin in regions where malaria is endemic, however sickle cell trait does not provide total protection nor invulnerability to the disease.
Now just this brief summary shows the complicated nature of the sickle cell trait. To suggest that a simple mutation produces a beneficial trait for Nature to select from is simply incorrect.
Regarding the term mutations.
Many biologists regard all changes in genetic make up as mutations. Some are random errors/damage but the majority are not.
Molecular Evolution makes this point
http://www.tempoandmode.com/wp-content/ ... oels08.pdf
All models recognize that most random changes to the genome are deleterious, because they will tend to disrupt highly organized genetic information. It is the relative proportions of mutations that are advantageous, neutral or nearly neutral that is debated.

DNA replication is remarkably accurate. The DNA copying machinery in eukaryotes usually makes a mistake less than once in every million nucleotides. This incredible copy fidelity is achieved by a sophisticated error-checking system involving base selection, proofreading and postreplication repair.


James Shapiro (evolutionary biologist) states
Genome restructuring is a normal part of cellular life

http://shapiro.bsd.uchicago.edu/Shapiro ... 0Dogma.pdf

Now in case you are tempted to discard this biologist's work as product of some sort of a lone wolf or other, just check out all the supporting citations in the paper, some 154 on total.
Plus check out the various cell function responses to various stimuli in his table 1 page 16 -21,
some 50 in all, as a start.
Go to any source in epigenetics and you will read a similar appraisal. The genome is a fluid structure.
There is no such thing as a static genome that is just subject to random changes. The vast majority of genome changes are as a result of cellular processes. These changes, you seem (if I understand you correctly) to think are what you call neutral mutations.
The problem with that view is to show an example of a “neutral mutation” that is not part of a cell process. How many of these “neutral mutations” can you name?
Your very example of the sickle cell trait reveals a structure alteration as part of the cellular process.

All people have fetal hemoglobin in their circulation before birth. Fetal hemoglobin protects the unborn child and newborns from the effects of sickle cell hemoglobin. However this hemoglobin disappears within the first year after birth. Why?

Is Natural selection at work in the unborn and new born selecting for survival, and then after about a year removes this survival package? How does that work?
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Postby AstraSequi » Sat Mar 10, 2012 7:44 am

Luxorien - I like your signature. :)

Scottie - are you going to reply to the second half of my post? If you're conceding points, I'd like you to specify that.
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Postby Luxorien » Sat Mar 10, 2012 5:03 pm

AstraSequi wrote:Luxorien - I like your signature.


Thanks. I'm thinking of trying to convince my principal that this counts as "professional development." :P

scottie wrote:Since you have not disputed my last statement that NS does not explain how species arrive I take it we are both agree in agreement. Is that a correct assumption?


That is an incorrect assumption. I disagreed with one of the premises of your argument. It so happens I also diagree with your conclusion, though I suppose one does not necessarily follow from the other (though they often go hand in hand).

However it is also brought about by diminished production of one of the two sub units in the hemoglobin molecule.


Hemoglobin is tetramer. There are four subunits: two betas and two alphas. The point mutation I referred to earlier causes the beta chains to be wonky. As I said, there are a couple hundred variants of this gene. Another mutation in that same location on chromosome 11 causes the beta thalassemias you seem to be talking about. The alpha chains can also get fooked by mutations in two genes on chromosome 16.

I'm confused as to what all this has to do with the fact that heterozygotes have malaria resistance. What is your point here? That there are even more mutations that can confer malaria resistance?

The science of how these abnormalities came about is not known, despite your claim that it is.


The genes that control the construction of the subunits have been located. Variants of these genes have been described. We know the exact substitution that occurs. People with certain variants have sickle-shaped cells. People with "normal" versions do not. What is mysterious about this? The DNA sequence changes, the protein changes, causing the observed phenotype. What exactly are you arguing? That the change in the single nucleotide was not the result of the sort of DNA copying errors that happen all the time in cells?

Your hetrozygous condition that you claimed has no symptoms has in fact several, some of them resulting in conditions as serious as sickle cell disease.


I said that they rarely experience symptoms, and that their sickle-shaped cells generally do not cause them significant harm. The fact that a small percentage have symptoms is irrelevant. The majority of heterozygotes suffer no ill effects. And none of this has any bearing on the fact that these mutations confer malaria resistance, which is of clear benefit to the organism. It seems we have a dispute over a matter of fact.

