scientific end of evolution theory (2)

Dear Peter,You write:
"My current opinion is that nothing that you have put forward
FALSIFY's ToE, that's true."You are of very short memory.
Three weeks ago I mailed the topic: "molecular genetic evidence against random mutation" and thus I falsified the NDT. Although not admitted by Percy (maybe she should do that to create some clarity) it still stands as a falsification of the atheistic version of evolution theory (=NDT). I recommend you to read the thread again. Maybe that will open your eyes.
In the meantime I also provided a falsification (do you know what a falsification is, and why it is not so good for a theory?) of natural selection and thus demonstrated the NDT not to be valid on the level of the genome. What else do you want me to falsify?
Best wishes
Peter

you haven't done anything of the sort borger, and if you think you have then you don't understand science very wellyou cannot falsify random mutation unless you can isolate mutation as one of the variables. When you look at the fly genome you cannot seperate the variables mutation and selection. You can only assume that selection has no affect (based on what little you actually know about the gene, which is in effect, nothing)so until you can isolate mutation from selection in an experimental setting, you cannot possibly "falsify" random mutationpehaps the worst thing about it is that you seem to think that your interpretation of this article is the only correct one, despite the fact that it has been read by many other scientists and peer reviewed by experts who don't seem to think it falsifies NDT. Thats nothing but arrogance

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Originally posted by peter borger:
Dear Mark,
Could you please point out exactly where you think I use fallacies (mailnumber and quote) to support my view. It will make it a lot easier for me to respond,

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Peter

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Yup, here she is....http://EvC Forum: evidence that intelligent design can't explain -->EvC Forum: evidence that intelligent design can't explainI never said you used fallacies to support your view, just that you allow yourself the luxury of not being able to show function/non-function of a sequence, yet absolutely require it for phylogenetic analysis that supports evolution.

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You also wonder:

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"Functioning transposons are just as good an evidence of common descent as functional gene sequences. Why does them having function represent a falsification?"

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As mentioned before, you cannot take DNA sequences in the same spot of the chromosome that we do not know the function of as proof for common descent.

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In the very same thread you are assuming the total non-functionality of the GLO pseudogene.Functionality doesn’t have to be known for phylogenetic inference, but it does have to be known if your argument depends on the lack of function of a particular sequence.Since you have used the GLO vit c pseudogene as your evidence;1/ Please cite the studies where human, chimp, orangutan, & macaque had their GLO genes knocked out, which you claim shows lack of function.2/ Assuming you can cite the studies of the knockouts above, how can you show the sequences never had a secondary function at some point, never, ever, EVER? Remember, you are claiming a falsification here, you need to be in possession of this knowledge.If you cannot show that a nucleotide sequence never had function, then you cannot make a judgement on neutral rate mutation, as regards falsification of neutral theory, or the NDT for that matter.Mark------------------
Occam's razor is not for shaving with.[This message has been edited by mark24, 08-07-2002][This message has been edited by mark24, 08-07-2002]

dear monkenstick,You write:
"you haven't done anything of the sort borger, and if you think you have then you don't understand science very well"Over the past few weeks I tried to discuss the concepts of non-random mutation and genetic redundancy and why they violate NDT. Apparently nobody understands these concepts and therefore I recommend you to read something about the topics to try to conceive the problem for ToE. It doesn't make sense to discuss the topics with people who don't understand the concepts.And:
"you cannot falsify random mutation unless you can isolate mutation as one of the variables. When you look at the fly genome you cannot seperate the variables mutation and selection. You can only assume that selection has no affect (based on what little you actually know about the gene, which is in effect, nothing)"Why don't you have a careful look at the figure presented in my first posting? You will notice that in all subpopulation of D. mel. the mutations are not introcuded at random. That falsifies NDT, whether you like it or not."so until you can isolate mutation from selection in an experimental setting, you cannot possibly "falsify" random mutation"Well, actually I didn't, but D. mel's 1G5 gene did."pehaps the worst thing about it is that you seem to think that your interpretation of this article is the only correct one, despite the fact that it has been read by many other scientists and peer reviewed by experts who don't seem to think it falsifies NDT. Thats nothing but arrogance"After disbelief the namecalling starts.I wish you well,
peter

