quote:
Originally posted by peter borger:
dear Mark,
You say:
"Good grief, this isn’t in dispute!!!"
If mutations can be non-randomly introduced how can the NDT still be around? Once more, how do you conceive hot-spots in the DNA? Is a mechanism involved, or not? If not, how do you conceive hot-spots in the DNA? I am really interested in your opinion.
The NDT is around because it uses a different definition of random to you, you are putting words in peoples mouths in order to make your strawman.
http://
EvC Forum: molecular genetic proof against random mutation (1) -->
EvC Forum: molecular genetic proof against random mutation (1)
Is a mechanism involved in hot spots? Yup, no problem with that, in the same way the GC rich sequences in some way provide a mechanism for chiasmata to occur. I think you’re leaping ahead & assuming mechanism is analogous with design. After all, evaporation & condensation/precipitation is mechanistic. Plate tectonics is mechanistic. Solar eclipses are mechanistic,
ad infinitum.
If mechanisms occur naturally, & you are unable to tell the difference between natural & non-natural mechanisms, then it’s the same old ID argument again.
[QUOTE]Originally posted by peter borger:
[B]
And:
"1/ That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab."
First of all, the GLO gene is an inactive gene since it has been interupted at several sites. [/QUOTE]
[/b]
If I can interrupt you (pun unintended) right there. Non-transcribed DNA has been shown to have function. So interruption to transcription does not equate to non-function. Regulatory sequences etc.
[QUOTE]Originally posted by peter borger:
[B]
The sequence shown in the paper is the sequence of exon X. It is of interest since it demonstrates a non-sense mutation (introduction of a stop codon). Since the protein is not expressed at all, all positions in the DNA are completely neutral. [/QUOTE]
[/b]
There ARE non-transcribing DNA elements that have function. Do you think transposons are transcribed, the ones that are functional & not bang in the middle of genes, that is? So, you can’t equate lack of expression/transcription to lack of function.
Furthermore, it is possible for transcription sequences to be greatly shortened by non-sense mutations, yet still be transcribed (everything after the stop codon doesn’t get transcribed, unless, of course a new start codon appears further downstream the gene sequence..). Protein functions are then unknown, & not proven functionless.
[QUOTE]Originally posted by peter borger:
[B]
This means that natural selection does not act on the sequence since the protein is not expressed.
[/QUOTE]
[/b]
Natural selection may well act upon the sequence, you haven’t shown total lack of function, see above.
[QUOTE]Originally posted by peter borger:
[B]
So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). [/QUOTE]
[/b]
They are
completely at random, I’ve shown you the intended definition elsewhere. I don’t see what you hope to gain by mis-representing THE INTENDED MEANING of random as it pertains to random mutation.
Oh, my mistake, I do!
[QUOTE]Originally posted by peter borger:
[B]
Since the protein is not expressed at all, all positions in the DNA are completely neutral. This means that natural selection does not act on the sequence since the protein is not expressed. So, mutations should be introduced completely at random according to NDT (and according to Kimura with a neutral rate). If not, than a hot-spot is present in the DNA. It tells me that a mechanism drives the mutations. Since we presently do not know the mechanism we cannot say where exactly the mutations will occur. [/QUOTE]
[/b]
Taking this passage as a whole;
You still haven’t told me how you identify a hot spot in an ancestral sequence? A site can mutate once or a thousand times, how can you tell from a substitution from A to C,T, or G that it is a hotspot?
How can you tell that more mutations have occurred at a locus than at the neutral rate? It’s A,C,G or T?
More below.
[QUOTE]Originally posted by peter borger:
[B]
For the 1G5 gene there are much more data than the GLO gene and the hotspots are pretty clear. One may even be able to predict future mutations in the gene of Drosophila melanogaster. If you have a close look at the figure in Schmidt and Tautz article you will notice that some nucleotides change in different subpopluations at the same spot in the DNA, idependent from selection. Since we do not yet have such extended data for subpopulations of primates it is too early to say something about it. However, there are such data for human subpopulations, but these are not yet thoroughly scrutinised.
[/QUOTE]
[/b]
I’m not talking about the 1G5 gene, but your claim that the GLO pseudogene was wrecked by hotspots & not conventional random mutation. I’d still like to know how you can tell a random substitution from a non-random one in ancestral DNA.
[QUOTE]Originally posted by peter borger:
[B]
I am sure we will find the mechanism of non-random mutation.
[/QUOTE]
[/b]
Me too. I’m also sure it will be entirely natural, but that you will still call it evidence of design.
