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Author Topic:   molecular genetic evidence for a multipurpose genome
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 31 of 317 (20783)
10-25-2002 9:24 AM
Reply to: Message 23 by peter borger
10-24-2002 9:02 PM


PB
Will respond in more detail on your comments, but I can already reveal that the concept of a multipurpose genome --although it is a fact-- is not easy to understand.
M: Interesting. In your next post you claim the concept of a mutlipurpose genome is a hypothesis not a fact....do you know the difference?

This message is a reply to:
 Message 23 by peter borger, posted 10-24-2002 9:02 PM peter borger has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 32 of 317 (20840)
10-25-2002 8:32 PM
Reply to: Message 18 by Itzpapalotl
10-24-2002 7:47 AM


Dear Itz,
YOU SAY:
I don't know how resistance to mutation in genetic networks evolves or even if it has been selected for or is an accidental property of the organisation of genes, but that doesn't mean it can't have evolved. Before all the details of the interactions involved in the resistance to mutation of even one system is known speculating on weather it could or couldn't have evolved is futile.
MY RESPONSE:
If you have a close look at certain redundant genes --for instance the alpha actinin genes-- you can only explain them by 'neutral selection'. It has not been introduced in evolutionism for obvious reasons, although the meaningless term 'very weak purifying selection' has recently been introduced. It is so obvious that there is no explanation for these redundacies (another one is the src-kinase gene family coprised of 8 members) within evolutionism's paradigm. Why stick to evolutionism?
Best wishes,
Peter

This message is a reply to:
 Message 18 by Itzpapalotl, posted 10-24-2002 7:47 AM Itzpapalotl has replied

Replies to this message:
 Message 33 by Itzpapalotl, posted 10-25-2002 9:52 PM peter borger has replied

  
Itzpapalotl
Inactive Member


Message 33 of 317 (20857)
10-25-2002 9:52 PM
Reply to: Message 32 by peter borger
10-25-2002 8:32 PM


hi peter B.
i looked up alpha actinin and found this:
J Biol Chem 2002 Jul 12;277(28):25609-16 Functional synergy of actin filament cross-linking proteins. Tseng Y, Schafer BW, Almo SC, Wirtz D.
which states: "The relative tolerance of cells to null mutations of genes that code for a single actin cross-linking protein suggests that the functions of those proteins are highly redundant. This apparent functional redundancy may, however, reflect the limited resolution of available assays in assessing the mechanical role of F-actin cross-linking/bundling proteins."
"Our studies support a re-evaluation of the notion of functional redundancy among cytoskeletal regulatory proteins."
with regards to SRC-kinase not all of the interactions are known so it's difficult to even evaluate the mechanism of redundancy let alone speculate on its origin.
if you want to read about genetic networks and their resistance to mutation and its evolution Andreas Wagner has written several papers on this subject which can be found here: http://samba.unm.edu/~wagnera/Publications.html

This message is a reply to:
 Message 32 by peter borger, posted 10-25-2002 8:32 PM peter borger has replied

Replies to this message:
 Message 42 by peter borger, posted 10-29-2002 12:23 AM Itzpapalotl has not replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 34 of 317 (20863)
10-25-2002 11:44 PM
Reply to: Message 26 by Mammuthus
10-25-2002 5:06 AM


