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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 151 of 317 (21702)
11-06-2002 10:17 AM
Reply to: Message 150 by derwood
11-06-2002 9:30 AM


Hi SLPx
What a joke...
Just another example of an overemphasis on internet discussion board posts by the cretin, and utter hypocrisy.
Posts are, at least mine are, not designed to be easily transferred to a professional manuscript. I write them on the fly - between classes, at lunchtime, those ocasions that I am caught up on my work and have some time to kill... Typos? Lots. Odd sentences? Plenty. Incorrect word usage? Sometimes. Gasp - errors? On occasion.
I don't write - or set out to write - impeccable proclamations on science, and I don't expect it of anyone else, either, though it seems pretty obvious that the average creationiost believes their every utterance has scientific merit...
M: I also do my responses on the fly. Only on occassion does a creationist post make me go back to the literature to check. Sometimes with TB and sometimes with Borger...that is why I actually enjoy debating them.
Most of the rest either don't stick around or are just a source of amusement...especially when they think their every pronouncement is actually something special ...make you think of anybody posting recently about information theory?
SLPx:
When I first started posting to these boards (about 5 years ago), ......
M: Wow...you have been at this a long time!
SLPx:
Too many times did I have multi-page posts gutted or outright deleted.
So I said F*** it - why do all that work when the cretin will ignore, obfusate, dodge, twist, or edit and delete? Why not just point out their ignorance? It is easier to do, faster, and one does not have to worry about making errors!
M: You should have seen the old CNN evolution forum...there were hundreds of people posting and they regularly deleted posts without warning. But as far as I have seen, that does not seem to happen here.
I also am frustrated by the same thing i.e. you post a detailed response and the person ignores it or claims YOU never addressed their questions.
SLPx:
Last time I checked, randall still had numerous errors on his pages, including the ones I pointed out (I had pointed out several more before he tucked tail and ran).
M: He can afford to be lazy since the people who believe what he says would not recognize the errors.
SLPx
So, not only does the creationist rarely - if ever - 'correct' an error made by a fellow creationist, they actually seem to embrace their idiocy!
By the way - I will nbever correct you in public... You do the same for me, OK pal?
M: You spelled never incorre...I mean yes I will not correct you in public
ciao,
M

This message is a reply to:
 Message 150 by derwood, posted 11-06-2002 9:30 AM derwood has not replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 152 of 317 (21727)
11-06-2002 5:24 PM
Reply to: Message 125 by Minnemooseus
11-05-2002 7:37 PM


minnemooseus:
quote:
I personally can't seem to see a direct correlation between "increased diversity" and "increased information".
I never said there necessarily was a direct correlation (in fact I can easily think of counter-examples to the above). Let’s deal with what I said, not what someone else said. What I said is that the cheetah has clearly lost genetic information from its pre-bottleneck parent population. For example, we know the cheetah has a deteriorated immune system and it is likely it has lost some gene segments (via crossover) and thus potential antibodies. This is clearly a loss of information, no way around it.
Speaking of diversity, the information problem always spurs an incredible amount of diversity in answers evolutionists come up with when the hot potato is thrown in their lap! Check this thread and you will see that Quetzal & Mammuthus are now stumbing all over each other. Quetzal clearly implies in his response to your message that he does not believe the cheetah has lost genetic information from its parent population, while Mammuthus backpedaled and now agrees information was lost (he blamed me for not understanding him; yea). I suspect Quetzal also originally believed Mammuthus thought the opposite because of what he wrote: They have neither poor genetic content nor have they lost genetic information. Mammuthus apparently confused a lot of people with that statement.

This message is a reply to:
 Message 125 by Minnemooseus, posted 11-05-2002 7:37 PM Minnemooseus has replied

Replies to this message:
 Message 153 by Minnemooseus, posted 11-06-2002 5:39 PM Fred Williams has not replied
 Message 164 by Quetzal, posted 11-07-2002 1:57 AM Fred Williams has replied
 Message 167 by Mammuthus, posted 11-07-2002 4:24 AM Fred Williams has not replied
 Message 170 by Mammuthus, posted 11-07-2002 5:11 AM Fred Williams has replied

  
Minnemooseus
Member
Posts: 3941
From: Duluth, Minnesota, U.S. (West end of Lake Superior)
Joined: 11-11-2001
Member Rating: 10.0


Message 153 of 317 (21728)
11-06-2002 5:39 PM
Reply to: Message 152 by Fred Williams
11-06-2002 5:24 PM


Fred said:
quote:
What I said is that the cheetah has clearly lost genetic information from its pre-bottleneck parent population. For example, we know the cheetah has a deteriorated immune system and it is likely it has lost some gene segments (via crossover) and thus potential antibodies. This is clearly a loss of information, no way around it.
I know that I'm in way over my head, as far as discussing genetics, so I won't pursue this much.
To me, it seems that Fred has made a valid and interesting point in the above quoted. How the cheetah situation fits into the bigger question of organic evolution is perhaps now the question.
Moose

This message is a reply to:
 Message 152 by Fred Williams, posted 11-06-2002 5:24 PM Fred Williams has not replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 154 of 317 (21729)
11-06-2002 5:43 PM
Reply to: Message 126 by Fedmahn Kassad
11-05-2002 8:27 PM


quote:
For that matter, any species that gains one useful allele by your definition has increased information in the gene pool.
By the definition I have submitted here for debate, yes! Do you have an example of a randomly produced allele that is beneficial to the population as a whole? In other words, do you have an example where the mutated population is clearly more viable than the wild-type population? I’ve seen one questionable example. Maybe you’ll stumble onto that paper and post it here. There was one admission in that paper that questions their claim. Subsequent mutated type generations produced smaller offspring. Their case was very weak (if requested I’ll look for the paper). Perhaps you may have a better example?
With a complete definition of information, everyone knows evolution is impossible. Hence evolutionists reject a complete definition. So I have acquiesced for the sake of debate to use a watered-down version. I’m trying to spot you guys points. But you still can’t score. Wazz’s up with that? It’s really no fun arguing from a losing position, is it?

This message is a reply to:
 Message 126 by Fedmahn Kassad, posted 11-05-2002 8:27 PM Fedmahn Kassad has replied

Replies to this message:
 Message 162 by Fedmahn Kassad, posted 11-06-2002 8:03 PM Fred Williams has replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 155 of 317 (21730)
11-06-2002 6:04 PM
Reply to: Message 128 by Mammuthus
11-06-2002 3:09 AM


quote:
M: It was a good one and I have no mistake to admit. What you should admit is that you cannot demonstrate non-random mutation and are desperately trying to deflect the conversation away from this painful fact.
LOL! You hang in there Mams. Don’t give in! Keep fighting! Preserve that ego! Why has not a single evolutionist come to your defense on this silly breach of logic you have made? Even if I totally caved and said I don’t believe non-random mutations occur, your point would still be either bogus or a strawman! Is this really that hard to figure out? What I believe about non-random mutations has nothing to do with your error. Please Mams, tell us how Monkenstick’s citation is evidence against non-random mutation. Answer this one request and perhaps it will solve the simple riddle that seems so elusive to you.

This message is a reply to:
 Message 128 by Mammuthus, posted 11-06-2002 3:09 AM Mammuthus has not replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 156 of 317 (21731)
11-06-2002 6:13 PM
Reply to: Message 129 by Mammuthus
11-06-2002 3:10 AM


quote:
Fred's latest method of ducking all questions to him...he is too busy..and the dog (oh I mean the poodles he thinks turn into St. Bernards by genetic drift) ate his homework...
Hi Mams. I wrote this a while ago for the trolls at the old OCW board:
404 Not Found
While you are not a troll or classical evo-babbler, I do think you need to go out on a date or something.

This message is a reply to:
 Message 129 by Mammuthus, posted 11-06-2002 3:10 AM Mammuthus has replied

Replies to this message:
 Message 157 by mark24, posted 11-06-2002 6:22 PM Fred Williams has not replied
 Message 165 by Mammuthus, posted 11-07-2002 3:22 AM Fred Williams has replied

  
mark24
Member (Idle past 5195 days)
Posts: 3857
From: UK
Joined: 12-01-2001


Message 157 of 317 (21732)
11-06-2002 6:22 PM
Reply to: Message 156 by Fred Williams
11-06-2002 6:13 PM


Fred,
post 133 please.
Mark
------------------
Occam's razor is not for shaving with.