Now just this brief summary shows the complicated nature of the sickle cell trait. To suggest that a simple mutation produces a beneficial trait for Nature to select from is simply incorrect.


The most curious thing about your response is the way you zeroed in on the sickle cell allele and ignored other, more obviously beneficial, mutations. I mentioned sickle cell anemia as an aside, because I think it's a cool example of heterozygote advantage. It's incidental to the larger fact that some mutations increase an organism's chance for survival. The sickle cell allele is just the best example of the crucial point that the environment often determines whether a mutation is harmful or neutral.

Many biologists regard all changes in genetic make up as mutations. Some are random errors/damage but the majority are not. Molecular Evolution makes this point.


There is no semantic analysis of the words in that article which could lead to the conclusion that the authors regard mutation as anything other than a random copying error. Far from supporting your conclusions, this source directly contradicts everything you've been saying.

The "Molecular Evolution" article discusses mutation rates, and how they may differ from one organism to another, or even between parts of the same genome. Changing the rate of mutation does not change the fact that a mutation is a random copy error. The article even mentions that "mutations occur spontaneously in every generation, but not all mutations become permanent features of the genome" (1). A spontaneous mutation is one that results from the random chance of a copying error when DNA is replicated.

The authors go on to discuss the impact of selective pressures and genetic drift on the persistence of mutations: "For any given mutation, the chance of going to fixation (replacing the wild-type in the population) is dependent on the properties of both the mutation itself (its selection coefficient) and the population in which it arises (effective population size). These two things determine the balance between the two forces that shape substitution rates: selection and drift" (2). In other words, random copy errors get made, and the relative usefulness of those copy errors will determine whether they are quickly eliminated from the population, though genetic drift will play a part, especially in small populations. This article explicitly describes the very sequence you say is impossible: random mutation - positive selection for mutation - propagation of mutation throughout species - change in gene pool.

Another section of this article deals with "the debate between neutralist and selectionist schools of thought" (3). This is right before the sentence you quoted. The existence of advantageous mutations is assumed, while, as you quoted above, "it is the relative proportions of mutations that are advantageous, neutral, or nearly neutral that is debated" (3). I'm confused as to why you think this article supports your claim that beneficial mutations do not exist, when the text clearly treats their existence as a fact. I suppose you think that their mention of the high rate of harmful mutations somehow validates your view. Maybe you're arguing that the rates of mutation the authors mention are too low to produce advantageous mutations?

I don't see that this follows, either logically or experimentally. We can observe mutations happening in the lab. We can even make them happen more frequently in the hopes of snagging some mutations that are useful to us. It is a fact that random changes to DNA occur. It is also a fact that some of these changes will be deleterious, some will be neutral, and some will be beneficial. Even if we suppose that most mutations are harmful, the advantageous mutations whose existence you deny are still real. They still affect evolution.

There's another reason your article on molecular evolution contradicts your argument. It's about molecular evolution. They are including in their calculations mutations that never make it to the organism level. From a molecular standpoint, most changes in DNA will be harmful. Hence the repair mechanisms. But if you sample populations, you'll find mostly neutral variants, because harmful ones have already been eliminated by selective pressures. A few organisms will survive despite deleterious alleles, but most of the genetic variation we see at the population level does not affect an organism's survival.

Once again, this is highly relative. The terms neutral, deleterious and beneficial all depend on the environment. Additionally, rates of mutation are not constant and neither are selective pressures. As your article mentions, there are some portions of the genome that tolerate mutations more readily than others. So all of this is, to echo your own phrase, more complicated than the simple picture you're trying to paint. That was my purpose is bringing up sickle cell anemia: the value of a mutation is relative to the environment. It is the presence of these three types of mutations and not their relative frequencies that makes evolution by natural selection possible. Even if only a tiny portion of mutations are beneficial, that's enough genetic novelty to fuel speciation.

Futuyma puts it this way: "The neutral theory acknowledges that many mutations are deleterious, and are eliminated by natural selection so that they contribute little to the variation we observe" (320, Evolutionary Biology). He's discussing the same debate as the article you linked. This argument is about whether selection or drift affects molecular (not phenotypic, which is what you were talking about in your original post) variation. This (admittedly fascinating) scientific discussion has no direct bearing on phenotypic variations. It has more to do with improving the accuracy of our molecular clocks.