Dear Mammuthus,
Thanks for your reply.
YOU WRITE:
PB:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.
M: First off, you can sequence the mtDNA of 3 cheetahs and find no genetic variation to. It is historically known that they went through a bottleneck (perhaps down to a single breeding pair) and they are still today extremely genetically uniform. All as predicted by population genetics much less evolution.
MY RESPONSE:
Population genetics is the field of multipurpose genome and allele frequency variation, not the field of evolution. Nothing evolved here, just variation with respect to preexisting alleles in the gene pool.
YOU SAY:
Same goes for the musk oxen. The entire population of musk oxen in Greenland were a transplant of a few from Alaska...thus, they are identical in the sequences thus far studied. Of 37 modern muskoxen only 8 very similar haplotypes were found...though I have some upcoming surprises about 15 thousand year old muskoxen
MY RESPONSE:
I am curious. Same genepool as contemporary muskoxen? It would fit 'multipurposism'.
YOU SAY:
Very few W. nobilis exist so it would have been a much greater surprise if the 3 stands demonstrated genetic variability as that would be inconsistent with a bottleneck. Bottlencks can be observed expreimentally and in the wild. Your concept of morphogenetic fields cannot so is thus unsupported.
MY RESPONSE:
There is no W. nobilis in the fossil record. So, your bottle neck is utterly hypothetical.
YOU SAY:
As to your arguement that no one could "prove" that W. nobilis was not created 100 years ago...(you don't prove in science which you obviously do not know)...Find the closest relative of W. nobilis and you can determine how long ago it separated from that relative..thus much evolution has occurred and had to occur before the trees present as the genome does not spontaneously change after the organism is present, except for a few loci
MY RESPONSE:
The closest relative of the pine is one of the Araucaria family. It is known that they have very low variablity. Maybe Quetzal can repond to this in more detail, since he has got the papers on the DNA work done on this topic.
YOU SAY:
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
PB:
Indeed, and how do you think this works?
M: Are you being serious or joking? Are you really unaware of why thalidomide is a mutagen? Before I go into this I need to know if you have any knowledge of developmental biology.
MY RESPONSE:
How does the environment have impact on gene regulation, I mean. Not the effect of thalidomide. I know how it works. It is a vascular growth inhibitor and now in use to treat certain solid tumors.
PB:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.
M: And again, you have not provided any evidence for non-random mutation except for your poor tactic of redefining random to suit your purpose though it is not correct. There are lots of papers on subpopulation variation and they don't show non-random mutation. You still cannot tell me for the hottest of hotspots if a mutation will occur there in the next generation or not.
MY RESPONSE:
Remember the 1G5 gene and ancient mtDNA? I also like to have a look on the paper that do not show this in subpopulations. Could you please provide me with the references.
PB:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)
M: We can continue as you like. Your repeating non-random mutation is not making it any more valid....so please continue but actually supply something substantive.
MY RESPONSE:
What evidence do you need to accept non-random mutations? I showed you the 1G5 gene and the ancient mtDNA already, what else do you need?
PB:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.
M: Actually, you have previously denied other forms of mutation contribute to variation. However, you stated multipurpose genome was all about shuffling of existing sequences only with no acknowledgement of point mutations etc...do you wish to revise your premise?
MY RESPONSE:
Denial of mutations would be stupid. I probably refered to point mutations as not being relevant in generating novelties, and usually neutral or degenerate.
M: As to your questions, I think we may be talking past each other. I am not sure what you are asking me. I can give you examples of close species with different chromsomal content but I am not sure if that is what you are asking for.
MY RESPONSE:
Close species with different DNA content sounds multipurpose-like and differential losses of redundant genes. Yes, I am interested and could you please provide the references.
PB:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?
M: That is an easy one. Novel integration events have been observed including with HIV when the virus integrates into the genome of its host. The LTRs are identical..the divergence is post integration.
MY RESPONSE:
Sounds reasonable if the LTRs diverged. Can you refer to the paper.
PB: No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?
M: Please read any basic chapter on recombination and you should be able in 2 seconds to see why the reciprocal recombinant is lost.
MY RESPONSE:
I wasn't referring to reciprocal recombinations. Is not how genes duplicated at the first place. I should be done by unequal crossing over. By any means, the identical copies of histon genes and the hundreds of copies of identical tRNA genes are by definition REDUNDANT. How can they be stable in the genome? Concerted evolution? I wanna see the evolutionary relics in the genome, diverging from 0-100% over time.
For histons the mechanism of concerted evolutionism has been abandoned recently for obvious reasons. It is now purifying selection.
PB:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.
M: actually you deny that you are linked to your parents by common ancestry as well. It is not a plain statement but one supported by paleontology, morphology, biochemistry, and genetics....what have you got?
MY RESPONSE:
Inappropriate analogy. It has been observed that my parents are my ancestors. It is a biological observation.
You are wrong in your statement that it is supported by all these disciplines. It is inferred from the fossil record, although nobody ever demonstrated it beyond doubt (transitionforms). Morphology doesn’t say anything about evolution, and phylogenetics observations violate the rules wherever you look (IL-1beta, LDH, alpha-globin, maybe even cytochrome c) so you’re not on solid ground with your assertion. I do the same observations as you but I can explain them by inferring (anti)creaton-matter-interactions (for the appearance of new genera, extinctions, morphology). For the rest there is the multipurpose genome and non-random mutations (this is NOT deterministic mutations).
PB:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.
Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).
M: Ah, so now the mutlipurpose is now only semi-multipurpose on certain occasions? As to ZFX..you are not helping your case by posting this fallacy again (as discussed).
MY RESPONSE:
As mentioned the new theory is still in preparation/under construction. It took the neo-Darwinians almost a century to set up their non-falsifiable theory (untill I got involved ).
Fallacy? The ZFX gene doesn't change for 20 million years as demonstrated by biomolecular scientists and you call that a fallacy?
M:
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
PB:
Nice example of redundancy. I see no problems here.
M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.
MY RESPONSE:
No, all organisms have a tremendous amount of genetic redundancies. Why would al redundancies be the same? I don't see a reason for that. I already demonstrated redundancies for several organism including Arabidopsis and E coli. Leave out 10% of the genome and no problem for the organism. Apparently these genes --that do not demonstrate more change than essential genes-- are in the genome without selective constraints. It is a Darwinian paradox. Insoluble. Here, the multipurpose genome is far superior to Darwinism. You know that, but you are free to deny it.
PB:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.
M: Clear to you but that is not a prediction of any evolutionary biologist. Some cases do operate as you have said. In other cases a gene involved in one function takes on a new function i.e. homoglobins in bacteria versus multicellular organisms. And you the need organism to be selected on by its environment at the phenotypic level, not the gene to be selected for to pre adapt the organism to something..get it?
MY RESPONSE:
All according to the FACT of evolutionism, isn’t it. I was objecting to evolutionism, since it is NOT a fact. As demonstrated --and denied-- over and over. Moreover, evolutionism also has to explain the origin of these novel genes.
PB:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.
M: There is a lot of evidence for a manatee-elephant association. you up for reading it?
MY RESPONSE:
There may be a lot of manatee-elephant associations. There is also a lot of bacterium-elephant association. Next thing you are going to say is since there is an association they have a common ancestor through a Darwinian mechanism. Well a red car and a red bike have also significant associations. Both consist of metal, have wheels, and even have the same colour. Am I to conclude that they are made in the same factory?
PB:
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.
M: Except that it is a non-testable hypothesis just like plain old biblical creationism.
MY RESPONSE:
Actually extinctions are associated with an interval of roughly 26 million years. Case proven
How do you explain extinctions?
M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
PB:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.
M: LOL!!!!!!!!!!!!!!!!!!!!
MY RESPONSE:
What’s the fun about? Is it a funny book? I didn’t read it yet, maybe I should?
PB:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.
M: Glad you don't object to point mutations as that would make for some very strange demonstrations in front of the White House
You have falsified your own hypothesis. Two humans have the same repair mechanism (as do chimps and humans)yet any two individuals have different amounts and locations of mutations so it cannot be due to loss of repair genes.
MY RESPONSE:
Your assumption is that these organisms have the same repair mechanism. However, the expression and interaction is differently regulated per individual. As mentioned several times now, there are 2 types of mutations non-random and random. The random mutations is all evolutionism requires, according to evolutionism. However, the non-random mutations line up if you compare (sub)species and give an illusion of common descent. In addition, they are alternated by random mutations. The latter are interpreted as being generated after the species split off from a common ancestor. In my opinion the two types of mutations work simultaneously. So, I don’t see a problem here.
PB:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.
M: Go ahead an revisit Lamark and tell me what our current understanding is of epigenetics and how it relates to evolution and then how it relates to your hypothesis.
MY RESPONSE:
It is clear from my own field that some ‘adaptations’ occur that cannot have resulted from mutations in DNA alone, since the adaptations occurs suddenly and everywhere at the same moment. For instance, asthma. It is a desease affecting ‘solely’ Western societies, and its prevalence increased from around 1% 40 years ago to 10% now. That is within 1-2 generations. It suggests an effect of the environment/lifestyle on the development of the disease. It is my personal opinion that the disease is largely due to epigenetic modifications of chromatin and/or DNA structure that results in an alternative development of immune system and lungs (sometimes aggravated by genetic predisposition).
Similar observation have been done on rapid adaptations of human populations on high altitude. It is as if the info of adaptation is pre-existing.
PB:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get its protein?
M: 8% of the human genome is composed of HERVs so there are plenty of options...you have a lot of work cut out to support your assumption
MY RESPONSE:
If the IL-1beta was carried by a virus and integrated adjacent to IL-1 alpha then I expect to find the remnants of the virus there too isn’t it?
PB:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).
M: You have claimed multiple times that it was easy to support your hypothesis and very easy to refute evolution based on your hypothesis. Suddenly it is hard? How do you know if creatons are omnipresent or not since you have never measured one or observed one? How will you go about identifying such a particle?
MY RESPONSE:
Not refute, I provide an alternative. And that will take a bit of time. Falsifications of evolutionism can readily be found by scrutiny of current literature on the topic. As demonstrated.
PB:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.
M: Then the hypothesis is falsified as the ancient and modern muskoxen and bears have the same genetic content as modern representatives.
MY RESPONSE:
No, it is not. Apparently they didn’t loose their genetic content. It is not obligatory to loose genetic content, it is a possibility to get variation.
PB:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.
M: Syncytin for one.
MY RESPONSE:
Where does syncytin come from? I mean if it is a viral protein, the virus got it somewhere and integrated it into another genome. Where did the virus get it?
And you said in the previous letter: "Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids." Clear for the theory of evolutionism you mean. It can be envisagd that it was a unique old world monkey gene caputered by an endogenous retrovirus and later escaped from the genome. Where do you think viruses have their origin? In the genome of course.
PB:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.
M: You often seem rather prickly these days. However, you did not deny your lack of knowledge of the fields you are criticizing and have not indicated a willingness to inform yourself. If you did so you might bolster your credibility and not make so many errors.
MY RESPONSE:
Yes, I have a cold. It affects the temper I guess. However, all I do is giving a different interpretation on scientific observations. Nothing wrong with that in my opinion. I learned a lot from this discussion and if a thesis is not tenable I give in. That’s the scientific way. It would be rather unscientific to claim that a hypothesis is a fact while it still can be falsified. But, I am working on that.
PB:
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.
M: On the one hand you say that population genetics predicts this and thus it falsifies evolution...evolution is population genetics...again Daniel Hartl and Andrew Clark Principles of Population Genetics..there is even a "Cliffs Notes" version with less of the mathematical derivations for some of the equations they present.
MY RESPONSE:
Since when is change in allele frequencies evolutionism? It is easy to explain by a multipurpose genome. If population genetics is evolutionism than I AM an evolutionist too. But, it is NO evolutionism, since it doesn't say anything about the generation of new organisms, novel genes, etc. You know --and every educated biologist should know-- that you cannot present population genetics as evolutionism.
Best wishes, And have a nice weekend
Peter
[This message has been edited by peter borger, 10-26-2002]

