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Author Topic:   questions evolutionists can't or won't answer
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 36 of 141 (10545)
05-29-2002 5:55 AM
Reply to: Message 35 by Philip
05-29-2002 2:01 AM


Hi Philip:

Just a quick clarification on your reference here:

quote:
Thus the mechanism is natural selection involving genetic variation(s) (not metastatic mutations) that exist within all populations to ‘enjoy’ limited biodiversity. See Quetzel's non-mutational recapped NS mechanism under the thread "Falsification Theory of Natural Selection" (5/28/02); his evo-mechanism goes into great technical depth while covering the basics of NS as well.

(Thanks for your kind words, btw). If you'll look back over the post you referenced, you'll note that a key assumption in NS is:

1. There must be heritable variation for some trait. Examples: beak size, color pattern, thickness of skin, fleetness, visual acuity.

Without going into excruciating detail, the bit that I left out (because it wasn't germane to the specific topic) is that this variation is based on changes to the genetic code of the organism. Heritable variation occurs by mutational changes in an organism’s DNA (any change in the hereditary message – base pair substitution or insertion/deletion of new bases, etc) leading to the creation of new genetic material AND/OR creation of new genetic combinations through transposition (changing the position of a gene changes what it does), recombination (through cross-over during meosis), or genetic reshuffling (through sexual reproduction).

So it's still the old "mutationalist" explanation. NS operates on those genetic changes that cause changes in the phenotype of the organism. Sorry.


This message is a reply to:
 Message 35 by Philip, posted 05-29-2002 2:01 AM Philip has responded

Replies to this message:
 Message 44 by Philip, posted 05-29-2002 7:49 PM Quetzal has responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 45 of 141 (10632)
05-30-2002 6:04 AM
Reply to: Message 44 by Philip
05-29-2002 7:49 PM


Hi Philip:

I think I'm beginning to catch a glimmer of where our disagreement lies (I mean, beyond the obvious).

quote:
what you call ‘mutational’ is never ‘freak’ metastasis (AKA raw mutations).

In the first place, mutations leading to metastatic conditions (sorry if that's the wrong term - I'm not an oncologist) only occur in somatic cells. In addition, metastasis only occurs if the somatic mutation is of a specific type that modifies the protein product without killing the cell. In any event, a somatic mutation has no direct bearing on evolution or natural selection, since these mutations are not inherited. (The indirect exception would be if a tumor kills the organism before it can reproduce.)

The only mutations that can have any effect on evolution are therefore germline mutations. Even here, the vast majority are going to either be neutral (i.e., of no consequence to natural selection because they have no effect on phenotype) or will kill the cell (or at least render the developing organism unviable). Another fraction of these mutations will have effects that show up later in development which may kill the organism before it can reproduce - again, having no effect on evolution because the changed genotype is eliminated from the population before it can be passed on.

What's left, therefore, are the few mutations that are either mild enough to permit the organism to live long enough to reproduce, OR provide a genuinely beneficial phenotypical change. http://207.36.64.70/ubb/smilies/wink.gif[/IMG] When it's expressed, then I'll worry about it. These are the mutations that create the actual heritable novelty in a population. They are not "in the a priori (sic) population’s gene pool". They represent NEW additions.

However, you are correct: mutations alone - which as you can see are relatively rare - cannot completely account for the significant variation between individuals within a given population on which natural selection operates. Instead, NS operates on variation thrown up by recombinations or other changes in the genetic code which already exists in the gene pool - everything from random chromosome shuffling to transposition and cross-over. Just to complicate things, plants are especially liable to chromosome doubling (polyploidy), and some prokaryotes can swap genetic material - again creating the diversity upon which NS operates.

The above is, of course, grossly over-simplified. I hope I've made my position clearer, however.

quote:
The error of your ‘detailed’ mechanism is that entropic destruction occurs where mutation is uncontrolled in any 'reshuffling', transposition, etc

Actually, your error is your misunderstanding that mutation = cancer. As I explained, this is not necessarily the case.