This message is a reply to:
 Message 156 by Fred Williams, posted 11-06-2002 6:13 PM Fred Williams has not replied

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


Message 158 of 317 (21734)
11-06-2002 6:56 PM
Reply to: Message 131 by Mammuthus
11-06-2002 3:38 AM


Dear mammuthus,
Thanks for your response.
You write:
PB:
Maybe I should have said POORER genomic content. It is well established that distinct subpopulations of species have lost/diminished expression of different genes. In humans ADH, hemoglobin, CF are lost in distinct subpopulations, while other still have them. The redundant alpha-actinin 3 gene is lost in approx 18% in caucasion population without any survival effect.
M: Can you give an example of diminished expression?
MY RESPONSE:
LDH and ADH in asian populations.
M:
Or do you just mean lost?
MY RESPONSE:
Both diminished expression and lost genes is possible.
M:
However, none of this is obvious from the cheetah. There is no evidence that they lost a gene like alpha actinin 3. And again, they are not extinct so their "quality" is fine.
MY RESPONSE:
Non-scientific humbug. A fine quality of cheetahs? And what about the fine quality of the Allocasuarina? Also of fine quality? In a previous letter it was stated that they struggle to survive, characterised by degenerate sperm production, high newborns deathrates, etc. It demonstrates loss of genes, not monomorphism of genes.
In addition, I predict that even this empoverished genepool of the cheetah will still have genetic redundancies.
PB:
Maybe I should have said poorer compared to before the bottleneck. I really have to spell out everything I say, because you like to be deliberately obtuse.
M: You have a knack for vaguery that makes it impossible to always know what you are talking about. "poor" genomic content is a meaningless statement.
MY RESPONSE:
Talking about vaguery. According to Quetzal evolutinism predicts either statics or dynamics. That's not even vague, that's nothing! It predicts nothing!!! Compared to wild types, poor genetic contents are often observed in laboratory animals. Did you know that laboratory mice can vary in genomic content between 3-3.3 billion nucleotides per diploid genome? That is 10%.
PB:
Furthermore you assert that they didn't loose genes. How do you know? Did you count genes before and after the bottleneck? And what also wonders me is your assertion that reduced allelic variation is the culprit. How do you know? You assume it. The observation of monomorphic genes is not equivalent to a decreased fitness.
M: I guess you did not read any of the papers.
MY RESPONSE:
I do not see a link between my statements and your answer. Clearly, your conclusions are base upon assumptions. That's not science, that's wishful thinking.
PB: It doesn't matter for structural and metabolic proteins.
M: Do you know this or are you just saying this?
MY RESPONSE:
Obtuse again? It is known from elementary biological knowledge, and you also (should) know that's better to have the wild type than the mutant form for such genes.
PB:
It probably only matters for the immunological compartment. However, the immunological system generates its own mutations so over a few generations this system will be variable again. In addition, projects like HUGO show that we are not able to give the exact amount of genes of the human genome, indicating the high within species variability.
M: Why would we know a priori the exact number of genes? HUGO used extremely rough calculations and were wrong...and?
MY RESPONSE:
Are you going to say that all human subpopulation have the same genetic content (same amount of genes)? If so, you are wrong (as demonstrated in previous mails distinct subpopulation will loose distinct genes, since it is a random process). This has been sceintifically proven beyond any doubt.
PB: Variability not through gain of new genes, rather through random loss of preexisting genes. These genes are apparently not directly necessary for survival/reproduction and will get lost easily. All in accord with the multipurpose genome.
M: How do you know if the genes are new or not with the multipurpose genome?
MY RESPONSE:
New protein families. Although you probably doubt them, they are for sure around. For instance recombination proteins (RAG1 and RAG2)in mammals that are involved in gene rearrangemnt in B cells to optimise antigen-antibody interactions. They are found only in mammals with such adaptive immune systems, and they are new genes present in the multipurpose genome of mammals.
M:
Since you claim that no animals are similar due to common descent you therefore don't know if New World Monkeys developed before or after humans by your hypothesis.
MY RESPONSE:
This question cannot be addressed by science (similar to the origin of gene, as discussed before). It can also not be addressed by evolutionism. It can only be speculated upon and the answer depends on the paradigms one proposes.
M:
All genes could be new or old. They could have been created as the sequencing reaction occurred to give the appeareance of the appearance of common descent. How you going to test for that. I have also given you citations for novel genes in primates but you choose to ignore them. And do you really claim ALL variability you see is due to loss of genes?.....Hartl and Clark...Hartl and Clark
MY RESPONSE:
Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision.
PB:
Furthermore, your example of the cheetah also demonstrates that organisms have an excess of genes (redundancies) that can be lost. Still the organism survives: Redundancies of the multipurpose genome.
M: You still don't understand the concept of fitness do you?
MY RESPONSE:
Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness.
PB:
The multipurpose gene is subject to entropy. Redundant genes will get lost easily. In particular those genes not immediately required for survival and reproduction.
M: Then it is pretty freaking amazing that so many redundant genes are highly conserved....or now you are going to post the exact same above sentence but just put a "not" in fron of subject in the first sentence?
MY RESPONSE:
Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied.
Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG.
MY RESPONSE:
Going back in time subspecies become more and more one species. This origin-species has got the ultimate genetic variation because it still contains all preexisting genes.
M: I actually asked if you think each (not the species) individual genome contains the variation of the species? That would fit with Lamarkian dynamics.
MY RESPONSE:
No, I already said --and this is observed in populations-- that losses are at random. So, the genepool of all populations of (sub)species contain what is left over of the original multipurpose genome. It is easy to understand (sub)speciation from this stance. Remember Occam's rasor? The easier the solution the better.
PB:
Through genetic losses, and differential regulation of these preexisting genes it can adapt to a range of environments. For instance the Darwin Finches on isolated Galapagos isles. Cross breeding (as has been carried out) will increase the genetic variability through inbreeding of lost genes (distinct species lost different genes).
M: You forgot that selection acts on the random mutation in the Darwin finches with those best adapted to the new environment surviving and reproducing.
MY RESPONSE:
Selection is not in doubt here. Random mutation is in doubt here. Studies on birds beaks demonstrate that all the variation is already within the gene pool, selection of certain characteristics of the beak can be selected against. For instance, drought will give birds with small beaks a disadvantage due to hard seeds. They will be selected against, and these genes may be removed from the gene pool if drought persists. So, here we have a nice example of reduction of genetic content. The opposite is also possible. However, the loss of such gene can be restored in the population by breeding.
M:
The birds don't just fly out one day and there beaks morph....and please explain how cross breeding will increase genetic variability through inbreeding since cross breeding and inbreeding are opposites.
MY RESPONSE:
Slip of the pen. It should have read cross breeding, not inbreeding.
Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak.
M:
Hybrids are usually less fit than either parent species and populations of such hybrids usually die out unless the two species share a hybrid zone...look it up.
MY RESPONSE:
What hybrids? You mean a hybrid between sheep and goat, for instance.
So, please be specific and look it up.
PB:
Thus, the more variability is inbred the closer the organism will resemble the original 'kind' containing all original genetic info.
M:Inbreeding reduces variability. More inbred individuals do not look like the last common ancestor or do you think the Amish are more genetically similar to Homo erectus because they are more inbred than the average human population?
MY RESPONSE:
Here I also meant crossbreeding.
M:
Also you seem to imply that the first breeding pair of a species contains all genetic variation possible for that species and must reproduce through some alternative means to suddenly make a population appear that contains all the variation which is then subsequently lost..disregarding expanding populations for one thing...and you think evolutionary theory is in trouble???
MY RESPONSE:
I already explained how the multipurpose genome works. Preexisting DNA elements induce variability due to differential regulation, and is probably partially irreversibel due to the character of these elements. I guess you would call these elements retroviroids, or LINE's or SINE's. Or whatever you call them.
PB:
Whether the original kind can ever be backcrossed remains to be established. My guess is NOT, since regulatory elements like retroviruses may have an irreversible effect on gene expression. So, in my opinion, the original genome is plastic within preset limits.
M: To bad this is not a testable hypothesis...preset by whom?
MY RESPONSE:
As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over.
Preset by the multipurpose genome, of course. The Creator if you like.
PB:
Alleles of what? Regulatory networks? Immunogenes? Genes coding metabolism proteins? It all depends on the alleles you are referring to. Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles.
M: Hmmmm have you ever studied genetics? Are you really really sure that "Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles"? Ever hear of dominant mutants? Partial dominance? Penetrance? Genetics 101 Peter.
MY RESPONSE:
Yep, any idea about the mechanisms underlying dominant mutations, and penetrance?
PB:
Your explanation does not account for wild type alleles. You also have to consider the fact that monomorphic alleles (homozygous) genes is the rule rather than the exception in any organism studied. So, in my opinion, monomorphic genes cannot be the culprit. Loss of genes can be.
M: Funny then that for many genes heterozygosity is very high.
MY RESPONSE:
That point in the direction of non-random mecahnisms. All in accord with the multipurpose genome.
M:
In fact it is variable among species with those going through bottlenecks showing very little like W. nobilis to those with very high relative heterozygosity.
MY RESPONSE:
The Wollemi pine doesn't demonstrate very little, it demonstrates NO variation. Wanna play the same game as Quetzal, with his distortion of scientific observations?
PB:
No, it is an evolutionary problem. It cannot be explained by NDT, or the gain of new genes. It can be explained by the multipurpose genome: differntial loss and differential regulation of preexisting genes.
M: Okay, then you finally have a testable hypothesis. You can isolate a group of poodles like Fred says and you should get St. Bernards if you agree with his prediction..this is not a predicition of evolutionary theory but obviously one of multipurpose-ism.
MY RESPONSE:
No, it is YOUR prediction and based upon lack of understanding of the hypothesis of the MG. The actual prediction made by the MG is that due to lost genetic sensible-sequences --not due to genetic monomorphism as you may think-- it is impossible to get St Bernards, or backcross a wolflike animal. However, if you artificially select certain dogs you will be able to generate a wolflike animal from the complete gene pool of the subspecies of dogs. Thus, you bring together all genes that are still present in the gene pool in one organism. Next, you can start breeding with this 'restored multipurpose genome' and you can get the St Bernard, the poodle, the dachshund, the chihuahua, etc.
PB:
Non-random mutations have been demonstrated but every time evolutionist provide fallacies to overcome them.
M: If by demonstrating you are wrong is how you define fallacy then so be it. Monkenstick at least provided a graph..let's see yours.
MY RESPONSE:
I commented on his graph. What I meant is the comments of evolutionists in response to the adaptive mutations of Raddman (mail#52 mol. gen. ev. against random mut. thread). It demonstrates that evolutionists overbluff Raddman (a molecular biologist) by their assertions that "..the error prone polymerase has been selected for their ability to allow cell to cope with damage; the generation of variability [in the genome due to this error prone polymerase] may simply a non-selected byproduct". Well, dear evolutionists, do you really understand biology? I have the feeling that they don't, since it makes the polymerase redundant and since they are not under selective constraint evolutionism predicts highly variable DNA sequences with respect to redundant gene. Based on the MG, I predict that knocking out the errorprone polymerase doesn't effect the organism at all. So here you have another problem.
Contrary what evolutionists believe and propagate as fact, molecular biology is not in accord with evolutionism.
PB:
This is also clear from the Cairns excerpt in letter #52 in the "mol gen evidence against random mutaion thread" (Dr Page response to Fred). Let's have a look at this paper again and I will demonstrate where the evolutionist's reasoning goes wrong. I don't understand that it is not seen through by the molecular biologists involved.
M: Let's have a look at some of my and Quetzal's unanswered questions to while we are at it.
MY RESPONSE:
As mentioned before, I will answer (and rebut) all your questions. Easy, since evolutionism is false.
Best wishes,
Peter
[This message has been edited by peter borger, 11-06-2002]