This message is a reply to:
 Message 26 by Mammuthus, posted 10-25-2002 5:06 AM Mammuthus has replied

Replies to this message:
 Message 35 by Mammuthus, posted 10-28-2002 4:23 AM peter borger has not replied
 Message 36 by Peter, posted 10-28-2002 5:33 AM peter borger has not replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 35 of 317 (20931)
10-28-2002 4:23 AM
Reply to: Message 34 by peter borger
10-25-2002 11:44 PM


Hi Peter,
Hope you had a nice weekend...my replies follow below.
PB:
Population genetics is the field of multipurpose genome and allele frequency variation, not the field of evolution. Nothing evolved here, just variation with respect to preexisting alleles in the gene pool.
M: Do you even know what evolution is? That you made this statement demonstrates profoundly that you do not. Variation of allele frequencies over..what? Over time! That is evolution. And it really has nothing to do with multipurpose. Multipupose should mean Lamarkian evolution which has not been observed.
PB:I am curious. Same genepool as contemporary muskoxen? It would fit 'multipurposism'.
M: Nope, so it does not fit mulitpurposism.
PB:
The closest relative of the pine is one of the Araucaria family. It is known that they have very low variablity. Maybe Quetzal can repond to this in more detail, since he has got the papers on the DNA work done on this topic.
M: Fair enough. I will let Quetzal answer this since the two of you were debating the topic specifically.
PB:
How does the environment have impact on gene regulation, I mean. Not the effect of thalidomide. I know how it works. It is a vascular growth inhibitor and now in use to treat certain solid tumors.
M: I am sorry Peter but I find it almost impossible to believe that you do not know this. Have you ever heard of maternal environment effects in Drosophila? Do you not get how thalidomide is a non-genetic morphological mutation? Do you know what penetrance is? Phenocopy? This is all first year or even high school biology!
PB:
Remember the 1G5 gene and ancient mtDNA? I also like to have a look on the paper that do not show this in subpopulations. Could you please provide me with the references.
M: Pick up anything by Cann R and Wilson AC ...or Stoneking M. or Sajantilli A and Paabo, S. (search terms for medline). Luca Cavalli Sforza or Jim Neel's various books on the subject would not be bad sources either.
PB:
What evidence do you need to accept non-random mutations? I showed you the 1G5 gene and the ancient mtDNA already, what else do you need?
M: I have already told you what evidence multiple times Peter. In order for non-random mutation to abide by the rules you have proscribed you would have to be able to tell me with absolute certainty which sites would mutate in the next generation of any organism. If you just say probably this position or that one then it fits the evolutionary random mutation defintion and not yours.
PB:
Denial of mutations would be stupid. I probably refered to point mutations as not being relevant in generating novelties, and usually neutral or degenerate.
M: Read up on hox gene mutations. Not all are major changes as your hypothesis demands.
MY RESPONSE:
Sounds reasonable if the LTRs diverged. Can you refer to the paper.
M: I'll get them to you a little later. I am a bit under time pressure today. Alternatively, punch in LTR divergence into medline and you should get a lot of references on the subject.
PB:
I wasn't referring to reciprocal recombinations. Is not how genes duplicated at the first place. I should be done by unequal crossing over. By any means, the identical copies of histon genes and the hundreds of copies of identical tRNA genes are by definition REDUNDANT. How can they be stable in the genome? Concerted evolution? I wanna see the evolutionary relics in the genome, diverging from 0-100% over time.
M: There was just a paper on rDNA psuedogenes. They are relics. There are also tRNA psuedogenes in the genome. If you want to watch them diverge to 100% you will be out of luck. How do you identify a 100% divergent sequence? Everything you are asking for is present.
PB:
For histons the mechanism of concerted evolutionism has been abandoned recently for obvious reasons. It is now purifying selection.
PB:
Inappropriate analogy. It has been observed that my parents are my ancestors. It is a biological observation.
M: Oh really? Is your conception a biological observation? You and your parents never actually observed the fertilization event that lead to your conception. Paternity studies have shown an average of about 8% non-paternity in most populations...thus it looks like most ancestry is unknown. The analogy stands.
PB:
You are wrong in your statement that it is supported by all these disciplines. It is inferred from the fossil record, although nobody ever demonstrated it beyond doubt (transitionforms). Morphology doesn’t say anything about evolution, and phylogenetics observations violate the rules wherever you look (IL-1beta, LDH, alpha-globin, maybe even cytochrome c) so you’re not on solid ground with your assertion.
M: That you say morphology has nothing to do with evolution especially as fields such as evo devo are showing a tight link demonstrates your lack of knowledge not lack of support for my assertion. That you don't know how envirnonment impacts gene regulation also does your credibility harm. Your phylogenetics background is equally shabby as you constantly misquoted Page and Holmes as claiming species trees must correlate with gene trees even though all evolutionary biology texts explicitly state that this is not the case. If you misrepresent my assertions you can build a strawman and defeat it. However, you have not put a dent in the actual assertions I have made thus far.
PB:
I do the same observations as you but I can explain them by inferring (anti)creaton-matter-interactions (for the appearance of new genera, extinctions, morphology). For the rest there is the multipurpose genome and non-random mutations (this is NOT deterministic mutations).
M: However, non of what you state in this paragraph is observable or consistent with the data. In addtion, non-randomness is not observed so it is thus falsified. anti creaton matter etc is a non-testable or falsifiable hypothesis i.e. not science.
PB:
As mentioned the new theory is still in preparation/under construction. It took the neo-Darwinians almost a century to set up their non-falsifiable theory (untill I got involved ).
Fallacy? The ZFX gene doesn't change for 20 million years as demonstrated by biomolecular scientists and you call that a fallacy?
M: Too bad that the ZFX region has changed as you have consistenly ignored. Evolution is falsifiable. Your dillusions of scientific grandeur are also not particularly helping your cause. I am personally gratified when people attack scientific theories as that is when the really interesting discoveries are made. But you spouting nonsense is hardly an attack on the theory and you have already claimed your agenda with respect to evolution is your personal loathing of atheists. You have fallen back to making claims repeatedly that have been shown to be incorrect yet you persist in repeating these fallacies. Either bring substantive or correct data to the table or admit your lack of such data. It does not mean a hypothesis is wrong but you cannot claim you have support for your hypothesis that does not exist.
M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.
MY RESPONSE:
No, all organisms have a tremendous amount of genetic redundancies. Why would al redundancies be the same? I don't see a reason for that. I already demonstrated redundancies for several organism including Arabidopsis and E coli. Leave out 10% of the genome and no problem for the organism. Apparently these genes --that do not demonstrate more change than essential genes-- are in the genome without selective constraints. It is a Darwinian paradox. Insoluble. Here, the multipurpose genome is far superior to Darwinism. You know that, but you are free to deny it.