This message is a reply to:
 Message 44 by Philip, posted 05-29-2002 7:49 PM Philip has responded

Replies to this message:
 Message 48 by Philip, posted 05-31-2002 3:58 AM Quetzal has responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 49 of 141 (10740)
05-31-2002 10:11 AM
Reply to: Message 48 by Philip
05-31-2002 3:58 AM


quote:
--Calling things “NEW additions” seems rash from the ‘mega’ perspective of the ToE. I observe them as mere DIFFERENT LATENT manifestations, because:

Why is this “rash”? Any mutation that causes a change to the DNA code and hence final protein product would be a “new addition” since the new code sequence didn’t exist in the genome before the mutation. It is certainly not a latent manifestation – implying the new code was already present (as opposed to gene duplication, reshuffling, etc, which could fit under a very generous interpretation of “latent”). Remember, a mutation is merely a copying error in DNA that isn’t repaired by the cell’s own repair mechanisms. I would argue that any change in the protein product – whether a single-base substitution, a frameshift or even duplication constitutes a NEW addition.

quote:
1) They do appear grossly ‘walled in’ by genetic-structural boundaries of the organism. That every organism indeed has its genetic bounds is presently seen and expected.

I’m sorry, Philip, but I have no idea what you’re on about here. What are the “genetic-structural boundaries” of an organism. Could you please provide an example of genetic bounds – since you state they are “presently seen”?

quote:
2) What is new is never ‘significantly’ new: i.e., never beneficial enough to incrementally make a novel complicated biochemical (let alone cellular) labyrinth and/or algarhythm. Recombinant technology splices only in metastatic ways that benefit non-host organisms (e.g., for human exploitation).

I’m not going to argue with your jargon – although I’ve never heard the terms “labyrinth” and “algorithm” used in this context in biology (you wouldn’t be inventing terms just to confuse me, would you? You can point to some mainstream literature that uses the terms in this fashion, yes?). You are simply incorrect that novel biochemical structures are never created naturally.

The classic example is the evolution of an anti-freeze glycoprotein derived from a pancreatic gene that normally codes for trypsinogen in Antarctic fish. A reading error or frameshift mutation occurred in a small region spanning the boundary between the first intron and second exon of the trypsinogen gene plus amplification of a 9-nt Thr-Ala-Ala coding element from the trypsinogen progenitor to create a new protein coding region for the repetitive tripeptide backbone of the antifreeze protein. (The full article, Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish.) This is by no means the only example.

quote:
3) New is…never enough to incrementally make novel complicated labyrinths and/or algarhythms become another kind of life form. Speciation (even in the form of polyploidy) never forms new complex algarhythms and/or labyrinths, only new latent ‘traits’.

Again, I’m not entirely clear what you are trying to say. If you are attempting to argue against speciation in toto, I’m afraid I’m going to have to ask you to explain away a lot of very compelling evidence to the contrary, including ring species, rodent speciation (check out Madeiras Island studies on Mus musculus – six different species on one island – and they’ve only been there for 250 years!), the observed evolution of sticklebacks, the entire science of developmental genetics and molecular phylogeny, etc.

quote:
--This aspect of your mechanism must never be over-generalized in science until demonstrated. Else you, too, become religious while inferring polyploid mutations (the raw mechanism of the ToE) to cause of life’s complex labyrinths and algarhythms.

Once again, I have absolutely no idea what you’re on about. What aspect? You seem to be arguing that polyploidy – which is a whole ‘nother mechanism of speciation unrelated to anything we’ve discussed so far – is the ONLY mechanism. Wrong again. Polyploidy – chromosome multiplication. It’s very common in plant speciation, but relatively rare in animals. It is NOT a mutation.

quote:
4) The sums of ‘new’ additions never harmonize those exceedingly complex interactions of these labyrinths and algarhythms, which are so unique and ‘set-in’ … within every biodiversity.

Sorry, once again you’ve gone over my head. Could you possibly explain what you’re talking about in layman’s terms, without jargon? Thanks.

quote:
--Metastasis is a term that may be used in genetics. Non-oncologists and laymen may adopt this cancerous term, to express cancerous reproductive aberrations (genetics) in gamete cells.

Uhhh, okay. However, you’re back to insisting mutation = cancer. This is not the case.

quote:
--Polyploidy is an interesting phenomenon, but again limited to mutation spots …else you observe metastasis, decay, etc. No doubt metastasis arises in these [i]hot[/] spots as well. Randomness and decay, thus, are allowed ‘some’ free expression beyond the mainstream norm … as in your multi-tiered mechanism of NS involving beneficial mutations.

