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Author Topic:   molecular genetic evidence for a multipurpose genome
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 196 of 317 (22138)
11-10-2002 7:21 PM
Reply to: Message 92 by Mammuthus
11-04-2002 3:26 AM


Dear mamumuthus,
You say:
Just to point out Peter, I also brought up the Erlandson study of the entire region comparing insertions, deletions, and point mutations and you have not addressed those issues and claiming that the region remains invariant. Sorry, but that is patently false.
My response:
The Erlandson study doesn't rebut Dr Kim's observation that the assessed region of the ZFX gene is completly stable. No variability at all, not even at neutral positions.
Best wishes,
peter

This message is a reply to:
 Message 92 by Mammuthus, posted 11-04-2002 3:26 AM Mammuthus has replied

Replies to this message:
 Message 201 by Mammuthus, posted 11-11-2002 3:34 AM peter borger has replied

  
John
Inactive Member


Message 197 of 317 (22139)
11-10-2002 7:22 PM
Reply to: Message 195 by peter borger
11-10-2002 6:44 PM


quote:
Originally posted by peter borger:

You may be wielding Occam's rasor, I possess Athena's Owl.
best wishes,
Peter

You pagan infidel!!!!! Burn the witch!!! Burn the witch!!!!
------------------
http://www.hells-handmaiden.com

This message is a reply to:
 Message 195 by peter borger, posted 11-10-2002 6:44 PM peter borger has not replied

  
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 198 of 317 (22145)
11-10-2002 8:16 PM
Reply to: Message 95 by Mammuthus
11-04-2002 3:41 AM