This message is a reply to:
 Message 131 by Mammuthus, posted 11-06-2002 3:38 AM Mammuthus has replied

Replies to this message:
 Message 166 by Mammuthus, posted 11-07-2002 4:21 AM peter borger has replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 159 of 317 (21736)
11-06-2002 7:03 PM
Reply to: Message 133 by mark24
11-06-2002 4:29 AM


Hi Mark, thanks for your patience.
quote:
A bit wasn’t toggled. IT WAS ADDED!!!!!!
OK, but essentially it’s the same concept. A trigger is either induced, or it is not. I’ll repost it almost verbatim. Note that state 0 = pre-framshift, and state 1 = framshift:
1) To keep things simple, let’s assume the change is binary. So there are two states, 0 and 1. The default, or normal setting is 0, which codes for carbohydrate digestion. Setting 1 codes for nylon. In order for there to be new, or increased information, the original state 0 would have to be the unfavorable state. But it is clear that 0 is the favorable state (in general), and the study confirms that this method is a whopping 98% more efficient. So based on this knowledge, we actually lose information when we go from 0 to 1.
2) Was the mutation random? If so, then from 1) above we can again reasonably conclude that a loss of information occurred. What if the mutation was non-random, that is, environmentally induced? This means there was no net gain or loss of information because the information was already present. I haven’t studied the study you provided in-depth, but from the website you posted my bet is this is a non-random mutation. The author states that it’s been observed more than once. What an un-whitting admission he is making here! Given the odds that this specific mutation would be observable more than once certainly raises eyebrows that this may not be a random event. Another reasonable possibility is that certain portions (hot-spots) of the genome have been pre-programmed for hypermutation during environmental stress to toggle bits in an effort to find a possible combination that improves survival in the degraded environment.
quote:
Hot spots are not pre-programmed. Mutations occur with higher frequency at hot spots regardless of environment.
Do we know this for sure? No. I merely offered it as a reasonable possibility. From a design perspective it is reasonable, in fact the immune system behaves in a somewhat analogous way. But it’s only thinking-out-loud on my part, I’m not claiming I know or can prove this is actually what is going on.
quote:
Furthermore, if you can’t predict where the next mutation is going to occur, then it’s random (in the sense biologists mean it).
This is false, as I demonstrated to Quetzal in this thread (and I believe he agreed with).
quote:
1/ Let’s get back to the crux of the argument, does evolution require naturally arising new information in the genome? 2/ Does evolution require naturally arising information that never previously existed in the genome? You have tried to say evolution can’t occur because, 1/ can’t occur. If this were actually a physical restraint, you would have a point,
Apparently you are a theistic evolutionist?
quote:
but since scenario 2/ CAN be true, evolution is safe from information theory.
Evolution is not safe from info theory because nobody believes evolution has produced life exclusively by using pre-existing genes and rearranging them. If you want to believe this, fine. But observable evidence has already falsified this notion.

This message is a reply to:
 Message 133 by mark24, posted 11-06-2002 4:29 AM mark24 has replied

Replies to this message:
 Message 169 by mark24, posted 11-07-2002 4:47 AM Fred Williams has replied

  
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 160 of 317 (21737)
11-06-2002 7:09 PM
Reply to: Message 145 by derwood
11-06-2002 8:54 AM


quote:
Address the scenarios I mentioned, and I will address yours.
See post to Quetzal. I'm not interested in wasting time.
You made a specific claim. I agreed it would be an example of increased genetic information. Having problems finding your hypothetical example? Why then did you bring it up? All you did was make my case for me. If evolution were true you should be able to produce a myriad of examples, yet you can't produce one.
Bye bye evolution. It's a fairytale.

This message is a reply to:
 Message 145 by derwood, posted 11-06-2002 8:54 AM derwood has replied

Replies to this message:
 Message 172 by derwood, posted 11-07-2002 9:19 AM Fred Williams has not replied

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


Message 161 of 317 (21739)
11-06-2002 7:36 PM
Reply to: Message 147 by derwood
11-06-2002 8:58 AM


Dear Dr Page,
You write:
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
Dear Dr page,
Your definition was oldfashioned (as expected, since evolutionism is an outdated theory). If you include introns in your definition, you also have to include all regulatory elements: promoters, enhancers, silencers etc. Enhancers and silencers have been found 10-100 thousand bp up- and down-stream of the coding sequences of a gene.
So, here we have the upgraded 21st century definition of a gene: All sensible-sequences that contribute to regulated expression of another sensible-sequence (specifying either protein or RNA).
Maybe you didn't get it yet, but biology is moving fast.
best wishes,
Peter
--------------------------------------------------------------------------------
Hey look! It is Fred Williams long-lost love child!
MY RESPONSE:
New for me.
You:
But tell us all, Pete, what that has to do with referring to an exon as a gene?
I:
Ask dr Kim.
You:
And do you have a soure for your definition?
I:
It is elementary that genes are regulated by distant DNA elements. That you didn't know that is because it is not your field, I guess.
You:
You see, maybe you just don't know better-- you are an asthma researhcer-- so you can be forgiven}...
I:
Best wishes,
peter
[This message has been edited by peter borger, 11-06-2002]

This message is a reply to:
 Message 147 by derwood, posted 11-06-2002 8:58 AM derwood has not replied

  
Fedmahn Kassad
Inactive Member


Message 162 of 317 (21743)
11-06-2002 8:03 PM
Reply to: Message 154 by Fred Williams
11-06-2002 5:43 PM


quote:
Originally posted by Fred Williams:
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For that matter, any species that gains one useful allele by your definition has increased information in the gene pool.
By the definition I have submitted here for debate, yes! Do you have an example of a randomly produced allele that is beneficial to the population as a whole? In other words, do you have an example where the mutated population is clearly more viable than the wild-type population? I’ve seen one questionable example. Maybe you’ll stumble onto that paper and post it here. There was one admission in that paper that questions their claim. Subsequent mutated type generations produced smaller offspring. Their case was very weak (if requested I’ll look for the paper). Perhaps you may have a better example?