M: Depends. The bacteria placed back in the wild would probably not survive in competition against the bacteria with the 10% not deleted. Selection is not limited to immediate lethality. It is a Borger unable to understand paradox. Not a paradox for those who actually study the subject. Redundancies by your theory should be identical as they are all caused by the same particles interacting in the same field using the same mechanism. This result is not consistent with you hypothesis.
PB:
All according to the FACT of evolutionism, isn’t it. I was objecting to evolutionism, since it is NOT a fact. As demonstrated --and denied-- over and over. Moreover, evolutionism also has to explain the origin of these novel genes.
M: Evolutionary theory also covers evolution of new genes. There is even a field of reconstructing ancient genes and testing their enzymatic properties. You can deny facts as much as you want..it does not decrease their veracity.
M: There is a lot of evidence for a manatee-elephant association. you up for reading it?
MY RESPONSE:
There may be a lot of manatee-elephant associations. There is also a lot of bacterium-elephant association. Next thing you are going to say is since there is an association they have a common ancestor through a Darwinian mechanism. Well a red car and a red bike have also significant associations. Both consist of metal, have wheels, and even have the same colour. Am I to conclude that they are made in the same factory?
M: Poor analogy. A red car and red bike are not subject to heritable mutation and thus cannot evolve by natural means. Manatees and elephants can and do. Elephants and manatees have more in common by orders of magnitude than either does to bacteria so your argument is simply foolish. But from your answer I can assume you are not interested in reading up on the associations.
PB
MY RESPONSE:
Actually extinctions are associated with an interval of roughly 26 million years. Case proven
How do you explain extinctions?
M: Case falsified. 10,000 years ago there was a mass extinction. The peridicity of mass extinctions is not supported either. There are extinctions happening currently.
Extinctions are a wonderful source of novelty. If you knock out top predators, grazers etc. it opens up all the occupied niches to exploitation by groups that were prevented previously. Mammals fill most of the niches previouly occupied by dinosaurs.
PB:
Your assumption is that these organisms have the same repair mechanism. However, the expression and interaction is differently regulated per individual. As mentioned several times now, there are 2 types of mutations non-random and random. The random mutations is all evolutionism requires, according to evolutionism. However, the non-random mutations line up if you compare (sub)species and give an illusion of common descent. In addition, they are alternated by random mutations. The latter are interpreted as being generated after the species split off from a common ancestor. In my opinion the two types of mutations work simultaneously. So, I don’t see a problem here.
M: The problem is that now you have fallen back to admitting random mutation whereas before mutation was non random. Before all organisms were using the same repair mechanism and now each individual is unique. Your hypothesis is falling apart.
PB:
It is clear from my own field that some ‘adaptations’ occur that cannot have resulted from mutations in DNA alone, since the adaptations occurs suddenly and everywhere at the same moment. For instance, asthma. It is a desease affecting ‘solely’ Western societies, and its prevalence increased from around 1% 40 years ago to 10% now. That is within 1-2 generations. It suggests an effect of the environment/lifestyle on the development of the disease. It is my personal opinion that the disease is largely due to epigenetic modifications of chromatin and/or DNA structure that results in an alternative development of immune system and lungs (sometimes aggravated by genetic predisposition).
Similar observation have been done on rapid adaptations of human populations on high altitude. It is as if the info of adaptation is pre-existing.
M: How is anything about either condition work against genetics or evolution?
PB:
If the IL-1beta was carried by a virus and integrated adjacent to IL-1 alpha then I expect to find the remnants of the virus there too isn’t it?
M: It really would depend. If it is a retroviral insertion you would expect to find LTR's on both sides of the gene (though they can and do get removed by recombination). If the integration was reasonably recent the LTRs should still be recognizable as such. If the integration was extremely ancient, you will have the 100% divergence you asked for previously.
PB:
Not refute, I provide an alternative. And that will take a bit of time. Falsifications of evolutionism can readily be found by scrutiny of current literature on the topic. As demonstrated.
M: You claimed that your hypothesis was very easy to establish. Yet now you still persist in falling back on "it is not done yet" when there are holes in it. You might have thought of that before announcing your replacement of evolution You have not demonstrated falsification of evolution to date..but please keep trying. Especially the over reliance of many on neutrality...I am not a big fan of neutral evolution explaining everything either.
PB:
No, it is not. Apparently they didn’t loose their genetic content. It is not obligatory to loose genetic content, it is a possibility to get variation.
M: Previously you stated they must have lost information due to degeneracy and here you say the opposite. Which is it?
PB:
Where does syncytin come from? I mean if it is a viral protein, the virus got it somewhere and integrated it into another genome. Where did the virus get it?
And you said in the previous letter: "Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids." Clear for the theory of evolutionism you mean. It can be envisagd that it was a unique old world monkey gene caputered by an endogenous retrovirus and later escaped from the genome. Where do you think viruses have their origin? In the genome of course.
M: Chicken and egg question. In some ways we are like complicated viruses so maybe viruses were the first life forms on the planet. They are certainly profoundly successful organisms. But anyway, all envelope proteins were old world monkey derived it does not explain the presence of this retroviral component in organisms from bacteria to humans.
PB:
Yes, I have a cold. It affects the temper I guess. However, all I do is giving a different interpretation on scientific observations. Nothing wrong with that in my opinion. I learned a lot from this discussion and if a thesis is not tenable I give in. That’s the scientific way. It would be rather unscientific to claim that a hypothesis is a fact while it still can be falsified. But, I am working on that.
M: Hope you are feeling better. Like I said, I am also up for this type of arguing and I have learned a lot to because the discussion forces me to keep going back to my literature collections and read and re read papers. I find it productive no matter how it goes..with the exception of my debate with Wordswordsman which was a colossal waste of time.
PB:
Since when is change in allele frequencies evolutionism? It is easy to explain by a multipurpose genome. If population genetics is evolutionism than I AM an evolutionist too. But, it is NO evolutionism, since it doesn't say anything about the generation of new organisms, novel genes, etc. You know --and every educated biologist should know-- that you cannot present population genetics as evolutionism.
M: Population genetics is inextricable from evolution. Evolution deals with species which are composed of populations that are ultimately determined by their genetics. educated biologists know this You have "created" and artificial distinction between the fields as the principles of evolution are based on the principles of population dynamics.
Best wishes and hope you are feeling better,
Mammuthus
[This message has been edited by peter borger, 10-26-2002][/B][/QUOTE]

