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Author
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Topic: can some aspect of Darwinism be falsified?
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Bruce Fast
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Member # 924
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posted 21. May 2006 00:18
Zachriel: quote:
that is precisely the pattern, a scale-invariant hierarchy, which is *expected* by the Theory of Evolution.
Please show where this pattern is predicted prior to being established.
Zachriel: quote:
Once a niche has been filled, it will tend to remain filled, though populations may continue to diverge in order to fill ever smaller and smaller micro-niches within the larger environment, and to fill new niches created as the biosphere evolves. When catastrophes occur, then this may provide an opportunity for radiative adaptation from a node higher in the hierarchy.
So you are saying that evolution has grinded to a halt, that it will only reignite activity if a catastrophy happens?
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John A. Davison
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Member # 1425
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posted 21. May 2006 06:52
If evolution were ever to "reignite" it would be right now when man is altering the enviroment in such an incredible fashion. What do we see? - nothing but extinction.
The truth of the matter is that there is not a single tangible bit of evidence that the environment ever played any role whatsoever in the emergence of any living thing except possibly to act as a stimulus for the release of a latent prepared potential. Just as ontogeny proceeds inexorably driven entirely from within, so has phylogeny done the same. Evolution has been the steady loss of potentiality with geologic time exactly as ontogeny proceeds as cells progressively lose their options, first with respect to germ layer, followed by an orderly progressive loss of potentiality until the final cell types of nerve, muscle, gland and epithelium are finally and irreversibly expressed. Ontogeny and phylogeny are both prescribed, auto regulated and self teminating. Only ontogeny continues.
Ontogeny remains the ideal model for phylogeny.
"Neither in the one nor in the other is there room for chance."
Leo Berg, Nomogenesis, page 134
If not chance then what? My answer is the Prescribed Evolutionary Hypothesis.
What say others?
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Zachriel
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Member # 1793
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posted 21. May 2006 10:30
Bruce Fast (snipped from earlier in the thread): “kingdom, philum, class, order, family, genus, species in that order. Every bone in my ‘let's think like a Darwin’ body says that this pattern is in conflict with NDE.”
Zachriel: "that is precisely the pattern, a scale-invariant hierarchy, which is *expected* by the Theory of Evolution."
Bruce Fast: "Please show where this pattern is predicted prior to being established."
This comment makes no sense. The nested hierarchy of organic life, extant and extinct, was identified before Darwin proposed his Theory of Evolution. However, mathematics predicts such a nodal structure as a result of sequential, incremental, preferential addition. It applies to species, and it applies to recently discovered protein networks.
Bruce Fast: "So you are saying that evolution has grinded to a halt, that it will only reignite activity if a catastrophy happens?"
Zachriel: "and to fill new niches created as the biosphere evolves."
I meant to add somewhat to this statement. In an evolving system, there is also a scale-invariant process of change. Most change is tangential and minor, some change is substantial, and very occasionally change is revolutionary. This is analogous to self-organizing criticality in landslide patterns.
There's also contingency; a comet here or there, continental changes, varying planetary tilt, a kid stomping on ant hills, the vagaries of life, etc. (Cometary collisions also exhibit scale-invariance, but with decreasing frequency over geological timescales.)
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John A. Davison
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Member # 1425
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posted 21. May 2006 14:01
Isn't any one else going to present their version of the MECHANISM of organic evolution? Is this forum only going to provide a replay of my earlier blog
prescribedevolution.blogspot.com
where I sponsored the First Annual Tournament of Evolutionary Hypotheses, personally invited all the luminaries in the current evolutuionary scene, and absolutely nobody showed? In fact only two responded, Michael Behe and Jonathan Wells, each claiming they were two busy writing. I, logically enough, assumed that either no one else within cybershot had an hypothesis to offer or, more likely, were ashamed to present it, knowing full well how silly it would probably appear.
These two questions require answers it seems to me. If they are to be ignored, perhaps I should fold up my evolutionary tent and move on, perhaps to greener pastures. It wouldn't be the first time.
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Bruce Fast
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Member # 924
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posted 21. May 2006 18:11
I am quite determined not to loose the redundant H1 topic, however I have not had an opportunity to reasonably absorb the links tha Zachriel has put on line. PB, I am dying to see you drag this thread back onto your track.
However
Zachriel: quote:
Accuracy in genome replication varies, but typically one in 10^9 base-pairs or one in 10^6 genes are within an order of magnitude or so in most cases.
I presmume you are saying 10^9 per generation, yes? This would make for a less than consistant molecular clock, short generation rate organisms such as bacteria would experience mutations much more rapidly than long generation rate organisms such as trees, would it not?
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Zachriel
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Member # 1793
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posted 21. May 2006 20:51
Bruce Fast: "I presmume you are saying 10^9 per generation, yes?"