Once again you’re confusing mutation and polyploidy. Not the same thing.

quote:
--Note: (Correct me if I’m wrong…) You seem to be scientifically underplaying mutations in the mega-ToE. That in my perspective is ‘jumping the boat’.

Err, nope. That’s pretty straightforward neo-Darwinian evolution. Mutation is how novel genetic material is produced. Variation is only the first step – after that you start working with natural selection and all its various complex mechanisms.

quote:
Do you not need to DRASTICALLY ‘play up’ ka-zillions of incremental beneficial mutations (vs mere traits) for the mega-ToE to be viable? (I invite anyone to debate this)

Nope. Just a few beneficial mutations or genetic reshuffling of existing genes, plus natural selection (especially directional selection: try this website Examples of Beneficial Mutations and Natural Selection for some nice abstracts of recent articles. Here’s a good article on evolution of novel proteins in mammals, Positive Darwinian selection drives the evolution of several female reproductive proteins in mammals. Here’s a really good article on the genetic basis for evolution, Morphological innovation and developmental genetics. I like this one because it shows that a small number of genes may be responsible for major morphological changes.

quote:
--Does not reproductive metastasis (cancer) remain as the only viable mutational mechanism left for the mega-ToE at this point, Quetzel (or any one)?

Since cancer is a negative survival pressure, I’d say 1. There’s no such thing as reproductive metastasis, and 2. It’s not even ONE of the mechanisms for ToE, let alone the only viable one.

Philip, I say this with all due respect, you really need to read some basic biology – I’m not sure you even understand what you’re arguing against.


This message is a reply to:
 Message 48 by Philip, posted 05-31-2002 3:58 AM Philip has responded

Replies to this message:
 Message 50 by Philip, posted 05-31-2002 8:00 PM Quetzal has responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 51 of 141 (10816)
06-02-2002 8:41 AM
Reply to: Message 50 by Philip
05-31-2002 8:00 PM


quote:
Originally posted by Quetzal:
1. There’s no such thing as reproductive metastasis:

quote:
DORLAND’S DEFINITION of metastasis: The transfer of disease from one organ or part to another not directly connected with it.
WEBSTER’S:
1. (Theol.) A spiritual change, as during baptism.
2. (Med.) A change in the location of a disease, as from one part to another. Dunglison.

I’ve used the term metastasis, perhaps too loosely from your restricted ‘book’ perspective, I admit I can not find a better term at present to verbally express transfer of detrimental DNA to ‘non-direct’ parts of reproductive chromosomes: i.e., in gametes, diploid individuals, or other microbiological reproductive components of species. Perhaps you can suggest a better term.


Actually, my objection is that I don’t think there’s any reason to bring in a new term. It’s not a question of perspective – “book” or not, the way I use the terminology is pretty much the way every biologist uses it. As to your specific use of “metastasis”, I appreciate the clarification, but submit that “mutation” covers any change in DNA code sequence either pre- or post-zygote. Once again, mutation does NOT equate necessarily to disease. Your use of metastasis in this context is misleading, at best. Beneficial mutations DO exist (see the articles I referenced in my previous post for several examples). The fact is, most mutations of any stripe are simply neutral as far as the individual organism is concerned.

Although I accept the fact that you have a degree in biology, once again you bring in elements that are very non-standard, or at least used incorrectly, in the discipline. What do you mean by “non-direct parts of reproductive chromosomes”? The phrase doesn’t seem to make sense to me. Perhaps you could explain what you mean.

In addition, all sexually reproducing organisms are diploid. One copy of the chromosomes is received from each parent. This is one of the reasons that even germline mutations may not have any effect on the organism – they may have received a fully functioning copy from the other parent (c.f, heterozygous recessives.)

quote:
And the term labyrinth (Websters):
1 a : a place constructed of or full of intricate passageways and blind alleys
b : a maze (as in a garden) formed by paths separated by high hedges
2 : something extremely complex or tortuous in structure, arrangement, or character :
3 : a tortuous anatomical structure; especially : the internal ear or its bony or membranous part
Examples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, and the ka-zillions of biochemical labyrinths associated with each.

