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Author Topic:   molecular genetic evidence for a multipurpose genome
Fred Williams
Member (Idle past 4855 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 226 of 317 (22553)
11-13-2002 6:46 PM
Reply to: Message 184 by mark24
11-08-2002 8:08 PM


quote:
a gain in function of nylon digestion IS POSSIBLE.
As I have said over and over again, a gain in function is not necessarily a gain in information. It may be, it may not be. In the case of nylon, since fixing the mutation in the population would be a clear degradation to the organism, it’s a loss of information. You can shout from the mountain tops about your nylon munching bacteria as long as you want, but it won’t change reality.
You are on a road to nowhere, the information-less abyss. Scott on the other hand provided a hypothetical example of what I have said all along would constitute a gain in information by most info scientist standards (a substantial improvement over his tree rings = code goofiness). Too bad though that Scott was engaging in his characteristic begging the question fallacy. Anyway, here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO. I’ve spotted you the BING. Just go find the O!
quote:
I am just presenting a scenario that is possible.
In science, if something is observed countless times over throughout time with no observed exceptions, it qualifies as a Law of Nature. It also means it is justified to declare the opposite is impossible. It is impossible to let go of a rock off a building and not have it drop to the earth. It is also impossible for new information to be created naturalistically.
If you guys can produce evidence in the lab of something similar to Scott’s fantasy, then you would have found ONE example of new info in the genome. But you can’t even produce ONE example, despite countless experiments on various rapidly reproducing species. This is a bad sign for evolution. It means evolution of new complex organs and features is impossible.
Yet another bad day for evolution.

This message is a reply to:
 Message 184 by mark24, posted 11-08-2002 8:08 PM mark24 has not replied

Replies to this message:
 Message 229 by Itzpapalotl, posted 11-13-2002 7:24 PM Fred Williams has replied
 Message 243 by derwood, posted 11-14-2002 2:32 PM Fred Williams has replied

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


Message 227 of 317 (22554)
11-13-2002 6:48 PM
Reply to: Message 216 by Mammuthus
11-12-2002 5:17 AM