I believe this tactic is called moving the goal posts. In your original example, you didn’t say anything about benefiting the population as a whole. How exactly is an allele to do that, other than by adding to the genetic diversity as in the case of the cheetah? You have also added the criteria that the mutated population must be more viable than the wild-type population. Yet, with respect to the cheetah, you said
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If the cheetah lost a net sum of ONE useful allele from the parent population then it is patently obvious that its gene pool has LESS genetic information than the parent species. Do you agree or disagree with this?
Now your story is changing such that the allele has to benefit the population as a whole. Was that the case with the lost cheetah alleles? Since it is patently obvious that loss of a useful allele is a loss of information, it is patently obvious that gaining a useful allele is a gain in information. Remember, we are not talking about loss of an entire gene to qualify as a loss, so we don’t require production of an entirely new gene to qualify as a gain (based on your criteria, of course).
Concerning examples, based on your original criteria any number of new alleles would qualify. Surely you are aware that many human genes have many different alleles? These alleles are of course useful. Based on your cheetah definition, an increase in the number of alleles for human genes alone amounts to an increase in information. You are also certainly aware of any number of examples from other species. Therefore, a gain in information, based on your criteria, has been shown. Unless you want to move the goalposts again?
FK

This message is a reply to:
 Message 154 by Fred Williams, posted 11-06-2002 5:43 PM Fred Williams has replied

Replies to this message:
 Message 178 by Fred Williams, posted 11-08-2002 5:51 PM Fedmahn Kassad has replied

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


Message 163 of 317 (21749)
11-06-2002 11:54 PM
Reply to: Message 137 by Quetzal
11-06-2002 5:23 AM