dear Mammuthus,
You wrote:
quote:
--------------------------------------------------------------------------------
Originally posted by Mammuthus:
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
dear Mammuthus,
I know these papers and I know the evolutionary vision of the authors. Still this vision is not explanatory. Maybe you could respond on the specific questions to Dr Wagner. That would clear things up and you will --on the side-- prevent evolutionism from falling.
best wishes,
Peter
--------------------------------------------------------------------------------
***********************
Hi Peter,
You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,particularly studies of the ZFX/ZFY region so the burden is on you to demonstrate that your arguements are based on a real flaw in the data or arguments of the authors and not on your lack of understanding of population genetics, biochem, and randomness.
My Comment:
According to neutral theory at least a couple of mutations would have been expected in the ZFX region gene analysed by DR Kim. Of course, you will not find this in discussion of evolutionary papers. You have to find out for your self from the raw data. Therefore, I mailed Dr Kim for a copy of the paper. He was very kind to send me one, so I could have a close look at their data. The data show NO variation in this region for 20.000.000 years. What kind of evolution is that?
Similar things have been obsrved for the ZFY region in human and great apes. The observations can only be interpreted as NON-RANDOM evolution. I mailed this months ago and never got a response. Percy was the only one with an (irrelevant) remark. The ZFY region is also still open for discussion/rebuttal.
PB: 1) Do these data mean that approximately 450 bp changes occurred on neutral positions?
M: SORRY PETER BUT NOTHING IN YOUR LETTER INDICATES TO ME WHERE THIS QUESTION COMES FROM. ARE YOU REFERREING TO SOMETHING IN THE ARTICLE?
PB: No, I am refereing to the alpha actinin genes in human. The reference is mentioned in the letter. Look it up and we can discuss this topic in detail. I will demonstrate ho it violates evolutionism, you rebut. Okay?
PB: 2) Do these data mean that it would take about 10(exp)6 years for 3 random mutation to occur in the duplicated gene? Thus 150 million years for 450 neutral mutations?
M: ONLY IF YOU BELEIVE THAT DNA EVOLVES IN A CLOCKLIKE MANNER. I DON'T SO THE ESTIMATE OF TIME WOULD HAVE A TREMENDOUS VARIANCE ATTACHED TO IT. PURELY NEUTRAL LOCI MIGHT EVOLVE IN A CLOCKLIKE MANNER HOWEVER BUT IT IS DEPENDENT ON A LOT OF OTHER FACTORS I.E. EFFECTIVE POPULATION SIZE; MUTATION RATE ETC.
PB: So, you don't believ that DNA evolves in a clocklike manner. How does it evolve than? Through punctuated equilibrium, I guess? Sometimes it evolves, sometimes it doesn't? Pretty good theory. Dear mammuthus, maybe you didn't get it yet but according o neutralists DNA is ALWAYS evolving on neutral positions. It is a random phenomenon, they say. Probably you don't agree with the neutralists, and are a selectionist. If so, let me know and we will discuss how these redundant genes were selected than. I will let you introduce neutral selection.
PB: 3) Do these data mean that after each point-mutation there was neutral purifying selection? And, what exactly is it? I mean, what exactly is selection on neutral genes?
M: I HAVE NO IDEA WHAT NEUTRAL PURIFYING SELECTION IS SUPPOSED TO MEAN. SELECTION OCCURS ON GENES THAT PROVIDE AN ADVANTAGE OR DISADVANTAGE TO THE ORGANISM. NEUTRAL GENES CAN BECOME HOMOGENIZED BY GENE CONVERSION BUT IT IS NOT BECAUSE OF SELECTIVE CONSTRAINT.
PB: Selection on redundant genes? If a gene is inactivated in a population it clearly demonstrates that it doesn't have any selective advantage. That's the evolutionary problem with redundant genes, they are in the genome without selective constraints. How many times do I have to reiterate this observation? Also, redundant genes do NOT evolve faster than essential genes. How many times do I have to reiterate this observation?
PB: 3a) Is it independent from nearby genes? Independent from the rest of the genome?
M: IT DEPENDS. SOME GENES EVOLVE BY CONCERTED EVOLUTION USING VARYING HOMOGENIZATION PROCESSES SUCH AS GENE CONVERSION. BUT THIS IS NOT THE
CASE FOR ALL GENES.
Mol Biol Evol 2002 May;19(5):689-97 Related Articles, Links
Purifying selection and birth-and-death evolution in the histone H4 gene family.
Piontkivska H, Rooney AP, Nei M.
Institute of Molecular Evolutionary Genetics, Pennsylvania State University, 328 Mueller Lab, University Park, PA 16802, USA. oxp108@psu.edu
Histones are small basic proteins encoded by a multigene family and are responsible for the nucleosomal organization of chromatin in eukaryotes. Because of the high degree of protein sequence conservation, it is generally believed that histone genes are subject to concerted evolution. However, purifying selection can also generate a high degree of sequence homogeneity. In this study, we examined the long-term evolution of histone H4 genes to determine whether concerted evolution or purifying selection was the major factor for maintaining sequence homogeneity. We analyzed the proportion (p(S)) of synonymous nucleotide differences between the H4 genes from 59 species of fungi, plants, animals, and protists and found that p(S) is generally very high and often close to the saturation level (p(S) ranging from 0.3 to 0.6) even though protein sequences are virtually identical for all H4 genes. A small proportion of genes showed a low level of p(S) values, but this appeared to be caused by recent gene duplication. Our findings suggest that the members of this gene family evolve according to the birth-and-death model of evolution under strong purifying selection. Using histone-like genes in archaebacteria as outgroups, we also showed that H1, H2A, H2B, H3, and H4 histone genes in eukaryotes form separate clusters and that these classes of genes diverged nearly at the same time, before the eukaryotic kingdoms diverged.
Proc Natl Acad Sci U S A 2000 Sep 26;97(20):10866-71 Related Articles, Links
Purifying selection and birth-and-death evolution in the ubiquitin gene family.
Nei M, Rogozin IB, Piontkivska H.
Institute of Molecular Evolutionary Genetics and Department of Biology, Pennsylvania State University, 328 Mueller Laboratory, University Park, PA 16802, USA. nxm2@psu.edu
Ubiquitin is a highly conserved protein that is encoded by a multigene family. It is generally believed that this gene family is subject to concerted evolution, which homogenizes the member genes of the family. However, protein homogeneity can be attained also by strong purifying selection. We therefore studied the proportion (p(S)) of synonymous nucleotide differences between members of the ubiquitin gene family from 28 species of fungi, plants, and animals. The results have shown that p(S) is generally very high and is often close to the saturation level, although the protein sequence is virtually identical for all ubiquitins from fungi, plants, and animals. A small proportion of species showed a low level of p(S) values, but these values appeared to be caused by recent gene duplication. It was also found that the number of repeat copies of the gene family varies considerably with species, and some species harbor pseudogenes. These observations suggest that the members of this gene family evolve almost independently by silent nucleotide substitution and are subjected to birth-and-death evolution at the DNA level.
PB: Thanks for these refernces. If you read these articles properly, you will find ou that concerted evolution was a concept to understand the uniformity of these high abundance genes, for instance the histon genes, TcR genes, ubuiquitin genes. However, it isn't tenable anymore and recently it was replaced by birth and death evolution. It's a meaningless term that doesn't explain anything. It's what you believe in. Explain what you believe in, maybe I can believe in it too.
PB: 3b) Does this type of selection take place on the level of the organism? How?
M: AGAIN, YOU REALLY NEED TO LEARN SOME POPULATION GENETICS OR AT LEAST GET A GRASP OF WHAT RELATIVE FITNESS MEANS. EVEN IF A MUTATION IS NOT IMMEDIATELY LETHAL; IF IT PUTS THE ORGANISM AT A DISADVANTAGE IT WILL BE SELECTED AGAINST. YES; IT IS AT THE LEVEL OF THE ORGANISM
PB: Maybe I don'r read enough about population genetics. But that not the discussion here. Selection against redundant genes? Please explain. The topic was on neutral selection, remember. However, I am very curious to find out about selection against genetic redundancies.
PB: 4) Are there identical (=very recently duplicated) genes in known genomes?
Annu Rev Cell Dev Biol 2002;18:53-80 Related Articles, Links
Gene co-option in physiological and morphological evolution.
True JR, Carroll SB.
Department of Ecology and Evolution, State University of New York at Stony Brook, Stony Brook, New York 11794-5245, e-mail: jrtrue@life.bio.sunysb.edu
Co-option occurs when natural selection finds new uses for existing traits, including genes, organs, and other body structures. Genes can be co-opted to generate developmental and physiological novelties by changing their patterns of regulation, by changing the functions of the proteins they encode, or both. This often involves gene duplication followed by specialization of the resulting paralogous genes into particular functions. A major role for gene co-option in the evolution of development has long been assumed, and many recent comparative developmental and genomic studies have lent support to this idea. Although there is relatively less known about the molecular basis of co-option events involving developmental pathways, much can be drawn from well-studied examples of the co-option of structural proteins. Here, we summarize several case studies of both structural gene and developmental genetic circuit co-option and discuss how co-option may underlie major episodes of adaptive change in multicellular organisms. We also examine the phenomenon of intraspecific variability in gene expression patterns, which we propose to be one form of material for the co-option process. We integrate this information with recent models of gene family evolution to provide a framework for understanding the origin of co-optive evolution and the mechanisms by which natural selection promotes evolutionary novelty by inventing new uses for the genetic toolkit.
PB: I checked out this reference. It is a model, a proposal. The authors do not provide a single example that demonstrates that duplication and cooption has been observed. In fact, the redundancy in the alpha actinin genes opposes the whole putative concept of cooption. What I like to see are genes in the human genome on their way to cooption. That is, show me expressed genes (pseudogenes are irrelevant for this concept) that are moving towards genes with a (slightly) different function through selection. A prediction could be that in distinct subpopulations these duplicated genes have accumulated distinct mutations.
PB: 5) Is evolution a phenomenon driven by random mutation?
YES
PB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.
M: I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.
PB: No worries about that.
Best wishes,
Peter
[This message has been edited by peter borger, 11-10-2002]