dear Mammuthus,
I don not quite understand your reponses. You are attacking Svante Paabo's explanations on this region, not mine (see: REF2 in my previous mail). I was under the impression that Svante is your friend. So, please explain.
My comments:
M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.
PB: And that would invalidate all studies on neutral evolution, isn't it? So, you have to either deny Kimura's theory or you have to deny common descent.
M: The rest is easy. Jim Neel for example studied kinship among the Yanomamo and demonstrated that one male fathered about 95% of the children in one tribe...what do you think that does to Y chromosome variation? Gorillas live in single male dominated groups where the dominant silverback has almost exclusive mating priveleges...what do you expect the Y chromosome to look like?
PB: You mean the rape-and-run cultural practice of the Yanomami Indians? And this cultural aberration is taken as a common human trait to explain the invariable ZFY region? I would call that conclusion jumping. In addition, you are talking about one Indian tribe; I was talking about the complete absence of variability throughout the human population.
This is what I found in pubmed on paternity in Yanomami Indians. (I could find Jim Neel, do you have the reference? Thanks):
Microsatellite and HLA class II oligonucleotide typing in a population of Yanomami Indians.
Roewer L, Nagy M, Schmidt P, Epplen JT, Herzog-Schroder G.
Institut fur Gerichtliche Medizin, Humboldt-Universitat, Berlin, Germany.
We have used three different microsatellites (on chromosome 12 and Y) together with HLA class II oligonucleotide typing (DQA and DQB) to analyze families of Yanomami indians settling in villages in Southern Venezuela. There exist complex networks of biological relationship between villages as a result of wife exchange, village fissioning and changing patterns of alliances associated with inter-village warfare. Social status in this society is largely determined by the kinship system. Polygyny is common, especially among headmen, with additional wives, frequently being chosen among the sisters of the first wife. Our preliminary results mainly obtained from inhabitants of the village HAP show the expected allele distribution in populations with a high degree of consanguinity: (i) deficiency of observed heterozygotes at the autosomal loci and (ii) almost all men carry the same Y chromosomal allele. Nevertheless in the Yanomami village two thirds of the described autosomal microsatellite alleles were identified. Several paternities were clarified.
PMID: 8400691 [PubMed - indexed for MEDLINE]
PB: A rapid, natural selection driven fixation of any advantageous gene on the Y chromosome would therefore result in loss of variance throughout the entire Y chromosome (REF2). Because all non-recombining DNA sequences of the Y chromosome are replaced in a single sweep, this vision predicts that variability should be absent in all linked non-recombining Y chromosome genes. (A retrospective prediction?)
M: Nope, an observation and one you could falsify Peter. Take a group of genetically diverse mice and only let one male mate for 10 generations and then measure the Y chromosome versus mtDNA variation...I can already tell you what you will see...hardly a retrospective prediction.
PB: First of all 10 generation is not 10.000 generations. You assume that the cultural thing of Yanomami Indians is representative for the entire human population. You are free to have these believes, but it is conclusion jumping. You can never present it as fact. And thirdly, what about inbreeding? Evolutionary conservationists keep stressing that small effective populations are bad for survival (ask Quetzal).
PB:
A recent study in mice on the non-coding region flanking the SRY gene, which is directly responsible for inducing maleness, is revealing in this matter. The study compared the amount of variation within the species and related it to the amount of variation among species. Then, the authors compared this ratio to the ratio for a rapidly changing region in the mitochondrial DNA obtained in the same way.
M: Okey....now we have gone from humans to mice...why do I expect exactly the same result?
PB: This was introduced by Svante Paboo, not me. I referred to it. (REF2).
If any of the two regions were subject to a selective sweep, it would be demonstrated by a reduced variation within species. It was found, however, that the non-coding region of the SRY gene changed at a neutral rate. It implicates that, because of linkage of the major part of the Y chromosomal genes, the entire non-recombining part of the Y chromosome changes at a neutral rate. Therefore, it is unlikely that natural selection acts upon the Y chromosome (REF2).
M: So there was no selective sweep in the mice...whoo hoo!
PB: According to Svante Paabo (REF2).
But if natural selection did not act upon the Y chromosome the high degree of variability of the Y chromosome between primates apparently defies the theory of evolution, since the coding region of the SRY gene is very stable within a species (as observed before), whereas considerable variation is observed between distinct species.
M: Note to Peter, though you seem to not realize it...mice are not primates.
PB: According to the Science paper (REF2). All this information is from REF2. You are now doubting your evo-friends, not me.
Some part of the SRY protein show such high degree of variability between distinct primate species that one must conclude that part of the protein has NO function at all, or that the gene is subject to DIRECTIONAL selection, says evolution biologist Svante Pbo (REF2). However, directional selection is only demonstrated in cases involving intergenomic conflict, such as occur between host and pathogen, but is has never been observed for non-immune system related protein coding genes. Of course, one can always propose non-random, directed mutations. But, evolutionists will object to that.
M: The Y is full of HERVs to that are replicating and otherwise evolving at a completely independent rate i.e. in conflict.....and please show the citation that directional selection is exclusively demonstrated by intergenoic conflict.
PB: First of all, it is Svante Paabo remark in REF 2. Apparently you didn’t read REF2. What have HERV to do with the observation that no polymorphism are observed in this non-recombining region? Nothing, I know what HERV are. In the MPG hypothesis, they are (degenerate) jumping preexisting DNA elements in the genome to introduce variation due to differential regulation of gene expression.
PB:
The only remaining evolutionary explanation of the variability in the Y chromosome between species is by the mechanism of neutral evolution. Yet, the observation that more replacement substitutions than synonymous substitutions are present between species suggests that a neutral mechanism is not likely to be responsible for variation among species.
M: Well, that would be true if all of us used data from mice to determine what is happening in primates...but then you have proposed that fish should be just as genetically similar to chimps as to each other so what the hey...
PB: Again you doubt the references. Not me. It can all be found in REF2.
Do evolutionists really understand their own theories?
M: They do...you don't...to bad.
PB: I do understand molecular mechanisms that should be responsible for evolutionism, apparently you don’t understand them or you deny them (Denying physics to keep the hype alive, you can't do that Mammuthus ).
Read this one more time:
REFERENCE 2 says that the only way to understand the region is:
‘these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone’ (REF2).
It immediately implies NEUTRAL EVOLUTION in the whole region, since there is NO constraint on the region. And the funny thing on the region is that there has been DIRECTED EVOLUTION. It all ends, as usual, in a PARADOX. Is't a characteristic of false paradigms.
In conclusion, the falsification still stands.
Try again
Best wishes,
Peter
[This message has been edited by peter borger, 11-13-2002]