I think maybe you're trying to make a point similar to one I found in Evolution: The First Four Billion Years. It has to do with limitations on the possible forms that random mutation can produce. Brian Goodwin argues against the view that there is an "infinite diversity of possible forms for evolution to work with" (299). Instead, he contends that "there are constraints on the possible forms of organisms and their behavior, so that some forms can be generated, while others cannot" (299). This is not an argument against the ability of natural selection to produce new species. It simply points out that genetic variation is not unlimited. This fits with the common conception of natural selection as a force that works within certain ranges of possible change, modifying structures to perform new functions rather than creating new systems de novo.

I suppose this might lead one to think that natural selection can change species but cannot produce new ones. The problem with that logic is this: it fails to recognize the incremental nature of evolution and speciation. Yes, there are limits on what natural selection can do, and it's true that there are four other "forces" of evolution: genetic drift, migration, non-random mating and mutation. But given enough time, natural selection can produce enormous changes simply by moving in tiny steps. The "constraints" on variation do not prohibit the development of complex systems; they prohibit the rapid development of complex systems.

Now in case you are tempted to discard this biologist's work as product of some sort of a lone wolf or other, just check out all the supporting citations in the paper, some 154 on total.


I have already blathered on for way too long, so I'll just address this briefly. For one thing, the number of citations in the paper is irrelevant to its scientific rigor and/or significance. The paper describing the discovery of the double helix, for instance, cites only four sources. So I'm not sure why you think that these 154 citations somehow make this paper irrefutable. I could write a paper hypothesizing the existence of pink unicorns and cite a hundred solid scientific sources; it wouldn't make my conclusions true.

The other thing I would mention is this: my concern with the "evidence" that you present is generally not that you are citing unscientific sources. Rather, I think you misunderstand and thus misrepresent the meaning and import of the sources you do cite. Your links often seem to have little bearing on the point you are trying to make. And, as we saw with the piece on molecular evolution, you often pick out contextless tidbits from texts that directly contradict you.

All people have fetal hemoglobin in their circulation before birth...


None of the information in this paragraph or the next has anything to do with the existence of beneficial mutations.
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Re:

Postby wbla3335 » Sat Mar 10, 2012 7:59 pm

Luxorien wrote:The other thing I would mention is this: my concern with the "evidence" that you present is generally not that you are citing unscientific sources. Rather, I think you misunderstand and thus misrepresent the meaning and import of the sources you do cite. Your links often seem to have little bearing on the point you are trying to make. And, as we saw with the piece on molecular evolution, you often pick out contextless tidbits from texts that directly contradict you.

You're relatively new to this thread. I've been around a bit longer but am tiring of banging my head against the wall. In case you haven't delved too far back in the thread, I'll fill you in on what you're getting yourself into. Scottie is a creationist. I and others have tried explaining to him how science works, but he's just not getting it. He's not getting it because he's a creationist. There's something about early indoctrination that seems to close down certain brain functions. Scottie will cite reference after reference, completely ignore the intent of the authors of those references, and then provide his own interpretation that he thinks somehow supports the existence of his god. So, all the best to you.
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Re: Re:

Postby Luxorien » Sat Mar 10, 2012 8:30 pm

wbla3335 wrote:You're relatively new to this thread. I've been around a bit longer but am tiring of banging my head against the wall. In case you haven't delved too far back in the thread, I'll fill you in on what you're getting yourself into. Scottie is a creationist. I and others have tried explaining to him how science works, but he's just not getting it. He's not getting it because he's a creationist. There's something about early indoctrination that seems to close down certain brain functions. Scottie will cite reference after reference, completely ignore the intent of the authors of those references, and then provide his own interpretation that he thinks somehow supports the existence of his god. So, all the best to you.


I have been going back through the earlier posts and trying to catch myself up. It's quite a read. Thanks for the heads-up.

I learned a lot about hemoglobin, mutation, molecular clocks, and genetic drift. I also have had the opportunity and impetus to read some interesting papers and books. So far this thread has been a success for me. :)
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Re: Theories - Origin of Life

Postby scottie » Sun Mar 11, 2012 4:40 pm

Luxorien
"All people have fetal hemoglobin in their circulation before birth..."

None of the information in this paragraph or the next has anything to do with the existence of beneficial mutations.