This message is a reply to:
 Message 34 by peter borger, posted 10-25-2002 11:44 PM peter borger has not replied

Replies to this message:
 Message 39 by Tranquility Base, posted 10-28-2002 9:03 PM Mammuthus has replied

  
Peter
Member (Idle past 1479 days)
Posts: 2161
From: Cambridgeshire, UK.
Joined: 02-05-2002


Message 36 of 317 (20932)
10-28-2002 5:33 AM
Reply to: Message 34 by peter borger
10-25-2002 11:44 PM


quote:
PB:
Since when is change in allele frequencies evolutionism? It is easy to explain by a multipurpose genome. If population genetics is evolutionism than I AM an evolutionist too. But, it is NO evolutionism, since it doesn't say anything about the generation of new organisms, novel genes, etc. You know
--and every educated biologist should know-- that you cannot present population genetics as evolutionism.

Check the glossary ... evolution has been defined as the
change in allele frequency over time for a while now.
You are mixing theory with mechanisms ... perhaps this is your
problem.
Are you aware of the 'systems' concept of emergent properties?
Basically this says that effects at the level of the system
cannot necessarily be explained by investigating the
components.

This message is a reply to:
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derwood
Member (Idle past 1876 days)
Posts: 1457
Joined: 12-27-2001


Message 37 of 317 (20943)
10-28-2002 12:55 PM


PB:
"And apparently, you --like Dr Page-- seem to find it pleasing to be condescending."
Remind me - who was it that came in here, with no pertinent educational or reseach experience, claiming to have falsified evolution?

Replies to this message:
 Message 41 by peter borger, posted 10-29-2002 12:07 AM derwood has replied

  
derwood
Member (Idle past 1876 days)
Posts: 1457
Joined: 12-27-2001


Message 38 of 317 (20948)
10-28-2002 1:59 PM


PB:
"The ZFX gene doesn't change for 20 million years as demonstrated by biomolecular scientists and you call that a fallacy? "
Why do you keep misrepresenting this, Peter?
Again I ask if you know the difference between a gene and an exon.
I ask this because you keep saying "gene" and yet your citations only deal with a single exon.
Are you hoping everyone will simply forget all of your misrepresentations and hyperbolic statmnents?
Guess again...