EXAMPLE 1) The problem with this is that it doesn't even consider that these traits may be byproducts of genes which do serve functions which aid survival.An analogy to demonstrate why I think this is ridiculous.A person can use their hands to clap. Clearly being able to clap can have no survival advantages. So are hands redundant?EXAMPLE 2) It isn't hard at all to imagine why the ability to regenerate has been turned off in some human tissues. It's because once development has occured, regenerating functional tissue in complex organs is extremely problematic. I'll give the example of brain tissue, as I have some knowlege of developmental neurobiology. Cell differentiation in the developing brain depends both on temporal and spatial cues. Its an extremely complex cascade which involves crosstalk between cells as they are developing. Regeneration of FUNCTIONAl adult brain tissue is therefore extremely problematic, because the complex interactions of cells in development can't be "reset", because cells in an adult brain are terminally differentiated. Temporal and spacial cues relied upon in the development of brain are no longer there. They cant be reset without compromising the function of adult brain cells. The reason lower organisms have the ability to regenerate is primarily most likely because they don't have the problem of regenerating the complexity which higher animals have to.EXAMPLE 3) I don't know anything about botany, but remember that you are merely assuming that the trait is redundant, and that it doesn't offer any survival advantage. You can't really show that its redundant, until you can compare fitness of liana with and without this trait.KNOCKOUTS:"In humans, ACTN2 is expressed in all muscle fibres, while ACTN3 expression is restricted to a subset of type 2 fibres." My possible explanation for why ACTN3 is still present in the genome (i'm not as certain of my opinions as peter seems to be) is that act-3 offers a performance advantage. Difference in fibre composition in muscle is known to affect endurance/power, due to differences in metabolism/morphology between fibre types. The fact that act-3 is only expressed in a subset of fibre types indicates that it may have some role in the differences between those fibres. Loss of the gene doesn't show any obvious myopathy for the same reason that differences in muscle fibre composition are not treated as myopathies.

dear Monkenstick,You say:
"The problem with this is that it doesn't even consider that these traits may be byproducts of genes which do serve functions which aid survival."Actually these traits are not likely to be byproducts. A recent article demonstrates that the trait of musia is genetically determined and probably involves one gene (Science 2001, vol292, p1636-37 and ref's herein).And:
"A person can use their hands to clap. Clearly being able to clap can have no survival advantages. So are hands redundant?"Clapping for fun (which involves the musia gene) or clapping to scare of animals?And:
"It isn't hard at all to imagine why the ability to regenerate has been turned off in some human tissues."So actually we are talking (again) about the loss of a trait. I have already mentioned before (several times) that I am not that interested in the loss of traits, since it is not hard to conceive. I wonder how the original organism got the trait of regeneration.And:
"Regeneration of FUNCTIONAl adult brain tissue is therefore extremely problematic, because the complex interactions of cells in development can't be "reset", because cells in an adult brain are terminally differentiated."Maybe we simply do not know the mechanisms of de-differentiation, yet.And:
"The reason lower organisms have the ability to regenerate is primarily most likely because they don't have the problem of regenerating the complexity which higher animals have to."I notice a bit of a contradiction here. Since higher organisms are able to regenerate bones and liver it is not restricted to lower organisms. So, this is not an argument, let alone a reason.You say:
"I don't know anything about botany, but remember that you are merely assuming that the trait is redundant, and that it doesn't offer any survival advantage. You can't really show that its redundant, until you can compare fitness of liana with and without this trait."That experiment is not that hard to carry out. One only needs to compare the fitness of far-soared offspring and direct-neighborhood-of-the-parent-tree offspring. I predict that there will no difference in fitness.And, finally:
"Loss of the gene doesn't show any obvious myopathy for the same reason that differences in muscle fibre composition are not treated as myopathies."... and that makes it a redundant gene, isn't it?Furthermore, you did not respond to my reply in the previous letter, where you say that:
"you haven't done anything of the sort borger (about the falsification of NDT), and if you think you have then you don't understand science very well"Please read my posting on Drosophila's 1g5 gene. And, please explain to me how you think science works. (I always thought it was about theories and the validation of these theories through objective emperical research)Have a good one,
Peter[This message has been edited by peter borger, 08-08-2002]

