"You cannot gainsay evolutions intended meaning of random. Only the definer/author can do that."
"So, you agree that it is all a matter of opinions of experts?"
You have tried to reduce Futuymas definition (& all other evolutionary biologists BTW, in this context) of “random” to a mere opinion. Well, of course it is, in a sense. But then YOUR definition of random is opinion also. The question is, not whether definitions are opinions, but whether an opinion/meaning that is pre-defined in advance for context, for the purpose of subsequent discussion, can be gainsaid by another definition, that hasn’t been defined in the same context. Um, that would be a “no”!
As long as I defined potato as “spice, common ginger, latin name Zingiber officinale, makes curries taste nice!”, then no one is in any confusion that I don’t mean the same plant that makes chips, fries, crisps etc. You may not agree with my meaning of potato, but it simply doesn’t matter, I’ve defined a word, so when I subsequently use it, you all know what I mean. Same goes with evolutionary biologies meaning of “random”. You HAVE to accept it at face value or you won’t make any sense out of the ensuing discussion. To NOT accept this definition is up to you, but when you attempt a falsification of the NDT, AND AT THE SAME TIME REJECT THE GIVEN CONTEXTUAL DEFINITION, you have a fallacy.
You have accused me of using definitions as a debatorial tactic. Shame you can’t see the wood for the trees. It is YOU who are using this tactic. The word “random” HAS been defined in this context. It is YOU who are removing this defined meaning & inserting your own, not me. I couldn’t give a shit whether you like Futuymas definition, or not. Tough. He has gone to the trouble of defining the word in it’s evolutionary biology context of “random mutation & natural selection”, it’s you who seem to be saying. “Hey, you can’t define words & use them in your own context! I’M THE ONLY ONE WHO IS ALLOWED TO DO THAT. Here, let me redefine your meaning of random in order to falsify what you say.”
I’ve given a similar example before, but it clearly hasn’t sunk in, so…
I define “transport” as to mean “all means of moving people from location to another”. Using this definition, I maintain that slaves were transported across the Atlantic from Africa to the Americas.
Person X, who shall remain nameless, comes along with another definition of transport that is perfectly good within it’s own context. “Transport is a means of moving people & goods via four wheeled engines, namely cars & trucks from A to B”. THEREFORE PERSON X MAINTAINS THAT HE HAS FALSIFIED MY CONTENTION THAT SLAVES WERE TRANSPORTED ACROSS THE ATLANTIC? Cars & trucks don’t float, right? So it must be falsified.
Nope, fallacy by out of context redefinition.
This is exactly what you are attempting.
[I][b]In order to falsify the “random” part of the NDT, you need to show that a strict statistical meaning is intended & in context, to the exclusion of all other meanings, & do so with near zero tentativity. If you can’t do that, you falsify nothing, nada, zip, zero……..[/I][/b]
"You admitted the falsification one mail ago, and now you don't. So, it is you who gives me opposite signals and thus I should be tired, not you. [/quote]
ROTFLMAO!!!!!!!!! Sweet Jesu, you do enjoy taking things out of context, don’t you!
[QUOTE]Originally posted by peter borger:
“Adaptive evolution is caused by all loci being subject to the probability of mutation, that mutation being culled by natural selection.
So what? It’s hardly falsified, is it?"
HARDLY isn't synonymous to NOT.
(Thanks for admitting NDT has been falsified). [/quote]
“Hardly” may not be synonymous with “not”, the way you WANT it to mean, but it is synonymous with “not” the way I actually mean it. You really do think you can change intended meanings to suit yourself, don’t you?
When I “admit” the NDT has been falsified, I’ll say so, OK? Have you no shame?
"B/ You believe you have falsified neutral rate mutation/ neutral theory. Therefore phylogenetic analysis cannot be inferred because directed evolution cannot be excluded. Put simply, you are saying that because alleged neutral sequences display non-neutral behaviour, this must be directed mutation, because it’s supposed to be neutral.