This message is a reply to:
 Message 216 by Mammuthus, posted 11-12-2002 5:17 AM Mammuthus has replied

Replies to this message:
 Message 235 by Mammuthus, posted 11-14-2002 3:50 AM peter borger has not replied
 Message 237 by Itzpapalotl, posted 11-14-2002 6:32 AM peter borger has replied
 Message 244 by derwood, posted 11-14-2002 2:38 PM peter borger has replied

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


Message 228 of 317 (22563)
11-13-2002 7:06 PM
Reply to: Message 185 by Fedmahn Kassad
11-08-2002 9:06 PM


quote:
FK: That’s one of the silliest assertions I have ever heard. You are making no sense at all. Let’s walk through this. If a single individual is born with a *new* inheritable deleterious mutation, then your assertion is that the gene pool has lost information, despite the fact that the wild type is unaffected in the rest of the population. I guess then if that individual dies without leaving offspring, the population gained the information back? If a horribly mutated individual is born, survives a few minutes, and then dies, was there a loss and then subsequent gain of information when the individual died?
Technically, yes, albeit incredibly miniscule. Do you have a problem with this?
quote:
FK: On the other hand, if an individual is born with a beneficial mutation, then it is not a gain unless it is beneficial to the population as a whole? What kind of logic is that?
Sound logic!
Sound logic has a way of evaporating strawmen, such as your recent installment here. I never said restored information is not a net gain from the prior state. What I am asking you guys for is *new* information in the genome, such as a new algorithm for sonar, or an algorithm for the avian respiratory system, the origination of feathers, etc, etc.
quote:
To make sure I am clear on your definitions, do you consider sickle-cell to be a loss of information?
Of course I do!
quote:
Would you accept the opinion of Tom Schneider on the matter? If not, why not?
On sickle-cell? I don’t need to accept it, he already agrees it’s a loss of information.
I have discussed info science with Tom several times in the past. He obviously believes info can increase, because evolution demands it. So he labored putting together a paper explaining how it could happen. The problem is, he only used Shannon statistical probabilities, and he had to jump through hoops just to make it happen (or appear to happen).
It was another bad day for evolution!
BTW, DR Royal has a good refutation of Schnieder here:
http://www.trueorigins.org/schneider.asp
PS. I respect Schnieder’s use of Shannon info theory in his work to define and identify binding sites. I hope he stays focused on this instead of wasting time delving into the fantasy world of evolution.

This message is a reply to:
 Message 185 by Fedmahn Kassad, posted 11-08-2002 9:06 PM Fedmahn Kassad has replied

Replies to this message:
 Message 230 by Itzpapalotl, posted 11-13-2002 7:37 PM Fred Williams has not replied
 Message 231 by Fedmahn Kassad, posted 11-13-2002 8:15 PM Fred Williams has not replied
 Message 232 by Fedmahn Kassad, posted 11-13-2002 8:20 PM Fred Williams has not replied

  
Itzpapalotl
Inactive Member


Message 229 of 317 (22565)
11-13-2002 7:24 PM
Reply to: Message 226 by Fred Williams
11-13-2002 6:46 PM


quote:
here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO.
How about this:
L. Chen, A. L. DeVries, and C. H. Cheng. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc.Natl.Acad.Sci.U.S.A 94 (8):3811-3816, 1997.
Trypsinogen duplicated (clear molecular relics of origin) then mutated to give new benefit (resistance to freezing) to the population of these antarctic fish.
You might also want to read: M. Long. Evolution of novel genes. Curr.Opin.Genet.Dev. 11 (6):673-680, 2001.