"Maybe we simply do not know the mechanisms of de-differentiation, yet."Not only do cells have to de-differentiate, they then have to read temporal and spatial cues from their environments, and their axons have to read chemotaxic cues to synapse with the correct dendrites. These temporal and spatial cues are specific to the developmental period, they aren't present in adult brain.And:
"The reason lower organisms have the ability to regenerate is primarily most likely because they don't have the problem of regenerating the complexity which higher animals have to.""I notice a bit of a contradiction here. Since higher organisms are able to regenerate bones and liver it is not restricted to lower organisms. So, this is not an argument, let alone a reason."Liver and bone are made out of fairly simple (in comparison to other organs, appendages etc.) arrangements of relatively few cell types, arms and legs are not. (an arm requires epidermal, muscle, blood vessels, nerve etc. to regenerate in precise locations.)"That experiment is not that hard to carry out. One only needs to compare the fitness of far-soared offspring and direct-neighborhood-of-the-parent-tree offspring. I predict that there will no difference in fitness."This doesn't test fitness, because you've assumed the only purpose of the flaps is to carry them long distances. Gene knockout is the only way to be certain.And, finally:
"Loss of the gene doesn't show any obvious myopathy for the same reason that differences in muscle fibre composition are not treated as myopathies."... and that makes it a redundant gene, isn't it?No, because it can give the organism an advantage, muscle fibre compositions between sprinters and endurance runners are usually different, they do different tasks. If the gene in question affects muscle fibre types then it has a function and will be subject to selection.Furthermore, you did not respond to my reply in the previous letter, where you say that:
"you haven't done anything of the sort borger (about the falsification of NDT), and if you think you have then you don't understand science very well"The reason I don't think you have is because the gene is the result of Mutation and Selection. You've assumed something about the selection pressure on certain base pairs to deduce that mutation is non-random. You actually don't know the value of the variable "selection" for any of the bases. So its an assumption, and assumptions do not falsify scientific paradigms. Your assumption might be reasonable, but until you can actually isolate the variable of mutation in the absence of selection pressure, you can't "falsify" random mutation.

dear Monkenstick,You state:
"you cannot falsify random mutation unless you can isolate mutation as one of the variables. When you look at the fly genome you cannot seperate the variables mutation and selection. You can only assume that selection has no affect (based on what little you actually know about the gene, which is in effect, nothing)"However, you are wrong. The mutations in D. melanogaster subtypes are introduced non-random in the 1G5 gene and do not affect the aminoacid sequence of the specified protein. Thus, the positions are neutral.(I know it is hard to accept. The falsification of NDT, I mean)best wishes
Peter

Peter B,Message 49 please,Thanks,Mark------------------
Occam's razor is not for shaving with.

dear mark,Be patient. Your response needs a bit of my thoughts, but I will respond soon.Peter

like I said pete, you're assuming that they're neutral because they don't code for amino acids.There are many examples of conserved nucleotide sequences which do not code for amino acids, most of which are regulatory regions. Introns themselves neccessarily must have some selection pressure on their sequence in order for them to be recognised as introns, and not as exons.If you are going to claim that all nucleotides which don't encode for amino acids are selectively neutral then you've got big problems when it comes time to explain homology in junk DNA and pseudogenes.