This message is a reply to:
 Message 95 by Mammuthus, posted 11-04-2002 3:41 AM Mammuthus has replied

Replies to this message:
 Message 202 by Mammuthus, posted 11-11-2002 4:02 AM peter borger has replied

  
doctrbill
Member (Idle past 2764 days)
Posts: 1174
From: Eugene, Oregon, USA
Joined: 01-08-2001


Message 199 of 317 (22156)
11-10-2002 8:55 PM


How is it that Evo's are debating here? They're supposed to have given up -
quote:
In the 1970s and 1980s, hundreds of public debates were arranged between evolutionary scientists and creation scientists. The latter scored resounding victories, with the result that, today, few evolutionists will debate.
For more entertainment, (or ammo) See:
http://evolution-facts.org/default.htm
Enjoy.
db

  
monkenstick
Inactive Member


Message 200 of 317 (22167)
11-11-2002 1:05 AM


silly me, i thought the creationists lost when they couldn't produce a single peer reviewed article in defense of their insane mythology - it turns out they won some public debates or something - why hasn't anyone notified any of the scientific journals?

  
Mammuthus
Member (Idle past 6474 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 201 of 317 (22173)
11-11-2002 3:34 AM
Reply to: Message 196 by peter borger
11-10-2002 7:21 PM


quote:
Originally posted by peter borger:
Dear mamumuthus,
You say:
Just to point out Peter, I also brought up the Erlandson study of the entire region comparing insertions, deletions, and point mutations and you have not addressed those issues and claiming that the region remains invariant. Sorry, but that is patently false.
My response:
The Erlandson study doesn't rebut Dr Kim's observation that the assessed region of the ZFX gene is completly stable. No variability at all, not even at neutral positions.
Best wishes,
peter

********************************++
Interesting Peter...you now had to change your statement from the ZFX region to the "assessed" region of ZFX. Erlandsson did a more thorough study that falsifies your statement...and now you are also demonstrating that SLPx was correct that you were mis-defining the region as you have here backpedalled.....at some point you will be looking at a single base pair of ZFX for support

This message is a reply to:
 Message 196 by peter borger, posted 11-10-2002 7:21 PM peter borger has replied

Replies to this message:
 Message 207 by peter borger, posted 11-11-2002 5:43 PM Mammuthus has replied

  
Mammuthus
Member (Idle past 6474 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 202 of 317 (22174)
11-11-2002 4:02 AM
Reply to: Message 198 by peter borger
11-10-2002 8:16 PM


According to neutral theory at least a couple of mutations would have been expected in the ZFX region gene analysed by DR Kim. Of course, you will not find this in discussion of evolutionary papers. You have to find out for your self from the raw data. Therefore, I mailed Dr Kim for a copy of the paper. He was very kind to send me one, so I could have a close look at their data. The data show NO variation in this region for 20.000.000 years. What kind of evolution is that?
Similar things have been obsrved for the ZFY region in human and great apes. The observations can only be interpreted as NON-RANDOM evolution. I mailed this months ago and never got a response. Percy was the only one with an (irrelevant) remark. The ZFY region is also still open for discussion/rebuttal.
M: Sounds like selection not non-random evolution. As to expectations of mutations...there is a probability of mutation not an expectation that they occur. A perfectly weighted coin is expected to give heads and tails 50:50 but it seldom meets this expectation...try it and see. Erlandsson found point muations, deletions, and transpostion events throughout the ZFX/ZFY region...you can look at their raw data to...thus, the available data does not falsify evolution.
PB: So, you don't believ that DNA evolves in a clocklike manner. How does it evolve than? Through punctuated equilibrium, I guess? Sometimes it evolves, sometimes it doesn't? Pretty good theory. Dear mammuthus, maybe you didn't get it yet but according o neutralists DNA is ALWAYS evolving on neutral positions. It is a random phenomenon, they say. Probably you don't agree with the neutralists, and are a selectionist. If so, let me know and we will discuss how these redundant genes were selected than. I will let you introduce neutral selection.
M: Build up as many strawmen as you like Peter. I do not believe in an accurate clock because of selective sweeps, bottlenecks, and founder events among lineages that can completely screw up the coalescence time and give an inaccurrate date. Also, since it is a random process, there is only a probability of the clock ticking, not that it actually will for a given sequence. A real clock does not have this type of statistical fluctuation as a variable. If you actually would read some literature on the subject you would see why this is the case but...you won't. Your claims as to WHAT neutral evolution says are meaningless as you have steadfastly refused to educate yourself regarding evolutionary theory or population genetics...I could do the same as what you are doing as follows..creationism posits that big hairy priests insert bananas in their rectums thus causing the creation of kinds..why do you hold to this rectal banana theory Peter? Is it your evil oppressive christian imperialism that blinds you?...(M exits creationism mode)
PB: Selection on redundant genes? If a gene is inactivated in a population it clearly demonstrates that it doesn't have any selective advantage. That's the evolutionary problem with redundant genes, they are in the genome without selective constraints. How many times do I have to reiterate this observation? Also, redundant genes do NOT evolve faster than essential genes. How many times do I have to reiterate this observation?
M: How many times do I have to re-iterate that you don't know anything about evolution or population genetics? How do you know that there is no selective advantage? How do you know that removal of the gene is not slighltly deleterious? Most mutations are yet are maintained in the population regardless. Survival of the fittest does not mean the best. It means that a population has reached an optima higher than its competitors and produces more offspring...not that there is no consequence of losing the gene on long term fitness when faced with subsequent selection. How much selection do you think is required to homogenize a gene?
PB: Thanks for these refernces. If you read these articles properly, you will find ou that concerted evolution was a concept to understand the uniformity of these high abundance genes, for instance the histon genes, TcR genes, ubuiquitin genes. However, it isn't tenable anymore and recently it was replaced by birth and death evolution. It's a meaningless term that doesn't explain anything. It's what you believe in. Explain what you believe in, maybe I can believe in it too.
M: As I said, in some cases concerted, in others by selection..what did you not understand in my sentence. And what percicesly do you want to discuss? You claim that Nei's papers are meaningless i.e. you don't understand them at all...what specifically is it that you disagree with since it is not clear from reading the portions of the papers you posted and your response.
PB: I checked out this reference. It is a model, a proposal. The authors do not provide a single example that demonstrates that duplication and cooption has been observed. In fact, the redundancy in the alpha actinin genes opposes the whole putative concept of cooption. What I like to see are genes in the human genome on their way to cooption. That is, show me expressed genes (pseudogenes are irrelevant for this concept) that are moving towards genes with a (slightly) different function through selection. A prediction could be that in distinct subpopulations these duplicated genes have accumulated distinct mutations.
M: Actually the paper is based on experiments done by Carrol and others to support his model .....also not totally clear what kind of example you want...something like this perhaps?
Evol Dev 2002 Mar-Apr;4(2):111-23 Related Articles, Links
Gene expression and larval evolution: changing roles of distal-less and orthodenticle in echinoderm larvae.
Lowe CJ, Issel-Tarver L, Wray GA.
Department of Ecology and Evolution, State University of New York at Stony Brook, 11732, USA.
We describe the expression of the homeobox genes orthodenticle (Otx) and distal-less (Dlx) during the larval development of seven species representing three classes of echinoderms: Holothuroidea, Asteroidea, and Echinoidea. Several expression domains are conserved between species within a single class, including Dlx expression within the brachiolar arms of asteroid larvae and Otx expression within the ciliated bands of holothuroid larvae. Some expression domains are apparently conserved between classes, such as the expression of Dlx within the hydrocoel (left mesocoel) in all three classes. However, several substantial differences in expression domains among taxa were also evident for both genes. Some autapomorphic (unique derived) features of gene expression are phylogenetically associated with autapomorphic structures, such as Dlx expression within the invaginating rudiment of euechinoids. Other autapomorphic gene expression domains are associated with evolutionary shifts in life history from feeding to nonfeeding larval development, such as Otx expression within the ciliated bands of a nonfeeding holothuroid larva. Similar associations between evolutionary changes in morphology and life history mode with changes in regulatory gene expression have also been observed in arthropods, urochordates, and chordates. We predict that recruitment of regulatory genes to a new developmental role is commonly associated with evolutionary changes in morphology and may be particularly common in clades with complex life cycles and diversity of life history modes. Caution should be used when making generalizations about gene expression and function based on a single species, which may not accurately reflect developmental processes and life histories of the phyla to which it belongs.
PB: 5) Is evolution a phenomenon driven by random mutation?
YES
PB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.
M: Apparently so since NOT a single one of these demonstrates a non-random mechanism.
M: I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.
PB: No worries about that.
M: If by no worries you mean you will avoid answering Quetzal then I see what you mean by no worries.