Dear Quetzal,
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I've had a good look at figures of Dilwynite- and Wollemia pollen and it is easy to discriminate between the two. So, this argument fails. Show me the figures where they demonstrate that the pollens of dylwinites and wollemia pollen are indistinguishable.
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Q: I gave you the reference, look it up for goodness sake!
PB: I’ve seen a full colour photograph of dylwinites and wollemia’s pollen and even a blind person can see the difference. Present the figures here you refer too. Or send me a copy (Dr P. Borger Uni of Sydney). If you are right I will admit it, but you are wrong, I’ve seen the pollens. I can send you a copy, if you wish.
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Probably so, or probably not? Of course this the evolutionary vision and I am aware of it. It does however NOT explain the invariability in the region that are usually highly variable regions. That was my point and still is my point. It tells me that DNA sequences are stable throughout time and that difference between individual trees is not likely to be due to pointmutations, but rather through differential gene regulation. Differential regulation probably involves the histon code.
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Q: So, anything written by an evolutionary biologist, botanist, geneticist, etc is by definition incorrect according to your view? Continue to believe whatever you wish. You’ve been shown to be wrong — repeatedly.
PB: Mantra’s. Dr Page’s club?
Q: I have cited multiple references, and every single article ever published on Wollemia nobilis. If you wish to continue arguing that the authors of these studies are completely wrong, there’s not much I can do to convince you otherwise.
PB: Listen Quetzal, I take time to provide you with an alternative vision, so at least you could give me the impression that you actually try to respond to that. Otherwise, be silent, and I don’t waste my time. For the last time, the authors demonstrate NO variability and even for me as a non-native English speaker that is something completely different than LOW variability. Even to an evolutionist this should be obvious.
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Demonstrate where the data are erroneous and incomplete, back it up with refernces.
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Suggest you actually go back and read all the references I’ve provided. Your interpretations have been shown to be erroneous. The data is incomplete because Peakall hasn’t completed the study — the initial sequencing was done on only 18s (by Peakall), and rcbl by (Setaguchi et al), references for which you have already been provided. This means that your assertion that this flipping tree somehow proves multipurpose genomes are absolutely stable and evolutionary theory completely overthrown is based at best on limited data from an initial study.
MY RESPONSE:
These data are the only data published in peer reviewed scientific journals, you mean. All sequences analysed thus far were found to be invariable between the different stands. So, my claim stands as long not proven otherwise.
You also like to exaggerate. The tree violates molecular evolutionism, so evolutionism cannot be true, and thus cannot be presented as fact. That’s what you want to do, present it as scientific fact, while it isn’t. The tree brings further doubt upon evolutionism. You know that. You simply ignore it, like you do with all evidence against evolutionism. You’re a faithful believer.
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Of course I am not being taken seriously by evolutionists. When I registered to this site it was one of the first things that came into my mind as a possible evolutionist's fallacy: O this guy doesn't understand anything about biology, so we don't have to take him seriously. I am used to that fallacy already.
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Q: If I didn’t think you were serious, I’d have ignored you completely. However, you have shown your ignorance or willful misunderstanding of even basic biology every time you type a new response.
PB: The usual response. I don’t understand this and I don’t understand that. I can assure you that I as a molecular biologist specialised in eukaryotic gene regulation I much better understand evolutionism and the underlying mechanism than Dr Page (he is anatomist by education) or you (a conservationist). So, it is you who doesn’t understand the molecular mechanism involved in evolutionism. So, don’t even try it. I know it is a common fallacy of evolutionists. Either this fallacy or complete silence. Evolutionism is NOT in accord with molecular biology.
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Furthermore, I don't know exactly how you make up your mind but I have the feeling that as long as an evolutionary vision hasn't been put forward, you simply do not know what to say about the data. For the rest you adapt to any evolutionary explanation that comes by, without objectively looking at the plausibility of the explanation. In contrast, I can immediately recognise whether molecular data are in accord with evolutionism or not. And I don't buy far-fetched evolutionary explanations anymore, since I can make up stories myself.
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Q: Yet another personal attack. Nope, wrong again. Since I’m not the one actually performing the original research, I tend to listen to the folks that are.
PB: Nope, you do NOT listen to molecular biologists who say that evolutionism is not in accord with current understanding of contemporary biology. Everyone can see this now. You do not accept any of my mails of being relevant against evolutionism. You only listen to evolutionary explanations. You cannot think beyond that outdated paradigm. Don’t play the innocent, Quetzal, since it won’t work. I can see right through your biased responses.
Q: When what they are saying contradicts other things — either my own personal observations or some other scientist — I dig into the subject in more depth and make up my own mind. On the other hand, I tend to only reference articles in these discussions which I agree with — otherwise I wouldn’t post them. Not my fault if the articles contradict your little fantasies. And I agree — you’re great at making up far-fetched stories.
PB: If so, than you also know that the Wollemia violates molecular evolutionary rules. Even Dr. Peakall acknowledged it.
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Finally, the case of Wollemia is extreme AND unusual. Even Dr. Peakall acknowledged that. If it is so common, give me the references please that show NO variability in subpopulations of organisms.
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Q: I did — I referenced several plants, a couple of mammals, etc. Pay attention. If you can’t keep up, take notes.
PB: No you didn’t. These references demonstrate LOW variability. You are distorting the scientific content. NO doesn’t equal LOW.
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All your answers are biased by the axioma "evolution is true". You are unable to think beyond this axioma. Probably --most likely-- the axioma you live with is wrong, and I provided a different explanation, that may be wrong but --most likely-- it may as well be right.
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Q: Whether it’s true or not is what we’re discussing, isn’t it? So far, you’ve shown a grand total of zip, zilch, nada that indicates you’ve falsified evolution as you’ve claimed. You haven’t even raised a decent question yet. The only thing you’ve done is make unsupported assertions and refused to answer direct questions.
PB: And the denial continues. Welcome to Dr Page’s club (I guess Mammuthus is a member too, now). Listen, Quetzal, one cannot discuss with people who deny scientific observations. It clearly demonstrates that evolutionism isn’t science; it’s just another -ism. If you demonstrate that the trees are variable in the expected regions I will be the first to admit it, since I am a scientist, and I don’t deny observations.
Q: Tell you what: here’s my axiom (and so you’ll stop claiming I don’t know anything). For me, to understand biodiversity and the birth and death of populations and species — and how to preserve them - requires an understanding of the natural history and ecology of individual species, and the biology of the individual organisms that make up the species. Survival of populations in the wild is dependent on effective population size, distribution, and density. The number of birds crammed into a small forest fragment or the number of algae cells on a wet rock effects food supply, how heavily predators and pathogens strike, to what degree reproduction is delayed or effective, how long individuals live, which new competitors can force themselves into the community, etc. To understand life, you must specify the context — the parameters of which are a function of a particular time and place. To understand biodiversity, you have to understand the processes of speciation and extinction - the birth rate of new species and the longevity of the clades they in turn spawn. You have to understand the first order effects of any environmental change, and the second-order ripples they cause, the third-order changes caused by the second, etc. And you need to understand the natural history underpinnings of the creation of ecosystems — because no organism on the planet lives in isolation. That is where my axiom comes from. Creaton waves, magical multipurpose genomes, spurious non-random mutations do absolutely NOTHING to advance my understanding of the processes that are critical to my work. Every single plant, animal, insect or fungus that I’ve ever encountered; every single interaction in the wild I’ve ever studied, merely confirms what science tells me about evolution. Hope that answers your question Dr. Borger.
PB: And what does all this have to do with an axioma? Let alone with the axioma of evolutionism? Nothing at all.
Regarding your professional interests, I don’t understand your objections to a multipurpose genome, since it also explains these phenomena, including the Wollemi pine. You say: To understand biodiversity, you have to understand the processes of speciation and extinction - the birth rate of new species and the longevity of the clades they in turn spawn. As long as you hang it on an evolutionary framework, you will never understand the underlying mechanisms. It is impossible to draw sound conclusions from a false theory. My advice: have a look at the raw data and analyse them without bias. That’s the way that leads to objective truth.
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I could tell Dr Peakall about my vision, but I guess that I will have similar responses as I get from you, mammuthus, Dr Page. So, why bother. His assertion of an all-purpose genome was in response to the invariability between the two stands. Now there are even three stands. This is the context of his 'all-purpose genome': "Whatever crash-tackled the tree, one of the most conservative organisms that life has ever thrown up, must have been bordering on apocalypse. So seriously", Peakall told me, "the best genetic constitution hasn't been able to get it out of the canyon. But the flipside is, once it settled down in there its all-purpose genome has allowed it to do as well as it can. I think there's a lot of luck in this story." (The wollemi pine, J. Woodford in discussion with Dr Paekall. Page 171) So, Dr Peakall acknowledges --actually invents-- an ALL-PURPOSE genome.
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Q: I’m still waiting for you to contact him for an explanation. If you think he’s so dead certain about the reality of your assertion, you should be jumping at the chance.
PB: I didn’t know you were waiting. I will send him an email (do you still have his address?).
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You didn't provide an explanation. Even Dr Paekall didn't have an explanantion. Why? Because there is NO evolutionary explanation. You are free to think that you have provided an explanation, but I know better from a molecular stance.
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{Begin Borger mode}You’re just so wrapped up in your dogmatic assertion of creatons and multipurpose genomes that you can’t accept any other explanation.{/Borger mode} I’ve given you several explanations from pop gen and ecology that could account for the limited variation in this species. Try actually developing a logical argument against them — like tell me WHY clonality, or extreme bottleneck, or any of the other explanations don’t make sense. All you’re doing is handwaving — in fact, if you hand wave much more you’re going to achieve liftoff.
PB: Indeed. You (and a lot of other evolutionists) have been so brainwashed that you (they) are unable to think beyond the paradigm of evolutionism. I know your explanations. They do not make sense in the light of molecular evolutionary rules. I explained that several times. You don't listen.
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All mainstreams explanation you provided end in a dead alley. I wouldn't have had a problem with the Wollemia nobilis if there was only one stand with identical DNA. Now there are two (or three) identical populations that cannot have been cloned from each other, I --and with me Dr Peakall-- have a severe molecular evolutionary problem with the tree. I pointed this out in my previous letter, but you just don't seem to get my --and Dr Peakall's-- point.
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Q: Okay, so I stand corrected: you HAVE received a response from Dr. Peakall. Please post it so we can all see how much he supports your position.
PB: Being deliberately obtuse is another evolutionist’s fallacy, I’ve discovered on this site. I referred to an interview with Dr Peakall in Woodford’s book, as mentioned. I recommend you to buy a copy of this interesting book.
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Your idea is that small populations are highly susceptible to diseases since they are gentcally uniform. Maybe your idea is wrong. Judging the Wollemia the are perfectly able to survive under several different conditions. Even in the city of Sydney I've encountered them. So, that is the multipurpose genome in action. Furthermore, I wonder whether you can provide evidence for your assumption that genetically uniform populations are more prone to diseases or that this observation merely reflects loss of genetic information that leads to extinction upon unusual stimuli from the environment (diseases). I guess this is a chicken-egg problem, so my vision against yours.
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Q: Even in the city of Sidney you’ve encountered them? Amazing — and here I’d thought everyone was saying they were rare. Oh, you mean you encountered them in the controlled environment of a botanical garden or institute? Bit of a different story, that.
PB: No, they are not in a controlled environment and are free to contact with all possible pathogens imaginable (where do you get your info? Mine is first hand, I've seen them). None of the trees demised. Sounds a lot like the multipurpose genome to me.
Q: There’s quite a bit in the literature on disease and bottlenecks — my suggestion would be to read some conservation biology. Look up feline infectious peritonitis and check out the FIP outbreak in African cheetahs in East Africa during the 1980’s. There was also a mini-epidemic at the Los Angeles Zoo. In every other species that can be infected by this virus, the mortality rate is about 1%. The 1980’s outbreak in cheetahs was 60% fatal. Do some actual research for a change before you claim that the scientists studying an issue are wrong.
PB: Thanks. Could you make a link to these references? In addition, why didn’t all cheetahs die? Any idea?
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(I read somewhere that the current population of the oryx was bred from 2 individuals and the alleged extinct cape lion has been found in a Russian zoo and all descended from a couple left there by a circus in the previous century. The concept of inbreeding and enhanced susceptibility to diseases doesn't seem to account for these organisms, including Wollemia. It is a questionable concept.)
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Q: Of course you have references for your oryx assertion, right? I mean which species are you talking about: O. gazella, O. tao, O. beisa, O. leucoryx? Your extremely sloppy scholarship is showing again - you are once more making utterly spurious assertions about what scientists are doing with absolutely no effort on your part to either learn about or understand what it is you’re attacking.
PB: I was hoping you could bring some light in what I read. And, you being obtuse again, I didn’t bring it as scientific fact. So, please shine some light on this matter.
It is always fun to kick butt on a tangent, isn’t it? Characteristics of Dr Page’s club.