This message is a reply to:
 Message 226 by Fred Williams, posted 11-13-2002 6:46 PM Fred Williams has replied

Replies to this message:
 Message 240 by Fred Williams, posted 11-14-2002 11:46 AM Itzpapalotl has replied

  
Itzpapalotl
Inactive Member


Message 230 of 317 (22566)
11-13-2002 7:37 PM
Reply to: Message 228 by Fred Williams
11-13-2002 7:06 PM


quote:
Originally posted by Fred Williams:
quote:
FK: On the other hand, if an individual is born with a beneficial mutation, then it is not a gain unless it is beneficial to the population as a whole? What kind of logic is that?
Sound logic!
So all the diverse molecular and physical features associated with sexual conflict are not new information because they only favour one sex so cannot possibly benefit the whole population?. If a dragonfly evolves new genitals that remove rivals sperm this is also no new information as it doesn't benefit and in fact harms the rivals lacking this feature?.

This message is a reply to:
 Message 228 by Fred Williams, posted 11-13-2002 7:06 PM Fred Williams has not replied

  
Fedmahn Kassad
Inactive Member


Message 231 of 317 (22573)
11-13-2002 8:15 PM
Reply to: Message 228 by Fred Williams
11-13-2002 7:06 PM


You have an uncanny way of dancing around the periphery of an argument while avoiding the meat. I bet you have never heard that before, have you?
There were two main points in my post. The first is in response to your assertion that loss of a single useful allele in the cheetah population would be a loss of information. I say then that the appearance of a single useful allele would be a gain. No, you say. It must benefit the entire population. I asked you to justify this, and you passed. I take it then that you concede the argument, as you appear to be unable to refute my points.
Second I wrote the following:
quote:
To make sure I am clear on your definitions, do you consider sickle-cell to be a loss of information? On what basis? Because it’s deleterious? Does it matter what is happening in the genome, or is yours more of a qualitative argument? I am just trying to make sure your argument is consistent, because thus far it does not appear to be.
Your response:
quote:
FW: Of course I do!
Where’s the beef? I am not saying that it isn’t a decrease of information, but I want to understand on what basis you declare that it is a decrease. It appears to me that your definitions are inconsistent, so I am asking you to describe specifically what makes sickle cell a decrease of information. I don’t consider Of course I do to be a substantive response.
Finally, you say:
quote:
FW: Anyway, here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO. I’ve spotted you the BING. Just go find the O!
I have already asked, without receiving an answer, why the mutation must benefit the population as a whole. Under your scenario, an individual could have an incredibly beneficial mutation, it could spread through a small portion of the population, allow the subpopulation to colonize a new environment, ultimately lead to speciation for the subpopulation, and it wasn’t an increase because it didn’t benefit the population as a whole. I am really having difficulty taking these kinds of arguments seriously.
FK

This message is a reply to:
 Message 228 by Fred Williams, posted 11-13-2002 7:06 PM Fred Williams has not replied

  
Fedmahn Kassad
Inactive Member


Message 232 of 317 (22576)
11-13-2002 8:20 PM
Reply to: Message 228 by Fred Williams
11-13-2002 7:06 PM


quote:
Originally posted by Fred Williams:
quote:
FK: That’s one of the silliest assertions I have ever heard. You are making no sense at all. Let’s walk through this. If a single individual is born with a *new* inheritable deleterious mutation, then your assertion is that the gene pool has lost information, despite the fact that the wild type is unaffected in the rest of the population. I guess then if that individual dies without leaving offspring, the population gained the information back? If a horribly mutated individual is born, survives a few minutes, and then dies, was there a loss and then subsequent gain of information when the individual died?
Technically, yes, albeit incredibly miniscule. Do you have a problem with this?