I understand what labyrinth means. If you are referring to anatomical structures in the sense that they are irreducibly complex (a la Behe), then your use in the context of definition 2 above is at least slightly justified – although in this case you’re going to have to show that the examples you gave are, in fact, irreducibly complex – something Behe himself has failed to do. I’m not going to argue definitions with you, but I would like to point out that definition 3 is merely a reference to the shape – a labyrinth can be used as a descriptive metaphor for the convolutions and maze-like structure of the inner ear. I don’t suppose there’s any point in drawing your attention to the varieties of suture patterns in foraminifera (you’d love ‘em, they’re an almost classic example of the “golden mean” in action in nature) as an illustration of how convoluted – labyrinthine – structures can be formed quite easily in nature? My point is you are not justified in using the term as a falsification.

As for how complicated systems such as protein cascades can be formed (evolved ) naturally, that’s a subject a whole lot more complicated than can be realistically covered in an Internet forum post. With cooption, recruitment, exon shuffling, and a dozen other observed mechanisms that can be involved, my only suggestion here is for you to check out a recent book on evolutionary developmental biology. Alternatively, you can probably find this article in a good university library: Thornhill RH, Ussery DW 2000, “A classification of possible routes of Darwinian evolution”, published in The Journal of Theoretical Biology, 203: 111-116, 2000. Once you’ve caught up on some of the recent advances in evolutionary biology and microbiology, anatomy, etc, you may find the evidence more compelling. Happy reading!

quote:
The term algorithm= a step-by-step procedure for solving a problem or accomplishing some end
Examples are too numerous: ears, eyes, olfactory senses, sympathetics, reproductive systems, numerous other systems and the ka-zillions of biochemical algorithms associated with each: Positive and negative eedback loops of harmones, enzymes, etc. on the biomechanical level. Cascading events in blood coagulation, healing, inflammation, etc. etc. Time would fail to go into algorithms of the immune system(s), botanical and environmental algorithms

I’m aware what the term algorithm means. My question was how you were using it. Would you care to try an algorithmic approach to refute the evidence provided in the antifreeze glycoprotein article I referenced? The authors certainly don’t see an evolutionary problem in the development of this protein. Considering that in Algorithm Information Theory (at least as proposed by Kolmogorov-Chaitan) the amount of information is an abstract thing, not a concrete fact about the world, it applies only to a description of things, not to the things themselves. If DNA is information bearing, it is because we can make a sequence of abstract symbols out of it and apply AIT to that. Even so, we keep finding features of DNA that the simple code does not capture (eg, histone and methylation patterns). I bid you, “Good luck” in your refutation.

quote:
Originally posted by Quetzal:
2. It’s not even ONE of the mechanisms for ToE, let alone the only viable one.

quote:
Ah but it is the only viable one that I can conclude under the mutationalist scheme.

Perhaps it is the only viable one you can conclude. However, in this case, you’re pretty much a minority of one. You certainly have failed to show that disease metastasis even has any bearing on this discussion – let alone that evolutionary biologists are basing their theories on it as such.

quote:
Originally posted by Quetzal:
Philip, I say this with all due respect, you really need to read some basic biology – I’m not sure you even understand what you’re arguing against.

quote:
I’ve had too much biology (M.S.B.S), tutored and/or taught it on H.S., college, graduate, and post-graduate levels. Currently I have an applied working knowledge of it as a podiatric surgeon, etc. I admit my language is more crude compared to your scientific rhetoric (which I appreciate), but I believe I know what I’m arguing against:

No insult intended. My apologies if you took it that way. However, with your stated background I’m having difficulty comprehending why you consistently misunderstand basic biological concepts. Your genetics, developmental biology, microbiology, and biochemistry assertions are often simply wrong. I’m having a hard time reconciling the two.

quote:
1) A ToE that ‘forgets’ ‘beneficial mutations’ alone are the foundation of the mega-ToE.