Q: As to the cape lion — what’s your point? Two cubs were imported to South Africa from Siberia — but they’re a related subspecies. There are, however, 11 reported specimens of what may be descendants of the cape lion in Ethiopia. Even if they are — and aren’t hybrids with another lion subspecies - as far as I know no genetic tests have been performed (except to show the Siberian cubs were a separate subspecies). So asserting that they are or are not genetically homogenous is pretty speculative, even for you.
PB: They were pretty viable, weren’t they? No bottleneck phenomena?
Q: Of course you’re correct that there’s no risk of pathogens with Wollemia either. That’s undoubtedly why they’ve instituted a complete contamination barrier — including forcing the scientists studying the trees to wash their boots in antiseptic before working with the wild populations — because they’re unconcerned about the introduction of new pathogens.
PB: All according to current evolutionary paradigm, that (very) probably isn’t right. The multi-purpose genome makes it less likely that the Wollemi pine will immediately be killed by pathogens. Now, the pine is growing everywhere —not only in restricted areas-- , is able to encounter loads of potential pathogens, and nothing happened. So, the MPG is far superior here.
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My response: endstations can indeed go extinct. Either endstations stay unchanged for eons or they go extinct. Could & Eldredge wrote extensively on this observation.
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Q: No, you misunderstood — endstation as I used it IS extinction. Otherwise the population continues to evolve. When it can’t, it goes extinct. Gould and Eldredge wrote extensively on the mode and tempo of evolution, they didn’t talk at all about endstations or whatever. Now Vrba wrote quite a bit about extinction and selection sweep. Maybe you’re confused.
PB: Here you demonstrate that you are unable to think beyond the evolutionary paradigm. All organism we have ever observed or present in the fossil record are endstations and will eventually become extinct. There is no evolutionary mechanism that can bring them to another level, since it requires reprogramming if the genome.
[It can only be performed by fast (there possibly are also slow) creatons. ]
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Q: As to your comment on breeding, you are again in error. In fact, one of the main management concerns with relict populations is finding ways to preserve the existing genome of the organisms. For example, the Catalina mahogany consists of six adult trees in two karyotypes (of which one is a known hybrid). To prevent further hybridization, one recommendation I saw was to cut down the hybrid! Another example is another Australian relict, Haloragodendron lucasii, which consists of a total of 8 populations but only 7 genetic individuals. In fact, one population (of some 700 specimens), contained only 3 different genetically distinct individuals! Isolation, small population size, inbreeding depression, clonality, etc ALL contribute to homogeneity in genomes in once widely variant populations. Beyond that, speciation has nothing to do with 'loss of information' whatever that means.
PB: I presume that the individuals of these organism demonstrate genetic differences? So, there is no threat to evolutionism. Why bother about hybrids, it merely demonstrates that they are of the same kind. If these organism are able to form hybrids with other organisms what is the problem? Does the hybrid have more or less distinctive genes? Does the genepool increase by cutting the hybrid down?
Loss of information has nothing to do with speciation? Get familiar with contemporary biology is my advise.
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Q: Read what I wrote! It’s quite straight forward conservation biology. 700 specimens, all genetically related to only three individual genotypes in a single population. And yes, there are genetic differences — don’t tell me you don’t know what a karyotype is I’ll leave you to guess why your questions on the debate over the Catalina mahogany hybrid show you don’t have the first clue what you’re talking about.
PB: I know what a karyotype is. However, it doesn’t contribute to an increased gene pool. I was interested in the sensible-sequences in the subpopulations. Is there a difference with respect to order of genes and/or nucleotides? That would be far more interesting. And why do you leave me to guess? I am genuinely interested in this matter. So, please expand.
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PB: Please provide the reference for the lizard. I will check it on DNA analysis. I expect not to find the change at the nucleotide level (as for the bacteria), but rather on the level of gene expression. This has also been demonstrated in mice. For instance, the agouti-colour is non-mendelian inherited. It depends on a jumping DNA element (usually referred to as a retroviral element) that affect the expression of the agouti-gene.
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Q: I did give you the complete reference. (Hint: look at the original post. See the little line under the title? Click on it and you have access to the original article in the original journal). What the hell does color inheritance in mice have to do with population bottlenecks or even conservation of isolated populations? Nice attempt to baffle with bs by dragging in a complete irrelevancy in an apparent attempt to show off how much you know
PB: Thanks for the reference. I will check it out.
That you don’t understand or miss to see the link doesn’t make it irrelevant.
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Q: Evolution predicts both variation and stasis, depending on the particular organism and the environmental factors that effect it.
PB: Of course. I could have expected this. In other words evolutionism doesn't predict anything. Pretty bad for a theory.
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Q: Now you’re back to denying organisms have a natural history. Oh yeah, I forgot — magical creaton waves poofed them into existence de novo.
PB: Strawman attack. Natural evolutionary history or natural multipurpose history? That’s the question.
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Yes, and evolutionism doesn't predict anything. I will work on the inconsistencies if they are present. However, the rule on this planet is that species suddenly appear, do not change over time and then become extinct. Pretty much in accord with my hypothesis and not in accord with the gradual changes required by evolutionism.
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Q: I assume this is the Peter Borger Rule of Biodiversity? Again, depends on the organism in question, the environmental factors impinging on it, etc. Some lineages change — speciate — quite readily, others don’t. There’s a lot of interesting debate over the causal factors of this difference.
PB: A lot od uninteresting evolutionary oldfashioned outdated humbug you mean? Some lineages change others don’t sound like directed evolutionism (did you read davison’s papers). All in accord with the hypothesis of a multipurpose genome.
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Sensible-regions are regions that have a function and do therefore not change. These regions make sense, therefor sensible region. They can be protein coding regions, but also regions that code RNAs involved in regulatory mechanism, regions involved in lining up chromosomes during cell divisions, etcetera. More and more RNA consensus sequences are discovered that are required for gene expression. It will be a major part of the 'junk-DNA'.
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So sensible regions are exons? What happens when one of the various mutations occurs in these sensible regions?
PB: Quetzal, there are a lot more sensible regions than exons. Even introns are sensible, spacers are sensible, promoters are, enhancers are, silencers are, all tRNA gene are, all regulatory RNA genes are, masking sequences are, and every day we discover more sensible-sequences involved in gene regulation. Here you demonstrate that you are not up to date with contemporary molecular biology. For a recent definition of a gene ask Dr Page, I mailed it to him, very recently. Usually, mutations are detrimental for the sensible-sequences. I well established observation in biology.
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No, Dr Borger agrees with Dr Peakall that evolution is not sitting well here. He says: 'Wollemia is likely the exception that disproves the rule. The assumption has been made that genetic variability is good because it is the basis of natural selection. The Wollemi pine might actually proof that in some systems it is possible to have exceptionally low variability and stay reasonable happy' (page 170). In my opinion, the Wollemi pine is not an exception but the tree is the extreme of the multipurpose genome. It is proof for a multipurpose genome.
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Q: I’d like you to post the response from Dr. Peakall where he says evolution isn’t sitting well — not the Woodford quotation — the response to your email that you’ve apparently received from him. I’ve never said — nor has any biologist that I’ve ever read — that low variability is a guarantee of extinction, although it's usually a good sign the population is in serious trouble.
PB: It is an interview --for that matter a quotation-- in Woodford’s book. What’s your problem with his words? To me his words a pretty clear. It not greek or chinese, so how can it be so unclear to you?
Q: I also agree that Wollemi Pine isn’t an exception — just an extreme example of a normal distribution. As far as variability is good, although a gross oversimplification, in essence this is true. It’s the key to your question above concerning disease susceptibility. I’m surprised I have to explain this basic concept. The more genetically homogenous a population, the less likely it will contain adaptive variants able to survive or take advantage of new selection pressures. IOW, introduce a new pathogen into a population with lots of variation, there’s much more likelihood that there will be some individuals in the population with at least partial resistance to the pathogen. In a homogenous population, the odds of having an individual or group with resistance is much less, and hence if a pathogen effects one individual, it will effect ALL the individuals in the population.
PB: I also agree that the Wollemi pine is an extreme. Namely the extreme of the multipurpose genome. It is able to fight off pathogens due to the preexisting information in the MG.
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Q: No, youre changing your statement. You said that the DNA was incapable of variation.
PB: No, I didn't say that. Reread my first mail, where I roughly outlined the concept of the multipurpose genome.
Q: Since this is completely counter to all observations and published literature, I am more than justified in asking for evidence of YOUR claim. Show that there is a mechanism, structure, or chemical that prevents Wollemia (because that was the organism we were discussing) from varying.
PB: Of course I do not have to prove an absence. The authors already showed that where variability was expected it wasn't found. In addition, I didn't say that DNA is incapable of change, but the mechanisms my be different than assumed. Change at the single nucleotide level is not a major change inducing mechanism. Rather, shuffling of DNA elements that affect gene expression will do the trick. All evidence currently present points in this direction. You may call that evolution, I know it isn't. It is variation induction through preexisting genetic elements. Probably the genome of Wollemia --and other members of the Araucariacaea-- still specifies the most optimal array of DNA repair enzymes.
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Q: Sorry Peter, your message 16 on this thread specifically states the DNA is unvariable, i.e., not capable of variation. You have been challenged to show the mechanism by which DNA is prevented from variation. Your assertion = your evidentiary support required. Try again.
PB: Obtuse again? I asked to have a look at my first mailing, i.e. mailing #1 of this thread. Now you refer to message #16. Message #1 is able to cover all biological phenomena. Message #16 refers to sensible-sequences.
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As demonstrated above, I will. Present the literature if you are so sure.
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Q: I have. You have not produced ONE SINGLE PIECE OF EVIDENCE outside Woodford’s book. I have presented you with numerous articles from peer reviewed journals written by the scientists actually studying the issue. Your entire argument thus far rests on your continual restatement that they don’t know what they’re talking about.
PB: Why would I retract an sound scientific observation? As long Peakall and colleugues don't demonstrate variability I will not retract? Give me at least a good reason why I would retract on the invaraibility of the trees?
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Sometimes I wonder why do I still discuss with evolutionism-believers. They are so stuck in their own paradigm that they are unable to think otherwise. Even if it has been falsified over and over.
Free your mind and I will show you the world how it really is.
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Q: Thanks, I’ll decline. I get enough of a rush out of the real world — I don’t need to accept your fantasy.
PB: Of course you don’t have to accept a new theory immediately. Over the long run, however, you will have since it better describes what we observe and that is what it is all about in science. Description of observations.
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Dr Peakall was the first scientist I heard talking about an All-Purpose genome and he further opened my eyes. I think that Dr Peakall tries to get his data in accord with evolutionism since he has to 'publish or perish'. So he introduces things like the exception that proves a rule. With believers of evolutionism as the only peers for scientific journals he will have a pretty hard time to get it in if he didnt do that, dont you think so? The hypothesis of the multipurpose genome holds that stability ensuring DNA repair mechanisms (plus the redundant genetic code) keep the DNA sense-sequences from changing. The variation observed (since not all the tree are the same) is due to jumping/shuffling DNA elements that affect gene regulation.
Besides, you demonstrate that you don't understand my hypothesis. The hypothesis of MP is an alternative for evolutionism and often it is superior in explanations.
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Q: Please quote the response you received from Dr. Peakall. You’re spending a lot of words explaining to us ignorants here on this board what he really means. I challenged your interpretation using what Dr. Peakall actually wrote. Unless you can bring me Dr. Peakall’s exact response, then you are engaging in yet more baseless assertion.
PB: Since you are questioning Peakall’s words, it is you who should contact Dr Peakall, not me. I don’t doubt his words.
Q: Wait a sec, I just caught this — from the above, it now appears you are stating that there IS variation in the trees — which is what I’ve been saying for 9 pages. Have you retracted your assertion, and I missed it?
PB: Yes, if you have a close look at a trees’s stand --for instance there are 10 in Taronga Zoo-- and it is clear that they are not identical. This has also been observed in cloned sheep. So there is a mechanism beyond DNA sequences that is able to induce change. I guess one of them is determined by the histon code.
Q: As for not understanding your hypothesis — on the contrary, I at least understand what you’ve presented so far. I also understand that it’s completely spurious, based on utter lack of evidence and gross misunderstanding of basic conservation biology, genetics, ecology, etc. Misunderstandings which you repeatedly and effectively demonstrate all on your own every time you post. Keep it up — you’re making my argument better than I ever could.
PB: You are definitively a member of Dr Page’s club. Denial and ignorance.
How can I discuss with guys who ignore scientific observations? Impossible.
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What I mean is that all DNA elements required to phenotypic adaptations are already present in the multipurpose genome. For instance, the multipurpose genome has a program for sexual reproduction as well as a program for copicing. The environment simply demands which one (or both) is operative. If sexual reproduction hasn't been sensed for a while, this information is transmitted to the roots and the copicing program is initiated. Both programs can only be kept in the genome through preservation of the programs and that demand for an array of stability ensuring DNA replication mechanisms. It is an example of genetic redundancy and redundancies demand elaborate repair systems, otherwise they will be lost through entropy.