Dear Monkenstick,You say:
"like I said pete, you're assuming that they're neutral because they don't code for amino acids."I say:
Apparently, you don't get it. The data not only demonstrates fixed introns, they also show mutations in the coding region inducing alternative codons that specify the same aminoacid (due to the degenerate [better is: redundant] genetic code).
Furthermore, since you don't agree on the paper I recommend you to sent a letter to Schmidt and Tautz (I will back you up, since I do not understand how such papers can be publishes in evolutionary literature). The authors demonstrate that the complete region changes according to neutral evolution. It's not may personal opinion. If you don't agree on neutral evolution maybe send a letter to Kimura too; to tell him that his neutral theory of evolution is wrong (what do you need a neutral theory of evolution for, anyway? Neutral evolution? What is it?).I also recommend you to have a careful look at the figure, so you will notice that the mutations in distinct subspecies are introduced on the same spot and even the type of substitution is the same. This falsifies NDT, whether you like it or not. Why don't you read the complete thread?And:
"There are many examples of conserved nucleotide sequences which do not code for amino acids, most of which are regulatory regions. Introns themselves neccessarily must have some selection pressure on their sequence in order for them to be recognised as introns, and not as exons."Now you tell me something new!And:
"If you are going to claim that all nucleotides which don't encode for amino acids are selectively neutral then you've got big problems when it comes time to explain homology in junk DNA and pseudogenes."Firstly, there is NO junk DNA. This oldfashioned opinion is (going to be) demonstrated to be completely wrong, although it is still claimed by evolutionists as proof for evolution [have a look at the TALK-origin site, or read the "selfish gene" (Dawkins, who else. But what does he know about genes? He is a zoologist). It is a completely outdated view on DNA].
Secondly, I am not the one in big problems. That is the theory of evolution.Best wishes,
Peter

[QUOTE]Originally posted by peter borger:Firstly, there is NO junk DNA. This oldfashioned opinion is (going to be) demonstrated to be completely wrong, although it is still claimed by evolutionists as proof for evolution [have a look at the TALK-origin site, or read the "selfish gene" (Dawkins, who else. But what does he know about genes? He is a zoologist). It is a completely outdated view on DNA].
Secondly, I am not the one in big problems. That is the theory of evolution.Best wishes,
Peter[/B][/QUOTE]Say, PB, if you think that there's no such thing as junk DNA (or I prefer Syamsu neutral 'self-sustaining' DNA ) then what are they?Some say that from 3 million base pairs of human DNA, only 3% (correct me) can be considered real coding & functioning genes. And there are genomes bigger than humans': the lungfish had 800 million (correct me again if my estimates are wrong) and I suspect that their functional genes are juts about the same number as ours.

borger, you are right in that regions previously described as junk have been found to have function. You must remember that in order for this DNA to be evidence of design, the function has to depend on the sequence. You also have to explain the function of certain pseudogenes. I suggest you look at the thread "what is design" in the intelligent design forum. What function can you attribute to the urate oxidase pseudogene that indicates it was "intelligently designed"?[This message has been edited by monkenstick, 08-09-2002]