This is YOUR assertion – and I have to say it’s becoming a rather obvious strawman. I have argued consistently (and repetitiously, I’m afraid) that beneficial mutations are only ONE aspect of the ToE. Selection pressures operating on the phenotypical variations occurring in a given population of organisms – whether arising through mutation or the normal recombination/reshuffling of genetic material that occurs during gametogenesis – provide the foundation of the ToE. Your assertion is wrong, and ignores almost all of biology. You don’t even have to accept evolution to be aware of variation in populations and the statistical processes that change the relative frequency of expressed alleles. Just look in the mirror: unless you are a clone of your parents, you differ from them in many traits. Your cousin is even more different. “In the wild”, given that some of these traits can have an effect on the survival of an organism (an herbivore that runs very fast or jumps very high has a better chance of surviving a predator’s attack than one that runs slowly or doesn’t jump high enough), the variation that provides at least some survival advantage to an organism is the one that gets passed on. This is the type of variation that drives evolution. The origin of that variation is what I’ve been discussing in the last several posts.

quote:
2) The impossibility of such incrementally complex mutations forming labyrinths/ algorithms seen and expected to be seen everywhere in nature (without excuse).

Why is it impossible? For just one example, Bandyopdhyay PK, Garrett JE, Shetty RP, Keate T, Walker CS, and Olivera BM, 2001, “Glutamyl carboxylation: An extracellular posttranslational modification that antedates the divergence of molluscs, arthropods, and chordates”. In this article, the authors report the discovery that one of the key essential elements in the mammalian blood clotting cascade, carboxylglutamate (Gla), is a modification of much “older” protein found in simpler organisms.

quote:

In 1984, Gla was shown to be present in a highly specialized invertebrate system, venom peptides of the marine cone snails (Conus). It was found that a neuroactive Conus peptide, conantokin-G, which is a 17-aa peptide ligand produced in the venom of the fish-hunting cone snail, Conus geographus, contained five residues of Gla. This peptide targets a subtype of the glutamate receptor, the N-methyl-D-aspartate receptor. A variety of other Conus venom peptides, some in the conantokin family related to conantokin-G, but others with completely unrelated amino acid sequences, also proved to have Gla residues. These discoveries provided initial evidence suggesting that the role of this posttranslational modification in blood clotting might be only a small part of the total biological picture. Not only was Gla present in invertebrates (which was totally unexpected), but it was found in several entirely different structural and functional contexts. Biochemical experiments established that the posttranslational conversion of glutamate to Gla in Conus peptides had the same general requirements as had been established for mammalian -carboxylation, i.e., reduced vitamin K, carbon dioxide, molecular oxygen, and a recognition signal sequence. (emphasis added, references removed for clarity)

Impossible? Apparently not…

quote:
3) Respectfully, human error and self-deception regarding ‘cause-effect’ relationships in biology.

This certainly occurs. However, I think you need to provide specific examples showing how widespread the problem is, as well as how this refutes the ToE. This isn’t biblical inerrancy, after all. It’s science.

quote:
4) My own misconceptions as well, in this field (which is why I enjoy discussing/arguing with you). That I may mature in my science as a physician, and in my ‘spiritual’ well-being, too.

Okay, glad you’re enjoying the discussion. I obviously don’t expect to change your mind, but from my perspective it’s useful to get the actual science on the table. Viva los lurkers!

[QUOTE]

Hmm, not sure I understand this. If you’re arguing that the biochemical origins of life are not proven, I agree with you. However, since every OTHER phenomenon in nature IS understandable using natural laws without recourse to the supernatural, I have to say that I’m relatively confident that abiogenesis will ultimately be understood the same way. I’m content to wait. Fraudulent it certainly isn’t – nobody’s setting out to deceive anyone. The only true a priori bias I’ve ever encountered is from the religious side. After all, since you don’t profess a belief in the Egyptian or Norse pantheon alongside your particular flavor of the Christian god, I’d have to say that the only difference between us is that I believe in one less deity than you do…


This message is a reply to:
 Message 50 by Philip, posted 05-31-2002 8:00 PM Philip has responded

Replies to this message:
 Message 52 by Philip, posted 06-03-2002 1:56 AM Quetzal has responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 53 of 141 (10877)
06-03-2002 9:18 AM
Reply to: Message 52 by Philip
06-03-2002 1:56 AM


I'm a bit unhappy, after the last two lengthy posts I provided, that this is the best you can come up with. Philip, it appears you are studiously ignoring my specific points. If this discussion is to continue, I would ask that you take a little more time and address or rebut the points I've made. Especially since the examples and discussion I have laboriously provided are direct refutations of many of your assertions. Thanks.