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Q: I think Mammuthus already hit you on this one. However, so I understand you, are you saying that all organisms possess a multipurpose computer system that allows them to switch genetic programs at will?
PB: Obtuse again. Mammuthus didn’t hit anything substantial, so far. Read what I said about these two reproductive systems and try to understand it. One is activated if the other isn’t sensed any more. Ever heard of inter- and intracellular signalling?
Q: If every organism had a multipurpose genome — which is what you assert — every organism should be able to fill every niche on the planet at will. Great! I want to have a gill system that allows me to forego SCUBA gear. How do I turn on the ability to breathe water?
PB: The MG is limited and not all organisms have the same to start with. The MG will become more and more limited over time due to losses and entropy. I mentioned this over and over. It is not a difficult concept to understand.
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Q: Now we're getting somewhere. If I understand what you just wrote, any organism that can be shown to have developed any new (i.e., not transposed or whatever), completely novel gene will utterly destroy your theory? Please tell me that's the case, then we can stop these lengthy responses and all go do something useful.
PB: If you can unequivocally proof that this completely novel gene came about without the interference of creatons, it would be bad for the hypothesis. For instance, the TcR gene in mammals seem to drop out of the sky (O I see, the current story is 'birth-and-death-evolution and purifying selection'). What's wrong with the idea of creatons?. Nobody ever saw birth and death evolution, and nobody ever saw a creaton. So, there is no difference (except that evolutionism is scientifically accepted).
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Q: Great! Your hypothesis is falsified:
PB: Even if it was (but it isn't), so what? The hypothesis of evolutionism has been so many times falsified that unbiased well informed biologists (NOT evolutionists) don’t even take it serious any more.
QNurminsky DI, Nurminskaya MV, De Aguiar D, Hartl DL (1998), Selective sweep of a newly evolved sperm-specific gene in Drosophila, Nature 396:572-575
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The pattern of genetic variation across the genome of Drosophila melanogaster is consistent with the occurrence of frequent 'selective sweeps', in which new favourable mutations become incorporated into the species so quickly that linked alleles can 'hitchhike' and also become fixed. Because of the hitchhiking of linked genes, it is generally difficult to identify the target of any putative selective sweep. Here, however, we identify a new gene in D. melanogaster that codes for a sperm-specific axonemal dynein subunit. The gene has a new testes-specific promoter derived from a protein-coding region in a gene encoding the cell-adhesion protein annexin X (AnnX), and it contains a new protein-coding exon derived from an intron in a gene encoding a cytoplasmic dynein intermediate chain (Cdic). The new transcription unit, designated Sdic (for sperm-specific dynein intermediate chain), has been duplicated about tenfold in a tandem array. Consistent with the selective sweep of this gene, the level of genetic polymorphism near Sdic is unusually low. The discovery of this gene supports other results that point to the rapid molecular evolution of male reproductive functions. (emphasis added)
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Q: Here’s a brand new gene that was formed from bits and pieces of other genes — not a duplication event.
PB: A brand new (?) gene from bits and pieces preexisting in the genome you mean? Sounds like a paradox. By shuffling I guess. As predicted by the multipurpose genome you mean?
And the selective sweep evo-non-sense. It is equivalent to Noah’s Ark. Very unscientific, and easy to falsify (as I demonstrate for the putative selective sweep to explain the non-variable human ZFX region).
Q: Here’s the follow-up paper: Nurminsky D, Aguiar DD, Bustamante CD, Hartl DL (2001), Chromosomal effects of rapid gene evolution in Drosophila melanogaster, Science 291:128-130
PB: I will look into it. Bet it is non-random evolutionism, parasite-host related, or an immuno-gene.
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Rapid adaptive fixation of a new favorable mutation is expected to affect neighboring genes along the chromosome. Evolutionary theory predicts that the chromosomal region would show a reduced level of genetic variation and an excess of rare alleles. We have confirmed these predictions in a region of the X chromosome of Drosophila melanogaster that contains a newly evolved gene for a component of the sperm axoneme. In D. simulans, where the novel gene does not exist, the pattern of genetic variation is consistent with selection against recurrent deleterious mutations. These findings imply that the pattern of genetic variation along a chromosome may be useful for inferring its evolutionary history and for revealing regions in which recent adaptive fixations have taken place.
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Q: Note the comparison with D. simulans, which has a recent —observed — common ancestor with D. melanogaster and DOESN’T have the gene.
PB: Do you really understand these references, evolutionism and multipurpose genome? I don’t see a problem here. It is all in accord with a multipurpose genome and loss of genes, and selection against. Reread my mailing #1.
Q: As to proving it didn’t happen through creatons — lol. You haven’t shown anything even remotely resembling proof that the silly things even exist! Why on Earth would you think I have to prove their absence in this process?
PB: You’ve just found yourself another straw-man. You haven’t rebutted any of my claims anywhere in your mailings. All your references demonstrate is the multipurpose genome in action but discussed subject to the false paradigm of evolutionism. Get real, Q, nothing evolved here. It demonstrates the plasticity of the multipurpose genome and how variation is generated. I will spell out the papers and show you that my vision is as right —probably betterin explaining the data.
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Q: I just had to include this section. I'm only going to cite one article out of hundreds that explains how ridiculous this assertion is, and how little you understand of population genetics, speciation, etc: Close genetic similarity between two sympatric species of tephritid fruit fly reproductively isolated by mating time.
PB: Please provide the reference you cite from. That these organisms seem to be speciating can be due to loss of DNA compatibility, so I don't see a problem for my hypothesis here. Also Darwin thought he saw speciation on the Galapagos Archipelago in all the different 'species' of finches. However, we now know that they can still interbreed and are thus NO new species. It is in favour of the plasticity of the multipurpose genome (that is due to loss of genes, and differential gene regulation due to shuffling DNA elements).
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Q: In the first place, I did provide the full reference (click on the title). Amazing you can make the assertion that the speciation event is due to loss of DNA compatibility whatever that is.
PB: It needs a bit of an effort and a lot of free unbiased thinking to set up a new theory. All characteristics you seem to lack, judging from your mails.
Q: How’d you arrive at that bit of inference when you haven’t, by your own admission, even read the article? From the title? Lol!!!! You didn’t even read THAT correctly. It talks about mating time incompatibility - one of several pre-zygotic barriers (in this case, behavioral, not genetic, originall). Your turn — provide a reference that shows the 13 species of finches on the Galapagos still interbreed.
PB: Obtuse again? If your letter demonstrates anything here, it is the impossibility to discuss with brainwashed evolutionists. You’re almost Dr Page. I recommend you to read Nature and Science on the finches: the recent volumes not the volumes from Darwin’s age. Get updated with biological science, it would improve our discussion a lot.
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The regions that are expected to change over time, and were expected to demonstrate variability, have been analysed and didn't show variability. Why would one analyse regions that are not expected to give a lot of change? Dr Peakall knows what regions to analyse in Araucaria family and he did just that. With the know results. Furthermore, coppicing could explain the invariability within the three stands NOT between the three stands.
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Q: See above — way above.
PB: Where, in the blue sky? Watch them fly? Quetzal, neither you nor anyone else solved the riddle around the Wollemi pine’s DNA (yet). You know that, but you prefer to be deliberately obtuse/in denial/ignoring. I am not impressed. Neither by your rebuttal, nor by your knowledge on contemporary biology.
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Q: 1. With your extensive knowledge of population genetics, I'm sure you know that inbreeding depression and mutational load can counteract each other in very small populations. Although possibly an extreme example of this, the observation that Wollemia shows negligible variation at the loci thus far compared between stands could be related to this. In other words, there may not be significant change due to mutation because, if two of the stands were originally seeded from one tree (which hasn't been shown one way or the other), under even theoretically ideal conditions, the divergence would possibly be minimal over several generations.
PB: No, it is the extreme example of the multipurpose genome, characterised by stability of DNA sequences.
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Q: This is now the THIRD time you’ve failed to even address this issue beyond simply re-asserting your original claim. I can only assume that in spite of your vaunted, self-proclaimed expertise, you are unable to do so.
PB: I will not repeat myself again. I recommend you to brush up on molecular biology and molecular evolution, so you can judge for yourself where evolutionism clashes with molecular biology.
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Inbreeding depression and mutational load counteractions sounds interesting. Could you please provide a reference for this, since I am going to look into the genetics. I mean maybe an alternative genetic program has been switched on in this situation. Next, I will explain my vision on this topic.
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Q: Tell me something Peter: are you simply incapable of looking something up on your own? This is pretty basic stuff. Here’s some articles I happened to have on my hard drive without even bothering to check Pubmed or any of the journals:
Bataillon T, Kirkpatrick M (2000) Inbreeding depression due to mildly deleterious mutations in finite populations : size does matter! Genet. Res., 75 : 75-81
Willis, JH (1999), Inbreeding Load, Average Dominance and the Mutation Rate for Mildly Deleterious Alleles in Mimulus guttatus Genetics 153: 1885-1898
Colas B, Olivieri I, Riba M (1997) Centaurea corymbosa, a cliff-dwelling species tottering on the brink of extinction: A demographic and genetic study, PNAS 94: 3471-3476
Reinartz JA, Les DH (1994) Bottleneck-induced dissolution of self-incompatibility and breeding system consequences in Aster furcatus (Asteraceae), Am. J. Bot. 81: 446-455
Charlesworth D, Morgan MT, Charlesworth B (1992) The effect of linkage and population size on inbreeding depression due to mutational load Genet. Res., 59: 49-61
PB: Immediately clear. Mildly deleterious mutations = loss of (redunant) genes. Why are you so blind? Are you paid to be so blind?
Q: These should be enough to give you at least some education in the subject. Feel free to ask if you have any questions ONCE YOU’VE ACTUALLY READ THE ARTICLES. I’m getting really, really, REALLY tired of doing your research for you. For someone who throws their academic credentials at me every single chance he gets, you seem to be oddly incapable of looking up the basic concepts of the multiple scientific disciplines you claim to refute.
PB: I will read the articles and demonstrate where they support the multipurpose genome.
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A mutation not in the germ line and therefor not inherited by sexual reproduction. However, it can be expected that plants that rely on copicing will demonstrate somatic mutations --even in the 18sRNA or rcb genes. Why, since they tissue derived from rapidly dividing meristemes, and here mutations can be introduced easily. All sister cells grown from the mutated cell will also inherit the mutation. So, somatic mutations are expected. If not, the DNA is extremely stable, and in accord with the prediction done by the multipurpose genome.
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Q: How about we see what the actual data says — WHEN IT’S FINALLY PUBLISHED.
PB: Excellent idea. We will see what the data say. I don't need a data interpretation, I can do that myself. Unbiased. Keep me informed, since you seem to know Peakall.
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Q: 4. All of your junk DNA, redundancies, etc, would only appear/accumulate in separated populations of multiple organisms over many generations. With Wollemia we are essentially dealing with three organisms only (although that may change with more data), not three populations. That's the implication of the coppicing growth pattern from an original seeding.
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Q: You have once again failed to address this issue in any way whatsoever other than repeating your mantra. Try again.
PB: Now you are starting to comment on your own replies? Confused? I have to repeat my statements since they are right. Your statements are wrong.
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Q: No, we were talking about the tree. However, just to get rid of your horseshoe crab nonsense right from the start, the living members of this group consist of three distinct genera and five species.
PB: Show me the DNA analysis and the references. I have the feeling that you still don't understand what I am trying to convey. Speciation can readily be understood from a multipurpose genome, it doesn't need evolutionism.
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Q: No — you made the claim. You show ME the references that indicate the five species of horseshoe crab are genetically identical in accordance with your multipurpose genome.
PB: Quetzal, I did a prediction from the MG hypothesis. So, now I like to see the refernces about the genera and subspecies so I can check it. That's how science works. So, could you please provide me with these papers. I would be grateful.
Q: Your MG thingy is incredibly elastic, depending on what you’re responding to:
PB: That's the good part about the MG hypothesis. It can explain every biological phenomenon (sounds like evolutionism, isn't it?).
Q:
1. MG is indicated by invariant DNA (Wollemia) which prevents speciation.
2. MG is indicated by the existence of different species which have invariant DNA ()
3. MG can cause speciation, which, according to you, doesn’t exist.
4. Under the MG, genomic plasticity (in invariant DNA?) is due to loss of genes (but I thought it was invariant?).
You aren’t even consistent in what you claim for your spurious hypothetical genome.
PB: Excellent. You demonstrate here that you are able to rewrite MY hypothesis and than bring it down. How do we call that? Distortion, red herrings and Strawman attacks? CONGRATULATIONS!!!! You managed to introduce three fallacies in one response. (Nice try, try again)
In the meantime the MG still stands and is superior to eolutionism since it can explain ALL biological phenomena. Evolutionism can not.
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Q: That enough variation for you? 'Living fossil'' 'lol' another 'argument from journalistic sensationalism'. Peddle it to someone who doesn't know any better. As to the designation of organism in the case of Wollemia, pending further data, I'd have to say each stand likely represents a single organism (or close enough as no matter).
PB: Even if they were, the separated populations are expected to demonstrate variability. You keep denying that. Maybe you should talk to Dr Peakall about it, since you don't want to accept it from me.
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Q: The point is, if the stands DO represent only three individuals — rather than three populations — seeded from a single individual, almost no variation would be expected. And you’re right about one thing, I wouldn’t accept uncorroborated ANYTHING from you at this point. Go ahead and contact Dr. Peakall for his input. I might accept what he has to say about the organism he’s studying.
PB: I quoted Peakall already for you. What do you want? Peakall’s life act on a videotape?
Best wishes
Peter