This message is a reply to:
 Message 198 by peter borger, posted 11-10-2002 8:16 PM peter borger has replied

Replies to this message:
 Message 210 by peter borger, posted 11-12-2002 12:11 AM Mammuthus has replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 203 of 317 (22207)
11-11-2002 8:41 AM
Reply to: Message 180 by Fred Williams
11-08-2002 6:39 PM


quote:
Originally posted by Fred Williams:
...I wanted to play in a band (which I did for 17 years, then I grew up ).
Let me guess - you are an 'expert' keyboard player, too?

This message is a reply to:
 Message 180 by Fred Williams, posted 11-08-2002 6:39 PM Fred Williams has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 204 of 317 (22212)
11-11-2002 8:54 AM
Reply to: Message 192 by peter borger
11-10-2002 5:25 PM


quote:
Originally posted by peter borger:
Dear mark,
You write:
Peter,
Provide ONE example that hasn't been trounced, or retract this ridiculously overconfident claim. Sheesh.
I say:
1) the redundant Src kinase family,
2) the redundant alpha actinin family,
3) the 1G5 gene in D melanogaster
4) the swim reflex in conjunction with the gag reflex in newborn
5) the ancient mtDNA (is still open for discussion)
6) the ZFY region (nobody responded)
7) the ZFX gene/exon
8) the IL-1beta incongruence (and more)
9) the LCR16a gene
10)the wollemi's invariable DNA
And probably more.
Well, there is at least one lie....

This message is a reply to:
 Message 192 by peter borger, posted 11-10-2002 5:25 PM peter borger has replied

Replies to this message:
 Message 208 by peter borger, posted 11-11-2002 8:55 PM derwood has not replied

  
Quetzal
Member (Idle past 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 205 of 317 (22236)
11-11-2002 11:17 AM
Reply to: Message 189 by peter borger
11-09-2002 11:01 PM