Hello allI lurk here from time to time because I find it facinating that anyone can be a creationist/IDer/Elvis Presley worshipper/my god can beat up your god etc. etc. in 2002 (not that it ever made any sense).
I can only attribute this to the huge variation in education standards that exists in the world which make the discrepancies in wealth pale in comparison.The post at the bottom from Mr.Borger drew my attention.First, that is very arrogant of Mr. Borger to claim that Diethard Tautz and Karl Schmid do not know what they are talking about in their papers. (I will be glad to tell them next time I see them though they will both laugh and wonder why I am wasting the few minutes to type this here). Please explain why two people who studied biology (evolution in particular) , generated the data, analyzed it, and yes, even published it are less qualified to draw their conclusions than Mr. Borger?I could use Mr. Borger's logic to disprove creationsim. There is not one piece of physical evidence that supports the existence of Jesus. Therefore, the bible must be false, an intelligent designer does not exist and all ID based hypotheses are refuted. Ta da! Just disproved your side! So we can all get on with it and support the one true god...Homer Simpson..doh! This would be analagous to the I don't know what the pseudogene does so therefore it must do something and therefore it was designed and therefore evolution did not occur argument.More seriously though, I work on "junk DNA" have a Ph.D. in human genetics and have been a working biologist for 12 years. The last six on evolution and analyzing DNA from extinct animals such as mammoths. I can agree on Mr. Borger that Junk DNA is an awful term that was adopted prematurely (the only thing we would agree on . However, there are functionless sequences that could be considered junk DNA but to many functionally uncharacterized sequences given this designation.Mr. Borger says:
(Dawkins, who else. But what does he know about genes? He is a zoologist).Ok Mr. Borger...what exactly are your credentials??? Since you don't accept the hypothesis/views/data of those who are not specialists in exactly the field under debate, show me what your credentials are regarding 1)evolutionary biology 2) "junk DNA"....if you do not hold a Ph.D. in a field directly related to these topics I guess we can say what does Mr. Borger know about genes? He is just a (profession unknown).It seems from Mr. Borger's posts that he is intelligent but has had no exposure to science or scientific method. If he were truly interested in the topic he would take some classes in 1) scientific philosphy 2) biology 3) genetics 4)evolutionary biology and then with a few clicks at ncbi.nlm.nih.gov click on PubMed and actually find out about pseudogenes, hotspots, etc. rather than spout out that he is more able to evaluate a field than anyone who actually makes a living at it. As a biologist I would assume that I am in no position to evaluate the current state of particle physics. That does not mean I cannot develope an informed opinion on the subject but it will not be worth much unless I really study and work on the subject. Mr. Borger and others seem to just say they have refuted a biological principle without even demonstrating that they are informed on the subject.Sorry to single you out Mr. Borger but your post was inappropriate...in principle one could cut and paste the name of any of the anti-evolution posters on this board...except for Brad McFall who would require a Rosetta stone to understand in the first place.Well, enough of that...at least before I bring down the wrath of Percipient...which would be ashame on my first postMark..if you are reading this, I really enjoyed your probability of rain post...very clever.Well, back to lurking...better yet..working

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Originally posted by peter borger:
Dear Monkenstick,

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You say:
"like I said pete, you're assuming that they're neutral because they don't code for amino acids."

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I say:
Apparently, you don't get it. The data not only demonstrates fixed introns, they also show mutations in the coding region inducing alternative codons that specify the same aminoacid (due to the degenerate [better is: redundant] genetic code).
Furthermore, since you don't agree on the paper I recommend you to sent a letter to Schmidt and Tautz (I will back you up, since I do not understand how such papers can be publishes in evolutionary literature). The authors demonstrate that the complete region changes according to neutral evolution. It's not may personal opinion. If you don't agree on neutral evolution maybe send a letter to Kimura too; to tell him that his neutral theory of evolution is wrong (what do you need a neutral theory of evolution for, anyway? Neutral evolution? What is it?).

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I also recommend you to have a careful look at the figure, so you will notice that the mutations in distinct subspecies are introduced on the same spot and even the type of substitution is the same. This falsifies NDT, whether you like it or not. Why don't you read the complete thread?

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And:
"There are many examples of conserved nucleotide sequences which do not code for amino acids, most of which are regulatory regions. Introns themselves neccessarily must have some selection pressure on their sequence in order for them to be recognised as introns, and not as exons."

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Now you tell me something new!

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And:
"If you are going to claim that all nucleotides which don't encode for amino acids are selectively neutral then you've got big problems when it comes time to explain homology in junk DNA and pseudogenes."

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Firstly, there is NO junk DNA. This oldfashioned opinion is (going to be) demonstrated to be completely wrong, although it is still claimed by evolutionists as proof for evolution [have a look at the TALK-origin site, or read the "selfish gene" (Dawkins, who else. But what does he know about genes? He is a zoologist). It is a completely outdated view on DNA].
Secondly, I am not the one in big problems. That is the theory of evolution.

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Best wishes,
Peter

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