This message is a reply to:
 Message 137 by Quetzal, posted 11-06-2002 5:23 AM Quetzal has replied

Replies to this message:
 Message 168 by Mammuthus, posted 11-07-2002 4:40 AM peter borger has not replied
 Message 171 by Quetzal, posted 11-07-2002 5:17 AM peter borger has replied

  
Quetzal
Member (Idle past 5872 days)
Posts: 3228
Joined: 01-09-2002


Message 164 of 317 (21758)
11-07-2002 1:57 AM
Reply to: Message 152 by Fred Williams
11-06-2002 5:24 PM


Fred:
Quick correction - My response to Moose was intended to imply that there was no correlation between loss of genetic variability in a population and loss of some undefined "information" at the population level. See my post #139 on this thread for why I think the concept is misleading at best - and why your question probably can't be answered, even using your definition. Hope that clarifies what I "think", "imply", "suspect" or any other attribution to me you'd care to make.
As far as what I "suspect" Mammuthus meant (and I could be wrong), I think he meant that since the population is still extant - IOW there are still cheetahs living in the wild - they can't be considered (in the context of PB's particular assertion), to be "poor". OTOH, I don't think he is implying that they aren't in trouble. However, ASSUMING no new environmental pressures are brought to bear that further degrade their marginal fitness, and ASSUMING they survive in the wild at all, I think he's saying that there's nothing preventing the cheetahs from evolving (or "improving" if you like) like any other species.
IMO, for what it's worth, I think cheetahs may have already passed the point of no return in a conservation sense, and are more than likely doomed. But that's just my opinion based on what I've read on them concerning infertility, infant mortality, disease susceptibility, continuing habitat degradation/restriction, etc, and has nothing to do with whether or not they DO actually survive - or even thrive. There are enough relictual populations of various organisms running around today that by all rights should have been a historical footnote long ago to make these kinds of predictions pretty speculative.

This message is a reply to:
 Message 152 by Fred Williams, posted 11-06-2002 5:24 PM Fred Williams has replied

Replies to this message:
 Message 179 by Fred Williams, posted 11-08-2002 6:25 PM Quetzal has not replied

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


Message 165 of 317 (21760)
11-07-2002 3:22 AM
Reply to: Message 156 by Fred Williams
11-06-2002 6:13 PM


M: It was a good one and I have no mistake to admit. What you should admit is that you cannot demonstrate non-random mutation and are desperately trying to deflect the conversation away from this painful fact.
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FW:
LOL! You hang in there Mams. Don’t give in! Keep fighting! Preserve that ego!
M: Actually from all of your posts it is you who is constantly boasting, avoiding questions, and demonstrating profound ignorance...what's the matter Fred, fail out of grad school so your angry at the world
FW:
Why has not a single evolutionist come to your defense on this silly breach of logic you have made?
M: As opposed to the masses of people running to agree with your statements?
FW:
Even if I totally caved and said I don’t believe non-random mutations occur, your point would still be either bogus or a strawman!
M: LOL! duck and bob..duck and bob.....your error was to support non-random mutations and now you have to backpedal by all means possible out of supporting your claims..LOL!
FW:
Is this really that hard to figure out? What I believe about non-random mutations has nothing to do with your error. Please Mams, tell us how Monkenstick’s citation is evidence against non-random mutation. Answer this one request and perhaps it will solve the simple riddle that seems so elusive to you.
M: Ah and distortions from Fred..what a surprise...I did not say Monkenstick's post is evidence against non-random mutation There IS NO evidence for non-random mutation. Monkenstick provided evidence FOR random mutation...when asked to do the same for your position resort to the pathetic posting style you are so famous for...(your only claim to fame by the way).
M:
Fred's latest method of ducking all questions to him...he is too busy..and the dog (oh I mean the poodles he thinks turn into St. Bernards by genetic drift) ate his homework..
FW:
Hi Mams. I wrote this a while ago for the trolls at the old OCW board:
404 Not Found
While you are not a troll or classical evo-babbler, I do think you need to go out on a date or something.
M: However, you Fred are a classical internet troll. Up the dosage of Prozac there Fred..your psychosis is beginning to overwhelm you.

This message is a reply to:
 Message 156 by Fred Williams, posted 11-06-2002 6:13 PM Fred Williams has replied

Replies to this message:
 Message 180 by Fred Williams, posted 11-08-2002 6:39 PM Mammuthus has not replied

  
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