Alright Peter, last chance.
Ladies and gentlemen of the jury, we have before us a question that has yet to be answered. To wit: given the marked genetic homogeniety of Wollemia nobilis, can this observation be ecompassed by current scientific explanations? If so, are the explanations incorrect or inapplicable? If so, why?
Peter: I have enumerated below the explanations you have been given in this thread that purport to explain the observation in the case of Wollemia nobilis. You have rejected them outright without discussion as "just so stories", etc. This is your last chance to salvage something: explain, in detail, with references, why the following are not acceptable explanations for (or simply don't explain) the observation.
1. clonality. There are two aspects here that must be discussed:
a) Within-stand growth pattern (i.e., coppicing) would lead to the expectation that all mature trees within a given stand would be genetically identical - they represent a single organism.
b) Between stand homogeneity can be explained if all three stands were originally seeded by a single parent, followed by coppicing, it would again be expected that the stands would show not only an internally homogenous genotype, but between-stands as well.
2. genetic bottleneck. It has been observed in many wild populations that when a population passes through an extreme population crisis, much of the original variation is lost. Given the relictual nature of Wollemia, there is a high probability that this occurred.
3. inbreeding depression. Micropopulations, especially plants but also many animal species, that survive extreme bottlenecks or occupy highly restricted ranges, etc, are known to suffer from lack of genetic variability due to inbreeding depression. This observation has been made for both selfed and sexually reproducing species isolated from gene flow. Inbreeding depression, coupled with selection sweep on deleterious mutational load over generations, tends to greatly homogenize genotypes of the effected organisms.
4. genetic drift. A simple statistical random walk in isolated micropopulations can cause substantial loss of variation.
Your job, Peter, is to examine each of these four explanations, and provide detailed reasons why any (or a combination) of them are incorrect or impossible in the case of Wollemia. I may have missed one or two (like dominance, imprinting, lack of recruitment from non-Wollemia, etc), but those are something to go on. If you are unable to refute these explanations, then your assertion is falsified.

This message is a reply to:
 Message 189 by peter borger, posted 11-09-2002 11:01 PM peter borger has not replied

  
derwood
Member (Idle past 1875 days)
Posts: 1457
Joined: 12-27-2001


Message 206 of 317 (22258)
11-11-2002 2:07 PM


Can't remember which thread this should go in, so am posting it in several...
quote:
Originally posted by Fred Williams:
Maybe Scott is ready to shatter the world with the example he implies he has in his hand. Let’s see if he plays the card, or keeps us all in suspense!
What example? Oh yes - an example of a gene duplication and subsequent mutation that conferred a benefit to the population.
The series of gene duplications in what we now call the beta globin gene cluster, a group of 5 genes and a pseudogene. Epsilon-globin, which is expressed in the embryo, has a higher affinity for oxygen than does the adult-expressed beta and delta globin, thereby making it easier for an embryo to gets its 'fair share' of oxygen. Epsilon arose via a duplication from other genes starting with proto-beta.
Healthy embryos make for healthy offspring, and healthy offspring are beneficial to the population.
What about an insertion that confers pesticide resistence?
A Single P450 Allele Associated with Insecticide Resistance in Drosophila
P. J. Daborn,1 J. L. Yen,1 M. R. Bogwitz,2 G. Le Goff,1 E. Feil,1 S. Jeffers,3 N. Tijet,4 T. Perry,2 D. Heckel,2 P. Batterham,2 R. Feyereisen,5 T. G. Wilson,3 R. H. ffrench-Constant1*
Science 297:2253-7.
Some interesting findings:
From the abstract:
"Transgenic analysis of Cyp6 1 shows that overtranscription
of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated wit a single Cyp6 1 allele that has spread globally. The is allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6 1 gene."
From the paper:
"First, resistance to DDT was wide-spread, as expected, and second, resistance can persist in laboratory strains in the absence
of pesticide selection, which suggests that little or no fitness cost is associated with this mechanism."
"The observation that the nucleotide sequence around the first intron in Cyp6g1 (291 bp away from the site of the insertion) is identical in all the resistant alleles supports the concept of this global spread and suggests strong linkage disequilibrium or hitchhiking of nucleotide variation with the spread of DDT resistance."
I was especially interested in your Information Theory expertise on this, because: there is no change in the expressed protein, just more of it, and this confers an advantage. Is this 'new information'? If not, why not? If it is, how is so when the expressed protein has not changed?
The ref for how Gene duplication can result in altered phenotype is at the office, will post that later.
But I did come across this pertinent ref (pay attention Freddie and Borger), emphases mine:
*************************************************
Amplification-mutagenesis: evidence that "directed" adaptive mutation and general hypermutability result from growth with a selected gene amplification.
Proc Natl Acad Sci U S A 2002 Feb 19;99(4):2164-9
Hendrickson H, Slechta ES, Bergthorsson U, Andersson DI, Roth JR.
Department of Biology, University of Utah, Salt Lake City, UT 84112, USA.
When a particular lac mutant of Escherichia coli starves in the presence of lactose, nongrowing cells appear to direct mutations preferentially to sites that allow growth (adaptive mutation). This observation suggested that growth limitation stimulates mutability. Evidence is provided here that this behavior is actually caused by a standard Darwinian process in which natural selection acts in three sequential steps. First, growth limitation favors growth of a subpopulation with an amplification of the mutant lac gene; next, it favors cells with a lac(+) revertant allele within the amplified array. Finally, it favors loss of mutant copies until a stable haploid lac(+) revertant arises and overgrows the colony. By increasing the lac copy number, selection enhances the likelihood of reversion within each developing clone. This sequence of events appears to direct mutations to useful sites. General mutagenesis is a side-effect of growth with an amplification (SOS induction). The F' plasmid, which carries lac, contributes by stimulating gene duplication and amplification. Selective stress has no direct effect on mutation rate or target specificity, but acts to favor a succession of cell types with progressively improved growth on lactose. The sequence of events--amplification, mutation, segregation--may help to explain both the origins of some cancers and the evolution of new genes under selection.
********************************************
Looks like the ball is in William's court now.
Let the hand waving, insults, backpedalling, and story-telling begin!