Well, per replication. It also occurs in cell replacement. That's the estimate, about 10^-6 per gene per generation, but it varies considerably due to a number of factors.
Bruce Fast: "This would make for a less than consistant molecular clock, short generation rate organisms such as bacteria would experience mutations much more rapidly than long generation rate organisms such as trees, would it not?"
Molecular clocks must be calibrated and cannot be accepted without a lot of caveats. They rely upon the assumption of stochastically constant rates, that mutation rates may vary, but averages out over time. Also, fast mutating sequences become reach saturation making them ineffective.
The main problem is calibration. The mutation rate is observed in extant organisms then calibrated with well-represented fossil transitions. The best represented fossil transitions tend to be vertebrates for obvious reasons.
Though the data from molecular clocks must be carefully analyzed, it would be wrong to just wave your hands and ignore the evidence. If someone were to show you two strains of bacteria and claim one was hundreds of millions of years old, but your molecular clock indicated that they diverged in more recent times, it would behoove you to look for more evidence to resolve the discrepancy.
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Bruce Fast
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Member # 924
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posted 21. May 2006 22:59
Dr. Denton has presented that the phylogenic tree is nicely painted in the cytochrome C. (PB points to a few intriguing exceptions within the cytochrome C gene.) Dr. Denton charges that the only way for this ideal graph of the cytochrome C to be the product of NDE is for the molecular clock to tick almost perfectly with that molecule. This would seem to need to hold true despite the kingdom, despite the rate of evolutionary change of the organism, despite organism generation time, despite how "advanced" the organism is, and despite any other factor.
Do you feel capable of disregarding this puzzle also?
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Christopher D. Beling
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Member # 723
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posted 22. May 2006 05:12
Bruce, if I could comment on some of the H1 issues:
1 Is a repair mechanism really necessary ? I question the need to invoke a repair (voting) mechanism for H1. If we discard the short evolution time hypothesis, then I argue it is still possible that some mutation has occured on some of the H1 genes (but not all) – and that a repair mechanism is not necessarily required to explain the family of 8 H1 genes. First can we agree on what the mutation rates really are and use common units so there could be no misunderstanding. You keep on quoting “1% mutations (of nucleotides)/My” – but I don’t know where you get this number. My numbers are:
1e-10/nucleotide/generation [Hoyle]
1e-9 thru 1e-11/nucleotide/generation[Spetner]
1e-9/nucleotide/generaton [Denton]]
Then I also have
1e-8/ alelle/generation [Kondrashov 95, paper ref by P.B] which would equate to
1e-11/nucleotide/generation (?).
So, although the value can vary by an order of magnitude on either side it would be ok to accept a value of 1e-10/nucleotide/generation. Take 1 gen =10yr, then 1e5 gen=1My. This would give a rate of 1e-5/nucl/My. Taking a typical gene size of 1000nucl, this gives you a mutation rate R=1e-2 (1%)/gene/My. [correct?]. Please do confirm this is what you are doing and your source. Lets for sake of argument assume you agree and take this value. Let PX(t)=Prob of gene X surviving to time t against any mutation.
PX(t)=Exp[-Rt]=Exp[-1d-2*t], where t is in My
Lets assume that half of the H1 subtypes have been damaged deleteriously – (note redundancy has been found for H1o, H1c, H1d and H1d – there seems to be no knowledge on H1a, H1b, H1t and H1oo – which are not seen to be “rush in when needed types” - and which could be deleterious). This would give PX(t)=0.5 and t=ln(2)/1e-2= 70My - a number that is quite adequate to cater for the observed H1 subtypes over the period of the Mammals. Because this “random mutation can explain” hypothesis is out there and viable you cannot assert that there has been a repair mechanism at work. However, this does not exclude such a mechanism.
2 What is the cause behind the 8 subtypes ?
One thing that worries me is that you seem to be talking about just the redundancy of the H1 gene, as if there were only one such gene. In reality there are 8 different genes (H1o,H1a,H1b,H1c,H1d,H1e,H1t,H1oo) – i.e. with different AA sequences. If there was just one H1 gene and it was knocked out there would be certain reproductory failure. I would suggest the reason that we have 8 types is at least in part due to mutation of an original wild-type (perhaps Ho). The above calculation for 70My – assumed all mutations to be sufficiently deleterious to give some loss of fitness – this is unlikely to be the case. Many deleterious defects do not reduce fitness very much – many are close to being neutral. Variations in a gene family can occur as they do in the cytochrome c case without loss of functionality.