[QUOTE]Originally posted by peter borger:
[B]
And you state:
"Common descent & genetic drift remains the best explanation for non-vit c synthesis in primates, particularly given that the two prosimian primates that can synthesise vit c, fit in nicely at the bottom of the primate phylogeny, where they would be expected if evolution & common descent were responsible. That is, that vit c gene wrecking occurred after the prosimian divergence, leaving them unnaffected. A remarkable coincidence, don’t you think?"
You are free to believe that common descent and genetic drift are the best naturalistic explanations. However, if mutations are non-random these conclusion cannot be drawn.
[/QUOTE]
[/b]
I do still maintain that common descent & drift are the best explanations of non vit c synthesis. Whether the mutations are random, partly random, or COMPLETELY NON-RANDOM, matters not one iota to phylogenetic inference. A non-lethal/non-genetic death mutation is heritable either way. If it's heritable, then phylogeny can be inferred.
[QUOTE]Originally posted by peter borger:
[B]
2/ That you are able to attribute the existence of hot spots to design, when the cause of hot spots is UNKNOWN. God-Of-The-Gaps."
I (and others) have already explained that IF [my bold] the information is already present in the genome it makes it hard not to believe in design. Maybe you know a naturalistic explanation. I am very curious to hear about it. [/QUOTE]
[/b]
How can you tell if something is designed when you don’t understand the mechanism?
Also, there’s a VERY BIG IF in that sentence.
I find it odd that a designer would go to the trouble of creating vit c synthesis in an organism, then deliberately put a function wrecker in as standard. It’s like designing an aircraft so that the wings fall off. Is this evidence against design? It’s as good as evidence for design, so why not? J
quote:
Originally posted by peter borger:
3/ That non-random means directed, or pre-programmed in the sense of design, with regard to spontaneous mutations. If you think it does, rather than not-an-equal-chance-of-mutation-at-each-site, then you need to back this up. Remember, you have already told me you aren’t conflating the statistical & colloquial definitions of random/non-random."
At present the only well presented gene in subspieces of an organism is the 1G5 gene of D. mel. I invite you to study the sequences of the 13 subspecies extensively and have a careful look at the site of the mutations, and the type of substitutions. (Please do, since I am becoming a bit tired of repeating myself.)
And, what exactly did I tell you about conflating the statistical and colloquial definitions of random/non-random?
I think you’ll find it was me that warned YOU about statistical & colloquial definitions of random, not the other way around.
I’m sorry you’re getting tired of repeating yourself, because you’re going to have to get used to it if you continue to avoid pertinent questions.
For the THIRD time, & this time I’ll really labour the point.
quote:
Originally posted by peter borger:
That you are able to attribute alleged homologous hot spots to the wrecking of vit c synthesis by looking at extant sequences (see my last post), or even be able to attribute any of the extant pseudogene sequence to hotspots by looking at primate sequences. BECAUSE YOU CAN’T TELL WHERE THE HOT SPOTS WERE. The best you can tell is that a site has changed up to three times, eg from A, to either T,G, or C. That is, you can see the quality of mutation, but not the quantity. It is precisely the quantity you need to be able to divine in order to know whether a hot spot exists at that site. It cannot be done without having the original nucleotide sequence in the lab.
Let me put it another way, you
can take an extant sequence, mutate it a thousand times, then examine where the sequences mutate most in order to demonstrate where the hot spots are.
THIS IS DIFFERENT TO INFERRING HOT SPOTS ON ANCESTRAL SEQUENCES, FROM ALLEGED NEUTRAL EXTANT LOCI!!!!!!!!
The best you can see from an ancestral sequence is that a loci mutated
a maximum of three times, that is, from A to G, A to T, A to C, certainly not from within your paradigm. There is no way you can quantify a hotspot that has a thousand-fold higher probability of mutation than a statistically random probability. You may look at loci that appear to be random to you, but have mutated thousands of times more than adjacent loci, but because it started as A, & finished as A, you will never know.
This is probably best illustrated in the form of a question;
Q/ There is a single homologous locus in a gene in eight different related organisms. The locus is alleged to be neutral. Is there, or has there ever been a hotspot at this locus?
1/The nucleotides are A,G,T,C,A,G,T, & C.
2/The nucleotides are A,A,A,A,A,A,A, & A.
3/The nucleotides are A,A,A,A,A,A,A, & T.
No, I can't tell either.
Mark
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Occam's razor is not for shaving with.
[This message has been edited by mark24, 08-09-2002]
[This message has been edited by mark24, 08-10-2002]
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