Replies to this message:
 Message 209 by peter borger, posted 11-11-2002 10:17 PM derwood has replied
 Message 224 by Fred Williams, posted 11-12-2002 7:12 PM derwood has replied

  
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 207 of 317 (22281)
11-11-2002 5:43 PM
Reply to: Message 201 by Mammuthus
11-11-2002 3:34 AM


Dear Mammuthus,
You say:
Interesting Peter...you now had to change your statement from the ZFX region to the "assessed" region of ZFX. Erlandsson did a more thorough study that falsifies your statement...and now you are also demonstrating that SLPx was correct that you were mis-defining the region as you have here backpedalled.....at some point you will be looking at a single base pair of ZFX for support.
I say:
It was Dr Kim --the author of the paper-- who talked about the ZFX gene instead of exon and I was a bit sloppy of me not to notice that. Doesn't invalidate my example, however. The nitpicking begins, I presume. You could have saved yourself the mail, since Dr Page already nitpicked on this observation.
However, are you a neutralist or a selectionist?
Best wishes,
Peter

This message is a reply to:
 Message 201 by Mammuthus, posted 11-11-2002 3:34 AM Mammuthus has replied

Replies to this message:
 Message 215 by Mammuthus, posted 11-12-2002 4:49 AM peter borger has not replied
 Message 219 by derwood, posted 11-12-2002 10:42 AM peter borger has not replied
 Message 220 by derwood, posted 11-12-2002 10:42 AM peter borger has replied

  
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 208 of 317 (22301)
11-11-2002 8:55 PM
Reply to: Message 204 by derwood
11-11-2002 8:54 AM


Dear Dr Page,
There we go again, my comments to the ZFY region. I challenge you to rebut them. Last time I mailed them the only response I had was from Percipient. It was irrelevant. So give it a try.
The Y-linked zinc finger (ZFY) gene is located on the male-determining Y-chromosome and specifies a protein that regulates the expression of genes. The ZFY gene is actively transcribed in male and appears to be involved in sperm and testes maturation. A detailed study was recently performed that surveyed the 729 base pair intron present between the third and fourth exon of the human ZFY gene. The study was performed to provide a picture of the sequence polymorphisms in the Y chromosome, and 38 individuals were included representing a cross section of geographic origins. In addition, the homologous sequences of the intron was analysed in three primates: chimpanzee, gorilla and orang-utan.
The samples obtained from human subpopulations no polymorphisms were detected whatsoever. On the contrary, inspection of the corresponding homologous intron region in the primates reveals that several variable sites are distributed throughout the intron and include at least 39 substitutions (21 transitions and 14 transversions, and 4 indel mutations. Thus, at least 5% variation in this region is observed between human and great apes.
The absence of variation in the ZFY region in humans is very awkward, and, according to the authors, cannot be ascribed to a chance (=random mechanism). Introns are thought to be subject to neutral evolution, and variation within the human population is predicted on neutral positions. Confronted with the peculiar situation of the absence of variation, the authors must apply statistics to define an era when the common ancestor of all males lived. They estimate that ‘Y-chromosome Adam’ lived around 270.000 (range 0-800.000) years before present (REF1).
It should be noted that the non-variant intron sequences in the ZFY region provides a severe problem for evolution biologists, since molecular rules demand some neutral evolution, and thus, variation on silent positions. But, he authors state that ‘the invariance likely may results from a selective sweep, a recent origin of modern Homo sapiens, or a historically small effective male population sizes’ (REF1).
Because the X and Y chromosome have little sequence homology there is no recombination between the major part of these chromosomes, and most of the genes on the Y chromosome will behave as one linked genetic group. Hence, if an advantageous mutation occurs in a gene on the Y chromosome it will drag with it all the non-recombining parts of the chromosome. A rapid, natural selection driven fixation of any advantageous gene on the Y chromosome would therefore result in loss of variance throughout the entire Y chromosome (REF2). Because all non-recombining DNA sequences of the Y chromosome are replaced in a single sweep, this vision predicts that variability should be absent in all linked non-recombining Y chromosome genes. (A retrospective prediction?)
A recent study in mice on the non-coding region flanking the SRY gene, which is directly responsible for inducing maleness, is revealing in this matter. The study compared the amount of variation within the species and related it to the amount of variation among species. Then, the authors compared this ratio to the ratio for a rapidly changing region in the mitochondrial DNA obtained in the same way.
If any of the two regions were subject to a selective sweep, it would be demonstrated by a reduced variation within species. It was found, however, that the non-coding region of the SRY gene changed at a neutral rate. It implicates that, because of linkage of the major part of the Y chromosomal genes, the entire non-recombining part of the Y chromosome changes at a neutral rate. Therefore, it is unlikely that natural selection acts upon the Y chromosome (REF2).
But if natural selection did not act upon the Y chromosome the high degree of variability of the Y chromosome between primates apparently defies the theory of evolution, since the coding region of the SRY gene is very stable within a species (as observed before), whereas considerable variation is observed between distinct species. Some part of the SRY protein show such high degree of variability between distinct primate species that one must conclude that part of the protein has NO function at all, or that the gene is subject to DIRECTIONAL selection, says evolution biologist Svante Pbo (REF2). However, directional selection is only demonstrated in cases involving intergenomic conflict, such as occur between host and pathogen, but is has never been observed for non-immune system related protein coding genes. Of course, one can always propose non-random, directed mutations. But, evolutionists will object to that.
The only remaining evolutionary explanation of the variability in the Y chromosome between species is by the mechanism of neutral evolution. Yet, the observation that more replacement substitutions than synonymous substitutions are present between species suggests that a neutral mechanism is not likely to be responsible for variation among species.
The ultimate hypothesis evolutionists propose is that ‘these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone’ (REF2).
Do evolutionists really understand their own theories? The proposal that the sequence has been retained without conservation requirement would still imply that the SRY protein is expected to evolve at a NEUTRAL rate! The peculiar thing about the SRY proteins was, however, that they are much more variable than predicted by neutral evolution. To properly understand this one has to assume SELECTION ON NEUTRAL POSITIONS! I can imagine that evolution biologists really get frustrated solving the riddles around the SRY region. Despite several ad hoc hypotheses it all ends, again, in a paradox. Apparently, there is no evolutionary explanation for the high degree of dissimilarity of SRY region between distinct primates. It points in the direction of directed, non-random mechanism. It is clear that invariability of this haploid region in humans is ensured by specific DNA guarding and stabilising proteins. All in accord with the MPG hypothesis.
REF1) Dorit R.L. et al. Absence of polymorphism at the ZFY locus on the human Y chromosome. Science 1995, Volume 268, p1183-1185.
REF2) Svante Pbo. The Y chromosome and the origin of all of us (men). Science 1995, 268, p1141-1142.
Best wishes, and I hope for a lot of discussion, not a lot of abstracts. I can find abstracts myself.
Peter
[This message has been edited by peter borger, 11-11-2002]