[QUOTE]Originally posted by Philip:
Quetzal: I have argued consistently (and repetitiously, I’m afraid) that beneficial mutations are only ONE aspect of the ToE.
Selection pressures operating on the phenotypical variations occurring in a given population of organisms – whether arising through mutation or the normal recombination/reshuffling of genetic material that occurs during gametogenesis – provide [b]the foundation of the ToE

Philip: --Your quoted statement above is all that is necessary to refute. You just inferred normal recombination/reshuffling of genetic material and played-out all the freak mutations, rhetorically. You can’t do that Quetzel, not within the framework of the mega-ToE (supposed high level trans-taxonomic ‘speciation’) ... because:[/QUOTE]

This is getting a tad surreal. I'm not quite sure why you keep insisting that I subscribe to your (erroneous) version and/or misunderstanding of evolution. Nothing I have posted so far on this thread or any other is in any way controversial or unaccepted in the context of mainstream evolutionary biology and genetics. I'm quite sure that if I had posted anything incorrectly, one of the experts on this board would have been all over it with hob-nailed boots.

I haven't "inferred" anything when I talk about "normal" recombination during gametogenesis. This is such fundamentally basic biology - it's not even evolution!!! - that I'm surprised you would even question it. EVEN IN THE ABSENCE OF MUTATION, the process of meiosis in sexually reproducing organisms produces variation upon which natural selection can operate.

Cross-over: In prophase I, two non-sister chromatids aligned together swap sections while synapsed together. The process is called crossing over. It is reciprocal - the segments exchanged by each non-sister chromatid are identical (but often carry different alleles).

Each chromatid contains a single molecule of DNA. So crossing over is really just the swapping of portions of adjacent DNA molecules. It must be done with great precision so that neither chromatid gains or loses any genes. In fact, crossing over has to be sufficiently precise that not a single nucleotide is lost or added at the crossover point if it occurs within a gene. OTHERWISE YOU GET A MUTATION! This form of recombination can create new alleles in the recipient gamete. THIS IS NOT MUTATION!!!! It is a basic property of meiosis.

Random assortment: In meiosis I, the orientation of paternal and maternal homologous chromosomes during metaphase is random - hence during anaphase I each homologue separates and moves to its respective pole. The poles are separated in meiosis II. Therefore, although each cell produced by meiosis contains one of each homologue, the number of possible combinations of maternal and paternal homologues is 2^n, where n = the haploid number of chromosomes. In humans this translates to 2^23, or 8,388,608 possible combinations of chromosomes FOR EACH GAMETE!!!!!

Fertilization: If the parents differ genetically - each providing one of the 8 million possible combinations - new combinations of genes occur in their offspring.

This is one of the primary ways variation occurs within a population: the recombination of existing genetic material. Natural selection operating on the individual expression of this variety leads to changes in the frequency of alleles in the population. This is utterly uncontroversial and so basic that I'm aware the idea is presented in Jr High School biology texts. You must have slept through that part of all those biology courses you supposedly took.

quote:
--Incrementally, Mega-ToE mutations/recombination/reshuffling must become abnormal, albeit beneficial to be viable: That is innumerable incremental mutations must be eventually become uncanny to be 'selected':

This is your assertion. If you are going to continue to argue this point, you need to present evidence that meiosis in the absence of mutation is abnormal. Then you can present evidence that all mutations are themselves "abnormal". Mutations, as I've continually pointed out, are the source of novel genetic material. When the selection pressures on a population change, it is the presence (or absence) of these novel traits that determines the survival or extinction of the population. A very conservative estimate is about one non-lethal mutation in any given locus per 100,000 gametes. That means that a human baby, for instance, will be born with 1-3 mutations. Combine these mutations (most of which are neutral in terms of survival) with the recombination during meiosis, and voila, you have literally staggering amounts of potential variation upon which natural selection can operate.

quote:
--There can be nothing ‘normal’ about incrementally uncanny variations of ‘set in’ and highly interdependent complexities (not merely ICs )of organs, the higher-level organs, especially. Thus the mega-ToE of origins becomes increasingly impossible, the more interdependent the biological complexities become (see my foot example under the thread listed below).