Really
Well my full statement reads
"All people have fetal hemoglobin in their circulation before birth. Fetal hemoglobin protects the unborn child and newborns from the effects of sickle cell hemoglobin. However this hemoglobin disappears within the first year after birth. Why?
Is Natural selection at work in the unborn and new born selecting for survival, and then after about a year removes this survival package? How does that work?"


May I remind you that it was you who introduced the sickle cell as a beneficial mutation, that NS has (non randomly)selected to protect against against malaria.
So to ensure clarity of the point I raised.

It is a fact that fetal hemoglobin protects the unborn child and newborns from the effects of sickle cell hemoglobin. Unfortunately, this hemoglobin disappears within the first year after birth.
One approach to treating sickle cell disease is to rekindle production of fetal hemoglobin. The drug, hydroxyurea induces fetal hemoglobin production in some patients with sickle cell disease and improves the clinical condition of some people. (A non random process I am sure you will agree) :)

So again my question is quite a simple one.
If Natural Selection acting on random mutations is responsible for the fetal hemogoblin (which it has to be for the theory to be intact) and this hemogoblin protects against sickle cell, what is the process that removes this protection?
According to your theory it can only be a random mutation(s). Is it not?
So to get this straight.
Random mutation first removes overall protection from sickle cell and all the problems that brings, then random mutation partially restores partial protection to offset a particular disease, and you regard this as a beneficial mutation?
It is an interesting take on things, I'll grant you that.
Now I appreciate that this is an inconvenient fact that you may wish to ignore by claiming it's irrelevance, but the question still remains.
I asked the question not to seek an answer, because I knew that you couldn't provide one, and you sadly have responded in the time honoured fashion, i.e. ignore that which contradicts a position.

Now as regards Shapiro's essay that you have so casually dismissed, a simple question.
Point to any part of the science he refers to as being incorrect?
His works is based on the work of Nobel Laureate Barbara McClintock.
Are you equally dismissive of her work?

As regards your lengthy response to the molecular evolution, I think that deserves a separate post.
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Postby Luxorien » Sun Mar 11, 2012 6:13 pm

May I remind you that it was you who introduced the sickle cell as a beneficial mutation, that NS has (non randomly)selected to protect against against malaria.


Actually, I mentioned HIV immunity and antibiotic resistance as examples of beneficial mutations. I brought up sickle cell anemia as an interesting example of how the term beneficial can be relative. I said all this before, and you still keep talking about sickle cell anemia as though the existence of beneficial mutations stands or falls on this example.

The simple fact remains that beneficial mutations exist. That is the only point that I am making. Your argument against the efficacy of natural selection relies on the premise that a random mutation cannot be beneficial. This premise is demonstrably false.

If Natural Selection acting on random mutations is responsible for the fetal hemogoblin (which it has to be for the theory to be intact) and this hemogoblin protects against sickle cell, what is the process that removes this protection?


This argument fails on two levels. The first is that it assumes that fetal hemoglobin was originally produced throughout the life of the organism. This does not necessarily have to be true, and indeed is not true. So there was no protection that was subsequently removed. The second level at which this argument fails has to do with its relevance to the topic at hand. The fact that a single point mutation confers malaria resistance does not somehow go away because there is another mutation that can mitigate the effects of sickle cell anemia.

To put it another way: instead of addressing the examples of beneficial mutations that were mentioned earlier, you keep piling on additional examples of what you think are features that natural selection could not have produced. I can explain why your example of fetal hemoglobin is not evidence against natural selection:

<tangent>
In the course of the (random) gene duplications that led to the present series of hemoglobin genes, certain sequences were positively selected for, or achieved fixation through genetic drift. A mutation in the fetal hemoglobin's regulatory sequences can cause this hemoglobin to be produced throughout one's life, but this mutation has not occurred often enough, or has not been selected for strongly enough, to become very common.

There is no "protection" that originally existed that was selected against; fetal hemoglobin has always been produced during the fetal stage. It is possible that a mutation which causes this fetal hemoglobin to be produced throughout life could become quite common, but it doesn't necessarily follow that this must happen. It depends on whether this (random) mutation happens often enough and in the right individuals. It depends on how many people with sickle cell anemia are successfully treated, and a bunch of other factors that would affect the strength of the selection pressure on this mutation.