3 The “voting” repair mechanism
I think the 8 different subtypes makes the “voting” repair mechanism look questionable – unless the mechanism only checks the part of the AA sequences that are the same. I understand the “voting” system for the case of 3 equal identical H1 genes – but I cannot yet fathom this pattern: quote:
To get through an 8 H1s filter would require the following: 4 identical mutations (to the same amino acid, at the same position, in four copies of aminos) or 5 mutations where three are the identical mutations, or six mutations where two are identical, or seven simultaneous mutations, all in the same organism at the same time
Incidentally I fully agree that any “mechanism to create error correction” would not be brought into existence by its selective advantage and thus is a point against the NDE. The selective advantage would be far too small as you say. In addition the CSI in any such repair mechanism must be colossal – and irreducibly complex into the bargain. But there is still the question - does such a mechanism exist (point (1))
4 What conserves the mysterious H4?
H4 is different in type to H1. I think there is only a single version of H4 (?). If there is a mutation on H4, since there is no redundancy (“back-up”), then meiosis will simply not occur – there will be no reproduction - no passing on of the faulty H4. NS will act as a strong conserving force in this case. It is not to say there is no repair mechanism - only that we cannot affirm one. BTW I wonder – as with the Cytochrome c variation whether the variation we see in H4 is not due to mutation but due to design - different organisms requiring slightly different protein types for optimization?
[ 22. May 2006, 05:42: Message edited by: Christopher D. Beling ]
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Christopher D. Beling
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Member # 723
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posted 22. May 2006 06:12
P.B. You say
quote:
quote:
Well I have to agree – it is very hard to see, or logically argue, how NS could have any role in removing a lethal (or deleterious) mutated subtype of H1.
Which overturns Darwinian Theory
QED
I am not sure you can be dogmatic about this because I am not sure it follows logically. In my understanding (correct me if I am wrong) there are two different predictions of NDE. First; that deleterious mutations are removed by NS. Second; that positive mutations occur and these are admitted through NS. It seems to me that we have only argued against the role of NS in the first sense – which I guess is not a very major sense as NDE seems to rejoice in producing positive evolutionary advance rather than being able to conserve that which already exists! But an argument could go like this:
(i) We have a redundancy system (the H1 system) that is not conserved by NS.
(ii) This implies another mechanism X apart from NS is at work in maintaining a functional genome.
(iii) Since there exists a mechanism X other than NS, responsible for maintaining genomic purity, X could also be involved in evolutionary advance.
(iv) Thus it is quite possible that the Darwinian mechanism is not responsible for evolutionary advance.
Can you assert a stronger argument? The fact that the H4 gene is likely kept pure by NS seems that we cannot assert that always the unknown mechanism X is at work?
To me – the biggest argument against the NDE is Bill Dembski's 4th law, that was surmised by Peter Medewar, and Victor Weisskopf, that CSIformation can only remain constant or decay. This law forbids the increase of CSI via a stochastic mutation. This is backed by Richard Dawkin’s famous 12 second silence when he as asked to give an example of a positive mutation. Chris
[ 22. May 2006, 06:27: Message edited by: Christopher D. Beling ]
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Christopher D. Beling
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Member # 723
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posted 22. May 2006 09:49
David, you write:
quote:
By using "homologous" you are saying they evolved!
Recommend using origin neutral terms
Thanks for making me aware of the generally understood meaning of “homologous”. I was naively unaware of this implication of common descent. I had taken according to its etymological root – homo (equal) logos (speaking).
So let me henceforth say that the H1 subtypes are sequelogous genes and their products are sequelogous proteins. The H1 family of proteins are spalogs (well I guess they must all have very similar structure to do the work they do).
I have one worry though. In talking like this we make no presuppositions concerning the origin of the genes. This is good in that we are being totally empirical with no deeper theoretical inference. But there is still a problem if one does want to delve deeper into ID compatible evolutionary mechanisms. While there is little evidence for universal common descent there seems to be quite a lot of evidence for limited common descent – perhaps at around the genus or order taxonomic level. Indeed on this thread we have been thinking about the origin of the H1 gene family in mammals. It is quite conceivable that these 8 sequelogous genes derived from identical copies of an original pristine H1. (I am not saying that they did – only that it is a possibility.) This would classify as limited common descent, but would still be ID compatible – in that the origin of the original H1 would not have been by the ND mechanism, and universal common descent is not required or part of the theory. Thus in this very limited sense it is possible that the sequelogous genes should be considered "homologous" (and in the same limited sense "evolved"). The danger I admit is the associations of the word homologous with universal common descent – and thus its present imprecision. This indicates that it is best to stay away from it. What do you think about evolution in this limited sense - and how should such be referred to even as a hypothesis? Chris
[ 22. May 2006, 10:03: Message edited by: Christopher D. Beling ]
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John A. Davison
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posted 22. May 2006 16:03
The only really compelling evidence for common descent is the genetic code. Even between the classes of vertebrates there is no homology for the origin of the definitive germ cells as I established in the 1984 paper. Within the vertebrate class such morphological and physiological homology does seem to prevail however and within the vertebrate orders so far examined we can account for all of evolution without the introduction of any extra-chromosomal environmentally produced information whatsoever. Like ontogeny, the phylogenies of these taxa would seem to be purely endogenously driven with no role for allelic mutation of any sort; in other words, exactly as in in ontogeny, purely emergent in character. Ontogeny remains the best model for phylogeny. Neither has now or ever had anything to do with chance.