Replies to this message:
 Message 40 by peter borger, posted 10-29-2002 12:05 AM derwood has replied
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Tranquility Base
Inactive Member


Message 39 of 317 (20966)
10-28-2002 9:03 PM
Reply to: Message 35 by Mammuthus
10-28-2002 4:23 AM


Mammuthus & Peter
I recently read a population genetics article where the researcher pointed out that, without exception, their field of study related to microevolution. Yes, just as Erwin did (I feel like Brad dropping names wihtout refs like that) this researcher used the dirty micro word.
I am happy to call it evolution but I can understand creationists who don't want to call it that. In any case it has almost nothing to do with macroevolution.
Citing allelic frequency changes, and allelic mutations, as evidence for macroevolution is extremely misleading.
[This message has been edited by Tranquility Base, 10-28-2002]

This message is a reply to:
 Message 35 by Mammuthus, posted 10-28-2002 4:23 AM Mammuthus has replied

Replies to this message:
 Message 43 by Quetzal, posted 10-29-2002 2:02 AM Tranquility Base has not replied
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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 40 of 317 (20971)
10-29-2002 12:05 AM
Reply to: Message 38 by derwood
10-28-2002 1:59 PM


dear SLPx,
You are purposely obtuse. You know what I mean and you know that I am right. Better try to find an evolutionary explanation for these observations. In addition, you still owe me an evo-explanation for the incongruence of the IL-1beta genes, and for the stability of the ZFX region studied by Kim et al. Next we can discuss --if you like-- the redundant alpha actinin genes, the redundant src-kinases and where they violate molecular evolution and how you try (?) to save evolutionism from falling.
And please stop trying to represent me as someone not knowing the difference between genes and exons. Maybe you can provide this site with a contemporary definition of a gene? That would be great. Thanks in advance.
best wishes,
Peter

This message is a reply to:
 Message 38 by derwood, posted 10-28-2002 1:59 PM derwood has replied

Replies to this message:
 Message 58 by derwood, posted 10-30-2002 12:24 PM peter borger has replied

  
peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 41 of 317 (20972)
10-29-2002 12:07 AM
Reply to: Message 37 by derwood
10-28-2002 12:55 PM


Dear Dr page,
And, as demonstrated, I not only claimed it but I also demonstrated how to do it.
best wishes,
Peter

This message is a reply to:
 Message 37 by derwood, posted 10-28-2002 12:55 PM derwood has replied

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peter borger
Member (Idle past 7665 days)
Posts: 965
From: australia
Joined: 07-05-2002


Message 42 of 317 (20973)
10-29-2002 12:23 AM
Reply to: Message 33 by Itzpapalotl
10-25-2002 9:52 PM


dear Itz,
Thanks for your reply. About six months ago I encountered the redundant alpha actinin genes and I observed an evolutionary problem. Since Dr Wagner --the one you refer to-- seems to be the evolutionary expert in the field of genetic redundancy, I mailed him the letter below. Till now I didn't get a response. For obvious reasons.
"Dear Dr Wagner,
With interest I read your mini-review in Genome Biology. I am interested in the origin of genes and I recently found out about genetic redundancy. I am trying to understand it in the light of random evolution. Redundant genes usually demonstrate only moderate sequence homology. For instance the alpha-actinin genes. The a-actinins comprise a group of actin-binding proteins encoded by a multigene family. In skeletal muscle, they are a major structural component of the Z-lines that anchor the actin-containing thin filaments and maintain the spatial relationship between myofilaments. In humans, two genes (ACTN2 and ACTN3) encode the closely related a-actinin-2 and a-actinin-3 skeletal muscle isoforms. ACTN2 is expressed in all skeletal muscle fibres, whereas expression of ACTN3 is limited to a subset of type 2 (fast) fibres. A careful screening of muscle biopsies with dystrophic (118 specimens), myopathic (74), neurogenic (20) and normal (55) features demonstrated that all specimens contained normal a-actinin-2 expression. Deficiency of a-actinin-3 was identified in 51 of the 267 cases (19%), and was due to a common non-sense mutation that introduced a premature stop codon. So, the proper a-actinin-3 protein cannot be synthesised. Surprisingly, the deficiency was not associated with any particular histopathological or clinical phenotype [North et al, Nature Genet.1999, 21:353].
What troubles me is that I cannot think of any molecular mechanism that gave rise to such genes. As a biology student I always was taught that neo-darwianian evolution proceeds through the mechanism of random mutation and natural selection. According to theory, duplication gave rise to two alpha-actinin.
A close look at the redundant genes reveals that the differences are the result of point-mutations. Neutral evolution rate is about 10(exp)-9/nucleotide/year, and recent genome wide studies present evidence that purifying selection worked upon duplicated genes. The ACTN2 and ACTN3 genes are approximately 3000 bp, and share 85% sequence homology. Moreover, the ACTN3 gene is highly conserved within mammals, suggesting ancient duplication and rapid diversion.
I have a couple of questions regarding the evolutionary mechanisms involved in genetic redundancies. I was hoping that you can find the time to address them.
1) Do these data mean that approximately 450 bp changes occurred on neutral positions?
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?
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?
3a) Is it independent from nearby genes? Independent from the rest of the genome?
3b) Does this type of selection take place on the level of the organism? How?
4) Are there identical (=very recently duplicated) genes in known genomes?
5) Is evolution a phenomenon driven by random mutation?
I hope you can help me out with my questions. I would be very grateful. Thanks in advance.
Sincerely,... "
These questions are still unanswered and maybe you are able to address them.
[Or maybe it is a nice challenge for Dr Page since he is the PhD-ed evolutionary biologist of this site and he knows how it works. I cannot answer these questions, since am only a "asthma research creationist guy".]
best wishes,
Peter

This message is a reply to:
 Message 33 by Itzpapalotl, posted 10-25-2002 9:52 PM Itzpapalotl has not replied

Replies to this message:
 Message 44 by Mammuthus, posted 10-29-2002 3:28 AM peter borger has replied
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Quetzal
Member (Idle past 5872 days)
Posts: 3228
Joined: 01-09-2002


Message 43 of 317 (20975)
10-29-2002 2:02 AM
Reply to: Message 39 by Tranquility Base
10-28-2002 9:03 PM


quote:
Originally posted by Tranquility Base:
I recently read a population genetics article where the researcher pointed out that, without exception, their field of study related to microevolution. Yes, just as Erwin did (I feel like Brad dropping names wihtout refs like that) this researcher used the dirty micro word.
I am happy to call it evolution but I can understand creationists who don't want to call it that. In any case it has almost nothing to do with macroevolution.
Citing allelic frequency changes, and allelic mutations, as evidence for macroevolution is extremely misleading.