The theory of natural selection says that favorable variants will tend to increase in populations, but it does not say that every possible favorable variant must come into existence - that's the random part of mutation.
</tangent>

But there is no point in doing so (responding to your additional examples of what you think are problems for natural selection) because you still have not demonstrated that the point mutations mentioned earlier (HIV resistance, antibiotic resistance, malaria resistance, nylon manufacturing waste metabolism) are anything other than random mutations that happened to be useful and were therefore selected for. As long as beneficial mutations exist (and they obviously do because we can literally watch this happen), your conclusions are invalid.

You may want to argue that beneficial mutations are possible, but that they could not form complex systems because they don't make big enough changes to the genome, or because a bunch of them would have to happen at once for a complex system to evolve. But arguing that beneficial mutations do not exist is like arguing that HIV does not cause AIDS.

Now I appreciate that this is an inconvenient fact that you may wish to ignore by claiming it's irrelevance, but the question still remains.


I will answer as many irrelevant questions as I have time to address, but they remain irrelevant. Whether the beneficial phenotype of being resistant to antibiotics is the result of a random mutation is a matter of fact which can be verified in the lab. Instead of addressing this, or even of addressing the fact that a single point mutation can confer malaria resistance, you are hunting around for other examples of mutation's supposed failure to produce beneficial traits.

Those examples can be discussed also, but discussing them will not negate your earlier failures to disprove the existence of beneficial mutations.

Now as regards Shapiro's essay that you have so casually dismissed, a simple question.
Point to any part of the science he refers to as being incorrect?
His works is based on the work of Nobel Laureate Barbara McClintock.
Are you equally dismissive of her work?


As I said before, I do not necessarily question the scientific conclusions of the papers you cite. I question your ability to understand their meaning. As we saw earlier, you quoted from a paper that directly contradicts your argument. You went so far as to include in your quote a sentence that clearly stated that beneficial mutations exist. You ignored that sentence and bolded the part about most mutations being deleterious.

I'm not sure why you keep asking me to point to flaws in their research. My argument has never been that they are bad scientists. My argument is that these papers don't mean what you think they mean. You act as though the existence of transposable elements and epigenetics means that beneficial mutations don't exist. Is that really your argument?
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Postby AstraSequi » Mon Mar 12, 2012 5:16 am

Scottie - in case you didn't see my question above...
AstraSequi wrote:...are you going to reply to the second half of my post? If you're conceding points, I'd like you to specify that.
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Re: Theories - Origin of Life

Postby scottie » Tue Mar 13, 2012 3:12 pm

AstraSequi

My apologies,
Luxorien's interjection somewhat hijacked me, quite challenge to deal with matters on different fronts. :)

Anyhow I will return to you now, and ask Luxorien to be a little patient. I am sure he would appreciate the rest from parading his developmental potential to his principle. :)

I believe you refer to your final point of your post of Sun Feb 19, 2012 12:08 am. Page 39
My question was
Has this situation changed since Darwin's day?
Can someone help with some evidence.
Your reply
Most definitely. I suggest you read http://en.wikipedia.org/wiki/Speciation, and also any included citations if you want to investigate further. Please note in the opening paragraph, "Observed examples of each kind of speciation are provided throughout."

Thank you for the wiki reference, and I have studied it.
It does provide good descriptions of the different kinds of speciation evolutionary theory posits.
It goes on to exemplify this:-
One example of natural speciation is the diversity of the three-spined stickleback, a marine fish that, after the last ice age, has undergone speciation into new freshwater colonies in isolated lakes and streams.
 
It provides a single reference in support of this, a 2000 paper.
Historical contingency and ecological determinism interact to prime speciation in sticklebacks,
Gasterosteus
http://www.ncbi.nlm.nih.gov/pmc/article ... 133026.pdf

The first point I noted in the wiki discussion was, this example appears to be about variation within a species. Nobody as far as I am aware disputes that variation within a species does occur.
However that said, the referenced paper does clearly state:-
Studies on the genetics, mate choice, ecology and morphology of these fish indicate that they are reproductively isolated and exploit alternative trophic niches in sympatry (Schluter & McPhail 1992; McPhail 1994;Taylor & McPhail 1999). Consequently, they fulfill the principal criteria of biological species. It has been well argued that ecological speciation, divergent selection
involving exploitation of alternative trophic niches owing largely to resource competition, has been a major deterministic factor driving divergence in sticklebacks
(McPhail 1993; Schluter 1994, 1996a,b; Rundle et al. 2000).