"Neither in the one nor in the other is their room for chance."
Leo Berg, Nomogenesis, page 134
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Zachriel
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Member # 1793
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posted 22. May 2006 18:27
Bruce Fast: "Dr. Denton charges that the only way for this ideal graph of the cytochrome C to be the product of NDE is for the molecular clock to tick almost perfectly with that molecule. This would seem to need to hold true despite the kingdom, despite the rate of evolutionary change of the organism, despite organism generation time, despite how "advanced" the organism is, and despite any other factor.
"
The confusion occurs because the molecular clock is not defined by the rate of mutation, but the rate of fixation which varies according to population size. The molecular clock is still somewhat problematic, but not without some practical scientific value (such as a null-case for the study of selection).
Even without the clock, the phylogenic tree remains (with the "intriguing exceptions" noted).
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Shi
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Member # 1923
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posted 22. May 2006 19:45
John,
The power of the human brain may be considered as evidence for the PEH. It is often noted that an averarge human being uses only a small percentage of his total brain power. Our kids today use more brain powers than we did when we were young (they deal with the internet as 4 year olds). We use more of our brain than our ancestor hunters. But our ancestor has the same amount of brain cells as we have today. Gradual evolution shoud predict a gradual increase in brain size correlated with survival needs. The brain power in playing music, art, computers, prime numbers, searching for god etc should have no value to a hunter and should not arise as a result of the hunter lifestyle. Our brain power of today is dramatically higher than our closest animal relatives. So is the first human being in history. Why such a dramatice advance in brain power for the first human being? It is obvious that the first human is equiped with a brain that is way more powerful than necessary for reproductive survival. That same brain is going to observe and understand the future 4 billion years of evolution on earth. Evolution is the unfoldment of a preexisting potential. The future 4 billion years of evolution will be the unfoldment of the potential embeded in the first human brain, from the past 1% to the present 10% and onto the future 100%.
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Shi
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Member # 1923
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posted 22. May 2006 20:41
I agree with John that a new species is created by the creation of an individual that serves as the first individual of the species. This is analagous to the creation of a new paradigm of science. A revolutionary scientis serves as the first individual for a branch of science.
I just want to confirm with you guys the position of Darwinism in this respect. is it true that Darwinism says that a population become transformed into a new species together as a group?
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Christopher D. Beling
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Member # 723
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posted 22. May 2006 20:55
John,
quote:
First you agree with us and then you bring up mutation rates again as regulating evolutionary frequency. You can't have it both ways. Do you believe creative evolution is finished or do you not? If you think it is still going on, I ask for the evidence.
I think this depends on what you mean by evolution. For example the ISCID dictionary has 7 definitions for usages of the word evolution can mean that compare similarly with those given by Stephen Meyer (click here) – I was only referring to mutations in the limited sense of Meyer’s no (i) “Evolution as the History of Nature” and (ii) “Evolution as Gene Frequency Change. I must admit to being concerned about (iii) “Evolution as Limited Common Descent” – but I think that to some extent it is that possibility we are often discussing on this thread. From your past postings I believe that you are more prone to believing in some form of “Limited Common Descent” rather than “Universal Common Descent”. You write:
quote:
Within the vertebrate class such morphological and physiological homology does seem to prevail however and within the vertebrate orders so far examined we can account for all of evolution without the introduction of any extra-chromosomal environmentally produced information whatsoever. Like ontogeny, the phylogenies of these taxa would seem to be purely endogenously driven with no role for allelic mutation of any sort.
Thus you indicate that there could be a common ancestor at the origin of the vertebrate phylum – i.e. at the Cambrian explosion? How then do you account for the origin of 1183 novel genes in the vertebrate genome (- or more correctly the mammalian order) over between 100 – 60 Mya? How would the SMH encompass the production of so many novel genes? [I think we both have no difficulty with the "death of 30 genes" over the same period!]
Incidentally I do agree with Meyer that we all need to be very careful about how we use the word evolution. He refers to the “logical fallacy of equivocation” that is played regularly by Darwinists and which annoys me when every I see it being practiced. Accused “So you say that evolution didn’t happen?” – Defendant “no, that’s not what I am saying - I am saying that Darwinian phylogenetic evolution never happened” Chris
[ 22. May 2006, 21:55: Message edited by: Christopher D. Beling ]
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