"Better would be that I used a DNA region that behaves according to neutral theory to demonstrate that mutations are not RANDOM in this particular region, and that alone overturns NDT". I did not say anywhere in my mailings that I've overthrown neutral theory. Actually, Neutral Theory it is well established (although it depends on the DNA regions you study. [/quote]
OK, but neutral theory is part of the NDT that you claim to have overthrown, yet claim NT is well established. Duh?
"I have the feeling that you mix up "function" and "neutral rate of evolution". In biology it is accepted that functional --protein-coding-- DNA sequences demonstrate an open reading frame. Such regions can perfectly well change at a neutral rate, demonstrating that there is no selective constraint on the protein."
"I don’t deny that the original transcribed protein has been ruined. But I do not accept that there is no function at any locus, or never has been, unless you show otherwise. But given that there are pseudogenes/transposons that HAVE been shown to have function, it is imperative that you investigate for this possibility before claiming falsifications."
"Here you refer to pseudogenes, and in particular to the GLO example.
I don't get your point. The GLO gene is inactivated by a stop codon in exon X, and in the paper the authors claim that this is the reason why primates do not produce vitamin C". If other loci have functions than for sure they do not contribute to synthesis of GLO protein, since it is absent in all great apes. The degeneration is a perfect example of what happens to redundant genes (and the GLO protein is redundant --> see a previous letter) over time: degradation, information to synthesise Vit C more efficiently is lost. It is de-evolution. In fact, if we had had the present knowledge on vit C synthesis before, we had been able to predict which genes might be inactivated over time. In general, redundant genes are supposed to be inactivated over time, since they are not under selective constraint. [/quote]
You seem to be equating “function” with “coding sequences”. The ATAT box has function, yet is not a coding sequence. All those transposons (that don’t end up in the middle of a coding sequence) that you & I accept have function, are not in coding sequences.
Therefore, you still need to show that alleged neutral sequences are neutral at all loci, & have always been, since the wrecking event, or you cannot infer falsification from non-neutral rate loci in alleged functionless sequences. Put another way, you are making inferences from loci that you assume are neutral without demonstrating that they in fact, are. Since your “falsification” is based on so called aberrant behaviour of neutral loci, don’t you think you should make sure before coming to a conclusion?
"All I claim is that if a non-functional gene demonstrates a NON-RANDOM position you cannot claim it as proof for common descent, since it might be due to a mechanism. And, if a mechanism is involved the other mutations might as well be introduced similarly." [/quote]
If it’s heritable & mutable, you can infer phylogeny from it.
I agree, 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.
But, this is entirely different a proposition from being able to infer hotspots from ancestral sequences. 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.
"By comparison of subpopulations.
To stick to your example. In subpopulations we find the following sequences:
sequence 1: tattgattagtgg
sequence 2: -------------
sequence 3: --c----------
sequence 4: -----g---a---
sequence 5: -------------
sequence 6: -------------
sequence 7: --a--ag--a-a-
sequence 8: -------------
sequence 9: --a--gg--a-a-
[- = same nucleotide as sequence 1]
Furthermore, if it is demonstrated that the sequence is not under selective constraint my conclusion would be that in this particular DNA segment the mutations observed in the subpopulations are introduced NON-RANDOMLY. Why? Because the same spots and same nucleotides are involved (compare this with the 1G5 gene).
You’re going to have to spell it out, Peter, I’m afraid. I STILL can’t tell where the hotspots were in the ancestral sequence.
Take the 4th from last loci, for example, the nucleotide is either g or a. This would seem to suggest that the ancestral state was either g or a, let’s call it a, for the sake of argument. A perfectly plausible explanation would be that a single mutation from a to g got fixed in one population, & that population was directly ancestral to 1,2,3,5,6,8,10,11,&,13. There is absolutely nothing that specifically suggests that more than one mutation took place at this locus.