Ah, the old argument from incredulity raises its head. Pure assertion - care to take a stab at providing evidence of "uncanny variation", and what you mean by "set in"?

quote:
--At least call your theory of origins by its correct name: the Mega-ToM (the ‘M’ for ‘Mutants’ … since ‘Metastasis’ is an unacceptable biological term at present)

You can call it anything you want - and as often as you want. Your insistence on this point when I have patiently provided the actual scientific terms and mechanisms is becoming redundant. "My theory", as you put it, is absolutely, positively, wholly neo-Darwinian synthesis. I'm probably about as orthodox in this science as you can get.

quote:
--The perpetrated fraud, self-deception, obstinacy, and/or delusion here is maxed-out, precisely here ... by numerous 'scientists'. Why, exactly, I won't sermonize here. (Note: Your keenness in this subject is nonetheless appreciated)

Again, you should - as I asked previously - provide evidence that any biologist has deliberately "perpetrated fraud", indulged in "self deception", or is somehow deluded because they find that nearly every observation they make in nature adds more to the strength of the evolutionary edifice. The only obstinancy I see is yours.

quote:
--Now knowing you will perceive all this ‘Brad-like’, hypocritical, etc., I invite you to rebuke me here, but then, continue a logical rebuttal on the thread entitled: “Has human evolution stopped”. There, I logically explained why mega-evolution of the human foot has indeed stopped (and never started).

I have never accused you of Brad-like behavior. I have stated, and will continue to do so, that in many cases your use of non-standard terms is confusing. As far as the human foot goes, since I know sod-all about it, I'll take a look at the thread but doubt I'll have anything to do with the discussion.

Meanwhile, you can try your hand at refuting any of the evidence I've provided in this thread. More handwaving or ignoring my posts will ultimately get you on my ignore list.


This message is a reply to:
 Message 52 by Philip, posted 06-03-2002 1:56 AM Philip has responded

Replies to this message:
 Message 54 by Philip, posted 06-03-2002 6:22 PM Quetzal has not yet responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 118 of 141 (17516)
09-16-2002 6:42 AM
Reply to: Message 116 by Bart007
09-15-2002 3:14 PM


Hi Bart:

quote:
Isn't evolution suppose to flow the other way. You do not start out with phyla that evolve all creatures according to their phylum, that sounds a bit creationist. Evolution demands it start out with a single self-replicating somehing or other, that speciates over and over into many new species, which evolve into new genesus, which evolve into new groupings known as families, etc., etc., all the way up to new phyla.

Not really. This is a relatively common misunderstanding of linnean classification and "phyla" in particular. A critter is assigned to a phylum based on a shared body plan. All phyla were described within the last couple hundred years - using modern organisms. One of the key fallacies here is that means that all extinct organisms - whether they really share a body plan or not - are shoehorned into one of the 33 identified phyla alive today! Needless to say, this means that some of the really weird pre-Cambrian and Cambrian fossils are listed in one of the modern phyla - whether they share a common body plan or not - leading to serious misconceptions that all phyla magically appeared 580 million years ago. In point of fact, only about 13 actually show up in the fossil record during the Vendian and around the Paleozoic-Cambrian boundary (the so-called "explosion"). Here's a listing:

Era Phyla

Recent 13
Eocene 2
Cretaceous 2
Jurassic 1
Triassic 3
Carboniferous 5
Devonian 4
Silurian 1
Ordovician 1
Cambrian 9
Vendian 4

As you can see, only 13 phyla show up during/prior to the Cambrian. 20 phyla appear later. There IS, therefore, evidence of inter-phyla evolution. Why? Because "phylum" is simply a convenient term, not an intrinsic entity defining a discontinuity or barrier. Even then, stuffing organisms into existing phyla leads to problems: look up Asbestopluma or the Cladorhizidae - classified under phylum Porifera, but sharing none (or almost none) of the Porifera bodyplans. The whole thing is very arbitrary - and substantially more complex than a cursory examination of the issue would lead one to believe.