Hi TB:
I'm not sure I agree with you here. Although I've always cringed at the "artificial" distinction between micro- and macroevolution (primarily because it's been so badly misused), the terms ARE becoming fairly widespread in the lexicon. Although I really dislike "argument from quotation", these two passages underscore the reality of what is being discussed:
1. "Evolutionary processes that occur at rates fast enough to be manifested as change within a single species lineage (*within-species* patterns) are included within the domain of *microevolution*. By contrast, processes that occur at slower rates, so that their effects are manifested in *among-species* patterns, are consigned to the realm of *macroevolution*. Microevolution and macroevolution are thus considered to be parts of a more inclusive whole represented by the hierarchical nature of biological systems."
Brooks D & McLennan D. 1991. "Phylogeny, Ecology, and Behavior: A Research Program in Comparative Biology" University of Chicago Press, p. 16.
2. "Nearly all the factors that have been used to distinguish the origin of higher categories can be attributed to the same processes of speciation, behavioral adaptation and the gradual accumulation of morphological differences that characterize evolution at the levels of populations, species, and genera. There are no fundamental differences between the early stages in the radiation of placental mammals in the earliest Cenozoic and what is known to have occurred in the origin of the species flocks in the East African Great Lakes...Although formulation of a distinct theory of macroevolution does not appear to be justified, it may be convenient to retain the terms microevolution and macroevolution to describe the different patterns of evolution that are observed at the level of populations and species versus higher taxonomic levels and time spans exceeding 5-10 million years."
Carroll R. (1997) "Patterns and Processes of Vertebrate Evolution". Cambridge University Press, pg. 392 (emphasis in original).
I especially like the Carroll quote because he talks about the paleontological "pattern" observed in the fossil record, and brings in a modern example for illustration. This is the same issue - pattern, i.e. mode and tempo - that led Gould and Eldredge to formulate punk eek. Basically, both authors are saying, "yes, we can make a differentiation for different purposes", but both are saying that there is no fundamental difference in the processes between the two.
To close, you might find this article interesting - from the late SJ Gould himself: Tempo and mode in the macroevolutionary reconstruction of Darwinism.
[This message has been edited by Quetzal, 10-29-2002]

This message is a reply to:
 Message 39 by Tranquility Base, posted 10-28-2002 9:03 PM Tranquility Base has not replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 44 of 317 (20978)
10-29-2002 3:28 AM
Reply to: Message 42 by peter borger
10-29-2002 12:23 AM