Yes, actually I do. How can it possibly be a decrease in information when the rest of the gene pool is unaffected? Unless it somehow displaces a wild type allele, then information didn't decrease. Please respond with something more than a vague, qualitative argument if you intend to prove your point.
FK

This message is a reply to:
 Message 228 by Fred Williams, posted 11-13-2002 7:06 PM Fred Williams has not replied

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


Message 233 of 317 (22579)
11-13-2002 8:29 PM
Reply to: Message 220 by derwood
11-12-2002 10:42 AM


Dear dr Page,
In reposne to
--------------------------------------------------------------------------------
quote:
--------------------------------------------------------------------------------
Originally posted by peter borger:
However, are you a neutralist or a selectionist?
Best wishes,
Peter
----------------------------------------------------------------------
----------
You say:
Informed scientists understand that the two are not mutually exclusive.
My reponse:
Could you please point out where I say that they are mutually exclusive? It is a common characteristic of evolutionism to conlusion-jump. You once more proof it here,
Best wishes,
Peter

This message is a reply to:
 Message 220 by derwood, posted 11-12-2002 10:42 AM derwood has replied

Replies to this message:
 Message 245 by derwood, posted 11-14-2002 2:44 PM peter borger has not replied

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


Message 234 of 317 (22590)
11-13-2002 9:57 PM
Reply to: Message 213 by Mammuthus
11-12-2002 4:46 AM