So although they claim species divergence, they are still referred to three-spined sticklebacks (Gasterosteus aculeatus). I find that somewhat interesting.
Be that as it may that is not all.
In a more recent study found in the Journal of Fish biology we have this paper
Along the speciation continuum in sticklebacks
http://labs.fhcrc.org/peichel/media/pdf ... 09_JFB.pdf
The authors clearly depict their understanding of speciation, which again is quite clear.
Speciation involves the evolution of reproductive isolation among groups of individuals; isolation that is often coupled with genetic and phenotypic differences (Dobzhansky, 1937; Mayr, 1963; Schluter, 2000).

The introduction states that speciation is a continuum of 4 different stages, with the final one being
the complete reproductive isolation, and this reproductive isolation is always associated with chromosomal rearrangements and environment independent genetic incompatibilities.

The paper then goes on to examine these 4 stages in connection with the stickleback.
1) continuous variation without reproductive isolation
2) discontinuous variation with minor reproductive isolation
3) strong, but reversible, reproductive isolation
4) strong and irreversible reproductive isolation
Only stage 4 can be classified as a speciation event and the paper points to only one example

It asks the question
Why have these sympatric pairs not proceeded to the point of irreversible reproductive isolation? One possibility is the limited time frame for their divergence, given that most freshwater populations were colonized from marine ancestors only after the last glaciation (Taylor & McPhail, 2000; Reusch et al., 2001; Makinen ¨ et al., 2006).
Genetic incompatibilities (a possible route to complete isolation, see below) might take considerably longer to develop (Coyne & Orr, 2004; Bolnick & Near, 2005).
This explanation is not entirely sufficient, however, given that genetic incompatibilities have not been documented across the range of G. aculeatus, including among populations separated for millions of years. A telling exception will be described below.

Another possibility, then, is that the divergent selection is not strong enough to generate irreversible barriers through ecological speciation. Equivalently, assortative mating may not be strong enough, perhaps because trait divergence is not sufficient for females to reliably or profitably discriminate against heterospecifics. Finally, irreversible isolation in sticklebacks may require specific genetic changes, such as chromosomal rearrangements.

The conclusion of this study has this to say
Finally, achieving state 4 (strong and irreversible reproductive isolation) seems to require additional factors, such as chromosomal rearrangements, intrinsic genetic incompatibilities and extended periods of allopatry, all of which are less obviously linked to processes occurring along the rest of the speciation continuum.
Perhaps the greatest lesson that sticklebacks can reach is the value of plurality in the study of speciation. That is, speciation might often involve multiple and shifting geographic contexts and mechanistic drivers. This mosaic nature of speciation has also been suggested to characterize other taxa (Feder et al., 2005; Rundle & Nosil, 2005; Mallet, 2008; Nosil et al., 2009), and it might even be reasonably common in nature.
The solution to Darwin’s ‘mystery of mysteries’ might therefore be considerably more complicated that proponents of parsimony might desire.
Nature is not parsimonious.


So the observed examples that wiki points to (stickleback) is not so observed after all, is it. :)

The apparent necessity of Chromosomal rearrangements within the nucleus pose a significant problem, if speciation is the product of random mutations to the genome.

We know the nucleus of each differentiated cell appears to possess an epigenetic mechanism.
This mechanism regulates the position of each chromosome in the nucleus and thereby determines the way and timing of how expression takes place.
We also know chromatin structure, the variation in histone 3D structure and so on are indeed regulated by this mechanism.
So the control of chromosome activity in the nucleus clearly cannot be the product of a mutation in the genome.
We are observing levels of information and control above and beyond genome information.
All of these are not instigated or varied or regulated by mutations to the genome, and yet this study
(which is very detailed and is really worth studying in full) is concluding that chromosome rearrangement is a requirement for speciation, whereas neo darwinian evolutionary theory is fixated on random mutations of the genome.
Ones like Donald Forsdyke have long recognised this link between chromosomal arrangement and species specific traits, only to be castigated by the likes of Coyne and Orr with their gene centred views.

So I conclude that despite the wiki appraisal of speciation as being a darwinian process, the evidence suggests no such thing.
scottie
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