It is almost all at a click of the mouse
Hopefully you will address some of my questions but more importantly, you have not addressed Quetzal's rebuttal of your W. nobilis example of a "created" organism....looking forward.
cheers,
M
Hum Mol Genet 2001 Jun 15;10(13):1335-46 Related Articles, Links
Differential expression of the actin-binding proteins, alpha-actinin-2 and -3, in different species: implications for the evolution of functional redundancy.
Mills M, Yang N, Weinberger R, Vander Woude DL, Beggs AH, Easteal S, North K.
Neurogenetics Research Unit, Children's Hospital at Westmead, Westmead, Sydney, NSW 2145, Australia.
The alpha-actinins are a multigene family of four actin-binding proteins related to dystrophin. The two skeletal muscle isoforms of alpha-actinin (ACTN2 and ACTN3) are major structural components of the Z-line involved in anchoring the actin-containing thin filaments. In humans, ACTN2 is expressed in all muscle fibres, while ACTN3 expression is restricted to a subset of type 2 fibres. We have recently demonstrated that alpha-actinin-3 is absent in approximately 18% of individuals in a range of human populations, and that homozygosity for a premature stop codon (577X) accounts for most cases of true alpha-actinin-3 deficiency. Absence of alpha-actinin-3 is not associated with an obvious disease phenotype, raising the possibility that ACTN3 is functionally redundant in humans, and that alpha-actinin-2 is able to compensate for alpha-actinin-3 deficiency. We now present data concerning the expression of ACTN3 in other species. Genotyping of non-human primates indicates that the 577X null mutation has likely arisen in humans. The mouse genome contains four orthologues which all map to evolutionarily conserved syntenic regions for the four human genes. Murine Actn2 and Actn3 are differentially expressed, spatially and temporally, during embryonic development and, in contrast to humans, alpha-actinin-2 expression does not completely overlap alpha-actinin-3 in postnatal skeletal muscle, suggesting independent function. Furthermore, sequence comparison of human, mouse and chicken alpha-actinin genes demonstrates that ACTN3 has been conserved over a long period of evolutionary time, implying a constraint on evolutionary rate imposed by continued function of the gene. These observations provide a real framework in which to test theoretical models of genetic redundancy as they apply to human populations. In addition we highlight the need for caution in making conclusions about gene function from the phenotypic consequences of loss-of-function mutations in animal knockout models.
J Mol Evol 1996 Feb;42(2):247-56 Related Articles, Links
Evolution of the src-related protein tyrosine kinases.
Hughes AL.
Department of Biology, Pennsylvania State University, University Park 16802, USA.
A phylogenetic analysis of src-related protein tyrosine kinases (PTKs) showed that one group of these genes is quite ancient in the animals, its divergence predating the divergence of the diploblast and triploblast phyla. Three other major groupings of genes were found to predate the divergence of protostome and deuterostome phyla. Most known src-related PTKs of mammals were found to belong to five well-differentiated families: srcA, srcB, abl, csk, and tec. One srcA gene (fyn) has an alternatively spliced seventh exon which shows a different pattern of relationship from the remainder of the gene; this suggests that this exon may have been derived by a recombinational event with another gene, perhaps one related to fgr. The recently published claim that mammalian members of this family expressed in the nervous system evolve more slowly at nonsynonymous nucleotide sites than do those expressed in the immune system was not supported by an analysis of 13 pairs of human and mouse orthologues. Rather, T-cell-specific src-related PTKs were found to have higher rates of nonsynonymous substitution than were those having broader expression. This effect was particularly marked in the peptide binding site of the SH2 domain. While the SH2 binding site was highly conserved among paralogous mammalian members of the srcA and srcB subfamilies, no such effect was seen in the comparison of paralogous members of the csk and tec subfamilies. This suggests that, while the peptide binding function of SH2 is conserved within both srcA and srcB subfamilies, paralogous members of the csk and tec subfamilies have diverged functionally with respect to peptide recognition by SH2.
: Proc Natl Acad Sci U S A 1991 Jun 15;88(12):5232-6 Related Articles, Links
Interleukin 1 receptor antagonist is a member of the interleukin 1 gene family: evolution of a cytokine control mechanism.
Eisenberg SP, Brewer MT, Verderber E, Heimdal P, Brandhuber BJ, Thompson RC.
Synergen, Boulder, CO 80301.
Interleukin 1 receptor antagonist (IL-1ra) is a protein that binds to the IL-1 receptor and blocks the binding of both IL-1 alpha and -beta without inducing a signal of its own. Human IL-1ra has some sequence identity to human IL-1 beta, but the evolutionary relationship between these proteins has been unclear. We show that the genes for human, mouse, and rat IL-1ra are similar to the genes for IL-1 alpha and IL-1 beta in intron-exon organization, indicating that gene duplication events were important in the creation of this gene family. Furthermore, an analysis of sequence comparisons and mutation rates for IL-1 alpha, IL-1 beta, and IL-1ra suggests that the duplication giving rise to the IL-1ra gene was an early event in the evolution of the gene family. Comparisons between the mature sequences for IL-1ra, IL-1 alpha, and IL-1 beta suggest that IL-1ra has a beta-stranded structure like to IL-1 alpha and IL-1 beta, consistent with the three proteins being related. The N-terminal sequences of IL-1ra appear to be derived from a region of the genome different than those of IL-1 alpha and IL-1 beta, thus explaining their different modes of biosynthesis and suggesting an explanation for their different biological activities.
: J Mol Evol 1994 Jul;39(1):6-12 Related Articles, Links
Evolution of the interleukin-1 gene family in mammals.
Hughes AL.
Department of Biology, Mueller Laboratory, Pennsylvania State University, University Park 16802.
The phylogeny of interleukin-1 family genes shows that human interleukin-1 alpha (IL-1 alpha) is more closely related to IL-1 alpha of the bovine than to IL-1 alpha of the mouse, whereas human interleukin-1 beta (IL-1 beta) is more closely related to IL-1 beta of the mouse than to IL-1 beta of the bovine. The IL-1 receptor antagonist (IL-1ra) shows homology to the C-terminal region of both IL-1 alpha and IL-1 beta. In the C-terminal region, the IL-1 alpha genes of human and mouse have diverged more from each other at nonsynonymous sites than have either IL-1 beta or IL-1ra; because the same pattern is not seen at synonymous sites, it must be due not to a difference in mutation rate but rather to a greater degree of functional constraint on this region in the IL-1 beta and IL-1ra proteins than in the IL-1 alpha protein. But synonymous sites in IL-1 beta of mouse have evolved more rapidly than in IL-1 beta of human, indicating a higher rate of mutation in the former gene. In the N-terminal region of the protein, nonsynonymous sites have evolved at similar rates in IL-1 alpha and IL-1 beta. The first exon of the IL-1ra gene, which encodes the leader peptide, shows evidence of homology with the first exon of IL-1 beta, which is not translated. Thus, it seems likely that IL-1ra evolved by duplication of an IL-1 beta gene and loss of expression of exons 2-4.
Mol Biol Evol 2000 May;17(5):804-12 Related Articles, Links
Sex chromosomal transposable element accumulation and male-driven substitutional evolution in humans.
Erlandsson R, Wilson JF, Paabo S.
Max-Planck-Institute for Evolutionary Anthropology, Leipzig, Germany. riker1@biochem.kth.se
We sequenced the genomic region containing the human Y-linked zinc finger gene (ZFY). Comparison of ZFY to the related region on the X chromosome (ZFX) and to autosomal sequences reveals a significant accumulation of transposable elements on the sex chromosomes. In addition, five times as many retroviruslike elements (RLEs) are present in the ZFY region as in the ZFX region. Thus, transposable elements accumulate more rapidly on the sex chromosomes, and the insertion of RLEs may occur more frequently in the male than in the female germ line. When the accumulation of substitutions in Alu elements was analyzed, it was found that the Alu elements at the Y-chromosomal locus diverged significantly faster than those at the X-chromosomal locus, whereas the divergence of autosomal Alu elements was intermediate. The male-to-female mutation rate ratio was estimated to be 2.5.

This message is a reply to:
 Message 42 by peter borger, posted 10-29-2002 12:23 AM peter borger has replied

Replies to this message:
 Message 51 by peter borger, posted 10-29-2002 7:13 PM Mammuthus has replied

  
Mammuthus
Member (Idle past 6475 days)
Posts: 3085
From: Munich, Germany
Joined: 08-09-2002


Message 45 of 317 (20979)
10-29-2002 3:33 AM
Reply to: Message 39 by Tranquility Base
10-28-2002 9:03 PM


quote:
Originally posted by Tranquility Base:
Mammuthus & Peter
I recently read a population genetics article where the researcher pointed out that, without exception, their field of study related to microevolution. Yes, just as Erwin did (I feel like Brad dropping names wihtout refs like that) this researcher used the dirty micro word.
I am happy to call it evolution but I can understand creationists who don't want to call it that. In any case it has almost nothing to do with macroevolution.
Citing allelic frequency changes, and allelic mutations, as evidence for macroevolution is extremely misleading.
[This message has been edited by Tranquility Base, 10-28-2002]

**********************************************
You will then have to explain why this is misleading TB...I mean AQ

This message is a reply to:
 Message 39 by Tranquility Base, posted 10-28-2002 9:03 PM Tranquility Base has not replied

  
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