This message is a reply to:
 Message 204 by derwood, posted 11-11-2002 8:54 AM derwood has not replied

Replies to this message:
 Message 216 by Mammuthus, posted 11-12-2002 5:17 AM peter borger has replied

  
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 209 of 317 (22304)
11-11-2002 10:17 PM
Reply to: Message 206 by derwood
11-11-2002 2:07 PM


Dear Dr Page,
Your examples are all in accord with the multipurpose genome. Lets start with your reference:
From the abstract:
"Transgenic analysis of Cyp6 1 shows that overtranscription
of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated wit a single Cyp6 1 allele that has spread globally. The allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6 1 gene."
What does the MPG hypothesis predict (see mail #1):
The concept 'multipurpose genome' holds that:
1) DNA sequences —although plastic-- are stable throughout time,
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory],
4) the function of natural selection is to remove degenerate organisms, and
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).
Point #3 predicted your observation.
So, I do not see a problem for the MPG hypothesis here. The other examples are similar. They all involve differential gene regulation. As predicted by the MPG hypothesis.
The ball is back in 'your' ZFY region.
Best wishes,
Peter

This message is a reply to:
 Message 206 by derwood, posted 11-11-2002 2:07 PM derwood has replied

Replies to this message:
 Message 217 by derwood, posted 11-12-2002 10:30 AM peter borger has replied

  
peter borger
Member (Idle past 7664 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 210 of 317 (22312)
11-12-2002 12:11 AM
Reply to: Message 202 by Mammuthus
11-11-2002 4:02 AM