Nevertheless, more mutations may well have occurred, from g to c, & g to t, but since they never got fixed, those polymorphisms/alleles were lost. According to you, any mutation that gets fixed “early” in a phylogeny, then multiple speciation/segregation takes place, is evidence of hot-spots. Meaning, multiple sub-populations/species that exhibit that one, single mutation, are evidence of hot-spot style mutability, despite the FACT that only one mutation may have been responsible for the same character state across multiple populations. If I had to sum up my argument in one sentence, it would be; I can see qualitative differences, but not quantitative ones.
You need to explain this in such a way that mutations can be quantitatively determined, beyond A-T, A-G, A-C etc, & demonstrate that those mutations “fail” a Poisson distribution test, & can be determined as non-random. But showing there is one, or up to 4 character states at one locus doesn’t exactly pass muster on this score, especially since SNPs are subject to the vagaries of fixation, which further compounds the issue. The last loci on your examples, that actually shows no change, may have experienced five times the rate of mutation than the fourth from last, but because pure chance never got any of those mutations fixed, the extant alleles do not reflect the quantitative value.
"You claim to have falsified natural selection, specifically."
"No, I demonstrated that that there examples of protein-coding genes that do question the validity of natural selection as being responsible for the residence of these genes in the genome. For instance, the a-actinin genes, and in fact all other redundant genes." [/quote]
Then why do you claim to have provided a FALSIFICATION OF NATURAL SELECTION, here?
Originally posted by peter borger:
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?
I refer you to post 73, D/ & Endlers observations with Guppies, rather than paste them here again, in order to shorten an already long post.
[QUOTE]Originally posted by Peter Borger:
"Where does this example help evolution? Nothing was created here by evolutionary forces. All your example demonstrates is that PREEXISTING alleles may vary in frequency in response to the environment. This is the role of natural selection: choose from alleles that are already present in the population, so the organisms do not become extinct immediately. [/quote]
Wha? YOU claimed to have falsified natural selection (see your own words), not me. Now back up, or back off.
"Where does this example help evolution?” Natural selection is a part of the NDT , & you claim to have falsified both. Natural selection doesn’t create alleles, it affects their frequencies where selective pressure can be brought to bear. I’m not claiming that anything was created by “evolutionary forces”. I AM claiming that natural selection can be seen to be at work in Endlers observations. What did you think I was trying to show? Alleles exist at the genome level, so natural selection can be seen to to occur at the genome level, in direct opposition to your claim of falsification.
[I][b]Since you have claimed to have falsified natural selection, please explain Endlers observations on Guppy camouflage, without resorting to natural selection, or any of the mechanisms involved therein.[/I][/b]
NON-RANDOM mutations indicate that all information is already present in organisms. Why? Because, the proteins and/or RNA that directs this are specified in the genome………… [/quote]
Can you show me a protein that “directs” mutation? Cite please.
…………..and it is reasonable to assume that no selective constraint is on these proteins, since they are only induced in response to the environment. If no selective constraint is involved it requires another mechanism to maintain in the genome as a functional gene. It is my personal opinion that the major part of the genome contributes to these mechanisms. It should be realized that only the minor part of the 40000 genes of man are of known function. Yes, only a couple of thousands have been described (5% or so), the rest is just there. Function unknown. I postulate that these proteins may be involved in maintenance of genes and stabilize the genome. In addition, these proteins may be involved in directing mutations towards the genes in response to the environment. Time will learn.
However, since all these genes are around without selective constraint (e.g. 98 % of the genes of Arabidopsis is redundant) it clearly demonstrates that there is a creator who designed them (for later use).”
"How can you tell a naturally occurring system/object from a designed one?"
"By redundancies: convenient to have and ready to use if needed. The genome anticipates on changes" [/quote]
Can you show that selective constraint is not observed on redundant genes?
There IS work going on regarding evolution of redundant genes.
Genetic redundancy caused by gene duplications and its evolution in networks of transcriptional regulators.