This message is a reply to:
 Message 116 by Bart007, posted 09-15-2002 3:14 PM Bart007 has responded

Replies to this message:
 Message 119 by Bart007, posted 09-17-2002 2:38 AM Quetzal has responded

  
Quetzal
Member (Idle past 4008 days)
Posts: 3228
Joined: 01-09-2002


Message 123 of 141 (17667)
09-18-2002 7:53 AM
Reply to: Message 119 by Bart007
09-17-2002 2:38 AM


You can start by explaining how what I posted constitutes "special pleading". Also, the chart I used came from Mayr, not Morton (although Morton's site provided the Porifera reference). I'm sure he'd be pleased you consider his works "great". IMO, they're pretty good, but I wouldn't go so far as to say "great".

quote:
There have been estimates of up to 84 Phyla that appear in the Vendian/Cambrian period. Many have become extinct. Since the Cambrian era, not one new bauplane (i.e. Phyla) has arose.

Yeah, I've seen the figure before (I think, Wilson "Diversity of Life") concerning the total number of phyla that ever existed - including proctists, archea, bacteria, etc - but not limited to the Cambrian. The most recently discovered phylum was found less than ten years ago (the Gnathostimulida), and there is absolutely no evidence it existed in the Cambrian. I've also seen as few as 22, of which only a dozen or so appear in the Cambrian. Depends on the taxonomist.

However, you have some significant flaws in your diatribe, err, argument. For example, your assertion "84 phyla appeared in the Vendian/Cambrian" is incorrect (to say the least), as it completely ignores the emergence of terrestrial plants (for example) containing 12 phyla (depending on your classification scheme) all on their own - and which didn't appear until the Ordovician or later. Or phylum Uniramia which also evolved on land sometime either in the late Cambrian or early Ordovician - after the "explosion" was long over (of course, whether you consider Uniramia, Crustacea, and Chelicerata as phyla or superclass, and Arthropoda as phylum or superphylum depends on your cladistics teacher). Remember, phylum refers to body plan - it doesn't say ANYTHING about whether or not the organism that first developed the plan had an ancestor with a different plan.

quote:
It is ludicrous that PBS writes loaded sentences to browbeat unwary readers into accepting the materialistic evolutionary worldview. Here is such a typical browbeating statement by PBS: "The mutations that give rise to these control genes...". Neither PBS nor Science know anything about any mutations giving rise to control genes. PBS can only justify such a statement because they "KNOW" evolution is a "FACT". This is teaching (of science) at its' worse.

You're so right. It's terrible when those evilutionists invent stuff like control genes. Homeobox genes in the ribbonworm Lineus sanguineus: Evolutionary implications. You'll really like this next one - it has a much better table showing when various phyla first appear than Morton or Futuyma (fig. 3), and a really neat table showing relative numbers of Hox genes in existing phyla and the branch nodes (fig. 6): Fossils, molecules and embryos: new perspectives on the Cambrian explosion. In fact, I like this one so much I'm going to quote their conclusion:

quote:
In sum, the fossil record: (1) indicates that metazoans certainly originated significantly earlier than 570 Ma and probably earlier than 600 Ma, but is otherwise silent on this point, (2) suggests that minute bilaterians were present by at least 565 Ma and probably earlier, (3) indicates that larger bilaterians were present by 543 Ma, and (4) suggests that a number of the body plans that today characterize major taxa first appear during or ‘shortly’ before the interval from about 530 to 520 Ma, when the range of activities of benthic organisms increased markedly. Beyond this information, interpretations of the events in early metazoan history are based on the topology of the phylogenetic tree, the pathways of morphological change implied by the fossils and by the constraints imposed by our understanding of evolutionary processes.

While the time of origin of the Metazoa is not known, an age of 700 Ma or less would not conflict with the evidence now at hand, though it may have been significantly earlier. Is 170 million years long enough for the evolution of the Cambrian fauna from the earliest animals? Clearly, much of body-plan evolution was accomplished by changes in patterns of gene expression. Many genes that mediate the development of disparate phyla are conserved after over half a billion years of independent evolution in lineages that have evolved independent architectures. Gene regulatory elements were probably the most important actors in this process. The rapidity of this sort of
evolution has not been formally evaluated, but the use and reuse of established signaling pathways and other regulatory cascades seem likely to provide evolutionary shortcuts in the production of novel morphologies. We have every reason to believe that the pace of evolution as suggested by plausible interpretations of the fossil record could easily be achieved.



This message is a reply to:
 Message 119 by Bart007, posted 09-17-2002 2:38 AM Bart007 has not yet responded

  
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