Dear Mammuthus,
M: You will have to tell me then why they are not explanatory. You have shown on several occassions profound misunderstandings of the papers,
PB: By "profound misunderstanding" you must mean "comments on evolutionism just-so stories". By now you should have known that I prefer to think for myself. I can analyse the data for myself, and I can interpret the data for myself. The data that are not in accord with molecular mechanism of evolutionism, I mailed to this site. You choose to deny them. I don't mind. Deny as often as you like. It doesn't make your pet theory a better theory.
M: particularly studies of the ZFX/ZFY region so the burden is on you to demonstrate that your arguements are based on a real flaw in the data or arguments of the authors and not on your lack of understanding of population genetics, biochem, and randomness.
PB: I mailed my comments on the ZFY region again. Maybe you can respond a bit on it, now. Haven't had any substantial responses, yet.
PB: According to neutral theory at least a couple of mutations would have been expected in the ZFX region gene analysed by DR Kim. Of course, you will not find this in discussion of evolutionary papers. You have to find out for your self from the raw data. Therefore, I mailed Dr Kim for a copy of the paper. He was very kind to send me one, so I could have a close look at their data. The data show NO variation in this region for 20.000.000 years. What kind of evolution is that?
Similar things have been obsrved for the ZFY region in human and great apes. The observations can only be interpreted as NON-RANDOM evolution. I mailed this months ago and never got a response. Percy was the only one with an (irrelevant) remark. The ZFY region is also still open for discussion/rebuttal.
M: Sounds like selection not non-random evolution. As to expectations of mutations...there is a probability of mutation not an expectation that they occur. A perfectly weighted coin is expected to give heads and tails 50:50 but it seldom meets this expectation...try it and see. Erlandsson found point muations, deletions, and transpostion events throughout the ZFX/ZFY region...you can look at their raw data to...thus, the available data does not falsify evolution.
PB: Selection on neutral positions? Dear Mammuthus, at least 20% of this region is neutral. Ever heard of the neutral third codon positions of the redundant genetic code? The odds are against your simplistic presentation, as demonstrated on this site by your friend Fred. If you throw often enough the odds will be 50:50.
PB: So, you don't believe that DNA evolves in a clocklike manner. How does it evolve than? Through punctuated equilibrium, I guess? Sometimes it evolves, sometimes it doesn't? Pretty good theory. Dear mammuthus, maybe you didn't get it yet but according o neutralists DNA is ALWAYS evolving on neutral positions. It is a random phenomenon, they say. Probably you don't agree with the neutralists, and are a selectionist. If so, let me know and we will discuss how these redundant genes were selected than. I will let you introduce neutral selection.
M: Build up as many strawmen as you like Peter. I do not believe in an accurate clock because of selective sweeps, bottlenecks, and founder events among lineages that can completely screw up the coalescence time and give an inaccurrate date. Also, since it is a random process, there is only a probability of the clock ticking, not that it actually will for a given sequence. A real clock does not have this type of statistical fluctuation as a variable. If you actually would read some literature on the subject you would see why this is the case but...you won't. Your claims as to WHAT neutral evolution says are meaningless as you have steadfastly refused to educate yourself regarding evolutionary theory or population genetics...I could do the same as what you are doing as follows..creationism posits that big hairy priests insert bananas in their rectums thus causing the creation of kinds..why do you hold to this rectal banana theory Peter? Is it your evil oppressive christian imperialism that blinds you?...(M exits creationism mode)
PB: Maybe you don’t believe in an accurate clock. But the HVR-1 mtDNA sequences presented by Adcock et al (PNAS 2001, 98:537-542) demonstrate with respect to human reference sequence 29 differences for bonobo, 24 for chimp, 27 for neanderthaler. I do not even see a RUDIMENTARY clock in these data. How about you? It should also be noted that an ancient homo sapiens (dated 62,000 BP) demonstrates 10 differences compared to reference sequence. Let me guess, bonobo/chimp and man have a common ancestor around 150.000 years ago? Nice believes you're holding to.
PB: Selection on redundant genes? If a gene is inactivated in a population it clearly demonstrates that it doesn't have any selective advantage. That's the evolutionary problem with redundant genes, they are in the genome without selective constraints. How many times do I have to reiterate this observation? Also, redundant genes do NOT evolve faster than essential genes. How many times do I have to reiterate this observation?
M: How many times do I have to re-iterate that you don't know anything about evolution or population genetics?
PB: It is a known that evolutionism is so difficult to understand that not even evolutionists understand it.
M: How do you know that there is no selective advantage?
PB: How do you know that there is selective advantage? You are the propagator of an extraordinary claim. So you have to present the extraordinary evidence.
M: How do you know that removal of the gene is not slighltly deleterious?
PB: I know that your friends introduced very weak purifying selection, another meaningless term. For the redundant gene family of alpha actinins --as for the 1G5 gene-- you have to introduce neutral selection. As demonstrated. And as denied by evo's.
M: Most mutations are yet are maintained in the population regardless.
PB: So you are a neutralist?
M: Survival of the fittest does not mean the best. It means that a population has reached an optima higher than its competitors and produces more offspring...not that there is no consequence of losing the gene on long term fitness when faced with subsequent selection. How much selection do you think is required to homogenize a gene?
PB: You should know this, you are the evolutionist. However, how much selection does it require to purify a redundant gene?
PB: Thanks for these references. If you read these articles properly, you will find out that concerted evolution was a concept to understand the uniformity of these high abundance genes, for instance the histon genes, TcR genes, ubuiquitin genes. However, it isn't tenable anymore and recently it was replaced by birth and death evolution. It's a meaningless term that doesn't explain anything. It's what you believe in. Explain what you believe in, maybe I can believe in it too.
M: As I said, in some cases concerted, in others by selection.
PB: Yes, and that makes it such fabulous theory. Sometimes a bit of this, than a bit of that. Evolutionism is like cooking, isn’t it. How to cook the one kind into the other. The stories get better and better.
What happened to Occam’s razor. Mark Pullen will object to such theories, is my guess. What about it, Mark?
M: What did you not understand in my sentence. And what percicesly do you want to discuss? You claim that Nei's papers are meaningless i.e. you don't understand them at all...what specifically is it that you disagree with since it is not clear from reading the portions of the papers you posted and your response.
PB: The whole discussion is meaningless. If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.
PB: I checked out this reference. It is a model, a proposal. The authors do not provide a single example that demonstrates that duplication and cooption has been observed. In fact, the redundancy in the alpha actinin genes opposes the whole putative concept of cooption. What I like to see are genes in the human genome on their way to cooption. That is, show me expressed genes (pseudogenes are irrelevant for this concept) that are moving towards genes with a (slightly) different function through selection. A prediction could be that in distinct subpopulations these duplicated genes have accumulated distinct mutations.
M: Actually the paper is based on experiments done by Carrol and others to support his model .....also not totally clear what kind of example you want...something like this perhaps?
PB: Apparently these experiments have never been published. Or do you mean the reference below? If so, than I have to disappoint you. It is NOT an experiment it is interpretations of data. You know the difference, I hope. (If not, it explains a lot ).
Evol Dev 2002 Mar-Apr;4(2):111-23 Related Articles, Links
Gene expression and larval evolution: changing roles of distal-less and orthodenticle in echinoderm larvae.
Lowe CJ, Issel-Tarver L, Wray GA.
Department of Ecology and Evolution, State University of New York at Stony Brook, 11732, USA.
We describe the expression of the homeobox genes orthodenticle (Otx) and distal-less (Dlx) during the larval development of seven species representing three classes of echinoderms: Holothuroidea, Asteroidea, and Echinoidea. Several expression domains are conserved between species within a single class, including Dlx expression within the brachiolar arms of asteroid larvae and Otx expression within the ciliated bands of holothuroid larvae. Some expression domains are apparently conserved between classes, such as the expression of Dlx within the hydrocoel (left mesocoel) in all three classes. However, several substantial differences in expression domains among taxa were also evident for both genes. Some autapomorphic (unique derived) features of gene expression are phylogenetically associated with autapomorphic structures, such as Dlx expression within the invaginating rudiment of euechinoids. Other autapomorphic gene expression domains are associated with evolutionary shifts in life history from feeding to nonfeeding larval development, such as Otx expression within the ciliated bands of a nonfeeding holothuroid larva. Similar associations between evolutionary changes in morphology and life history mode with changes in regulatory gene expression have also been observed in arthropods, urochordates, and chordates. We predict that recruitment of regulatory genes to a new developmental role is commonly associated with evolutionary changes in morphology and may be particularly common in clades with complex life cycles and diversity of life history modes. Caution should be used when making generalizations about gene expression and function based on a single species, which may not accurately reflect developmental processes and life histories of the phyla to which it belongs.
PB: 5) Is evolution a phenomenon driven by random mutation?
YES
PB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.
M: Apparently so since NOT a single one of these demonstrates a non-random mechanism.
M: I am going to let Quetzal have first crack at a response to your post to him but I found several deep flaws in your statements that I will address if he does not.
PB: No worries about that.
M: If by no worries you mean you will avoid answering Quetzal then I see what you mean by no worries.
PB: You are lagging behind, I responded to all Quetzal’s points. He choose not to respond to all my replies. However, talking about avoidance. You are avoiding crucial questions of my mails with increasing frequency. Why, I wonder?
Best wishes,
peter

This message is a reply to:
 Message 202 by Mammuthus, posted 11-11-2002 4:02 AM Mammuthus has replied

Replies to this message:
 Message 211 by Quetzal, posted 11-12-2002 1:35 AM peter borger has replied
 Message 213 by Mammuthus, posted 11-12-2002 4:46 AM peter borger has replied

  
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