Biol Cybern 1996 Jun 74:557-67
In various organisms loss-of-function mutations of individual genes with unexpectedly weak or no phenotypic effects in the homozygous state have been observed. In several of these case, independent evidence shows that the respective gene products do have essential biological functions. An explanation emerging from detailed biochemical and genetic studies on such genes is that two or more genetically redundant genes contribute to that function, i.e., a group of genes that is able to substitute partially for a loss of function in one member of that group. The often-observed sequence similarity among redundant genes suggests gene duplications as a frequent source of genetic redundancy. Aside from this observation, the evolution of genetic redundancy is poorly understood. Genetic redundancy is potentially of great relevance to organismal evolution, since it may (i) 'protect' organisms from potentially harmful mutations, and (ii) maintain pools of functionally similar, yet diverse gene products, and thus represent a source of evolutionary novelty at the biochemical level. The question of how genetic redundancy evolves should ideally be answered by experimentation. However, the large time scales involved and insufficient quantitative understanding of the underlying regulatory pathways are likely to preclude such an approach in the foreseeable future. Preliminary answers are sought here by using a biochemically motivated model of a small but central part of a developmental pathway. Sets of transcription regulators are modeled that mutually regulate each other's expression and thereby form stable gene expression patterns. It is then studied how genetic redundancy caused by gene duplications might evolve in such networks. [I][b]The results obtained suggest that redundancy may, at least in some cases, be a global property of gene interactions within a regulatory pathway, rather than a local property of genes in that pathway. They also raise the possibility that duplications of a whole regulatory gene network, as may have taken place during the evolution of HOM/Hox genes in chordates, are less likely to be reversible (by gene deletions) than duplications of individual network genes. These findings are discussed with reference to experimental evidence on the evolution of HOM/Hox genes.[/I][/b]
Evolution of genetic redundancy for advanced players.
Curr Opin Genet Dev 1993 Dec 3:902-10
An ever expanding database on the sequence organization and repetition of genic and non-genic components of nuclear and organelle genomes reveals that the vast majority of sequences are subject to one or other mechanism of DNA turnover (gene conversion, unequal crossing over, slippage, retrotransposition, transposition and others). Detailed studies, using novel methods of experimental detection and analytical procedures, show that such mechanisms can operate one on top of another and that wide variations in their unit lengths, biases, polarities and rates create bizarre and complex patterns of genetic redundancy. The ability of these mechanisms to operate both within and between chromosomes implies that realistic models of the evolutionary dynamics of redundancy, and of the potential interaction with natural selection in a sexual species, need to consider the diffusion of variant repeats across multiple chromosome lineages, in a population context. Recently, important advances in both experimental and analytical approaches have been made along these lines. [I][b]There is increasing awareness that genetic redundancy and turnover induces a molecular co-evolution between functionally interacting genetic systems in order to maintain essential functions. [/I][/b]
Even the maintenance of those redundant systems, have potential explanations.
Evolution of genetic redundancy.
Nowak MA, Boerlijst MC, Cooke J, Smith JM
Nature 1997 Jul 388:167-71
Genetic redundancy means that two or more genes are performing the same function and that inactivation of one of these genes has little or no effect on the biological phenotype. Redundancy seems to be widespread in genomes of higher organisms. Examples of apparently redundant genes come from numerous studies of developmental biology, immunology, neurobiology and the cell cycle. Yet there is a problem: genes encoding functional proteins must be under selection pressure. If a gene was truly redundant then it would not be protected against the accumulation of deleterious mutations. A widespread view is therefore that such redundancy cannot be evolutionarily stable. [I][b]Here we develop a simple genetic model to analyse selection pressures acting on redundant genes. We present four cases that can explain why genetic redundancy is common. In three cases, redundancy is even evolutionarily stable. [/I][/b] Our theory provides a framework for exploring the evolution of genetic organization.
The inference of design you make here is primarily a god-of-the-gaps argument. Genetic redundancy is at a very early stage of understanding, so you infer design from an argument-from-personal-incredulity. This is an incredibly weak position from which to infer anything, let alone design.
Give me something that is well understood to infer from, please.
Occam's razor is not for shaving with.
[This message has been edited by mark24, 08-25-2002]
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