Dear mammuthus,
[no comments to the first part]
PB: Maybe you don’t believe in an accurate clock. But the HVR-1 mtDNA sequences presented by Adcock et al (PNAS 2001, 98:537-542) demonstrate with respect to human reference sequence 29 differences for bonobo, 24 for chimp, 27 for neanderthaler. I do not even see a RUDIMENTARY clock in these data. How about you? It should also be noted that an ancient homo sapiens (dated 62,000 BP) demonstrates 10 differences compared to reference sequence. Let me guess, bonobo/chimp and man have a common ancestor around 150.000 years ago? Nice believes you're holding to.
M: You know Peter, you are developing a Fred like habit of putting words in my mouth since your last sentence is utter bullshit and I never made the above statement.
PB: A bit prickly today? However, I am not putting words in your mouth, I was drawing a conclusion from the data in the PNAS paper. These data are a clearcut falsification of common descent and the molecular clock.
M: I guess since your arguments are so pathetically weak this is the only strategy left to you.
PB: Please mind your words, Mammuthus. "Pathetically weak... left to you" does not sound like an argument. Better explain how you see the molecular clock, and convince me with scientific arguments that your visions are right.
M: Did you even read how they calculated the clock rate in the damn paper?
PB: All the paper showed are the polymorphisms in the HVR-1 region of mtDNA and according to these data there is NO molecular clock.
M: I explained why I don't put much stock in molecular clocks, particularly recent events (last million years). You clearly did not understand it.
PB: I fail to see why the molecular clock wouldn't be valid during the last million years. Moreover, why would it become valid after a few million years? Is it hiding behind non-falsifiable experiments?
What is clear from this PNAS paper, is that the mtDNA demonstrated 10/62.000 years in one analysed ancient human, or 3-7/10.000-15.000 years for the other ancient humans. Considering human, Neanderthaler, bonobo and chimp it implicates that either they have a common ancestor around 150.000 years ago (or even earlier), OR polymorphisms are always introduced at the same spot. The latter is a NON-RANDOM mechanism. I don't understand it. You are the evolutionist so please explain.
M: I am not your Mommy and am not going to do your homework for you( again) look up molecular clocks and the controversy surrounding them yourself...otherwise stop arguing from ignorance..it is unbecoming of you.
PB: Are you a bit prickly today? However, although it is not compulsory to addressing questions I would appreciate it. The EXTRAORDINARY evolutionary claims require EXTRAORDINARY scientific evidence.
If you don't want to discuss evolutionary topics, why did you register to this board? I am under the impression that you registered to educate me on evolutionism (remember your first letter?). So, here is an excellent challenge to help me understand evolutionism. Please explain how you see it. [Or, maybe you could recommend a review on the controversy. Thanks.]
PB: It is known that evolutionism is so difficult to understand that not even evolutionists understand it.
M: And I see you had no answer to my question. My understanding is fine. That you do not is obvious.
PB: If it is not difficult to understand, please explain the PNAS data to me.
PB: How do you know that there is selective advantage? You are the propagator of an extraordinary claim. So you have to present the extraordinary evidence.
M: Ok Fred..I mean Peter.
PB: You are prickly! So, these are the questions you get prickly about? Why, I wonder?
M: This is how you want the debate to go? Let me know and I can change the tone of this very quickly and we can have a nice flame war.
PB: A nice flame War? Who are you really Mammuthus? A deep dark inside? Keep it scientific please. Besided, you claimed selection so proof it!
PB: I know that your friends introduced very weak purifying selection, another meaningless term. For the redundant gene family of alpha actinins --as for the 1G5 gene-- you have to introduce neutral selection. As demonstrated. And as denied by evo's.
M: And another non-answer.
PB: Your friend Wagner, among others. Evolutionary theorists on genetic redundancies introduced this concept. I introduced the concept of neutral seletion for the alpha actinin genes. You need this concept to explain these redundant genes. If you don't need this concept, please explain.
PB: So you are a neutralist?
M: What makes you say that?
PB: Your remark on stuff residing in the genome waiting for someting.
PB: You should know this, you are the evolutionist. However, how much selection does it require to purify a redundant gene?
M: Are you actually going to respond to my posts in context. What the hell does this have to do with what I said?
PB: I am rather curious about how much selection purification of redundant genes require. You are the proponent of an extraordinary claim....
PB: Yes, and that makes it such fabulous theory. Sometimes a bit of this, than a bit of that. Evolutionism is like cooking, isn’t it. How to cook the one kind into the other. The stories get better and better.
What happened to Occam’s razor. Mark Pullen will object to such theories, is my guess. What about it, Mark?
M: You are being really dim today Peter.
PB: Dim? I'd rather call it bright.
M: Do you beleive the environment is constant everywhere always?
PB: Usually the environment does not change a lot. Sometimes, environments change overnight. For instance after meteor impacts, ice ages, total earth crust crushes, etc. Fortunately organisms have a multipurpose genome that interacts with creatons, so they can immediately adapt.
M: Do you think selection acts at all times? Do you know if humans are under selective pressure now or not..I bet you don't know the answer to that one
PB: Of course! There is always selection. Selection AGAINST. The issue here is, since I reason from a distinct paradigm, we can never come to the same conlusions.
M: As to weaknesses of theories...your MPG is as weak as they come..stable but variable because of repair enzymes...falsified before it even gets to the starting blocks.
PB: Dear mammuthus, it is elementary that stable DNA sequences can't reside in the genome longer than one generation without repair mechanism. Even the simplest organisms have a complete set of repair enzymes. It is a prediction of MPG hypothesis. I checked it and it is true (PNAS 2002, 99:9509).
PB: I have the feeling that you don't understand the concept of the MPG. Maybe, you don't want to understand or you cannot think beyond the paradigm of evolutionism.
PB: The whole discussion is meaningless (Nei's paper). If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.
M: Great clarification Peter...so I will take it to mean you could not understand Nei's papers as all.
PB: Only just-so statements. Not much of a discussion. So, meaningless.
PB: Apparently these experiments have never been published. Or do you mean the reference below? If so, than I have to disappoint you. It is NOT an experiment it is interpretations of data. You know the difference, I hope. (If not, it explains a lot ).
M: So I guess you are willing to retract all of your papers now to Peter..I mean you did not actually see the change in gene expression..you inferred it from your experiments..I look forward to the retraction letter...
PB: If I have to retract, all inferred papers have to be retracted.
PB: You are lagging behind, I responded to all Quetzal’s points. He choose not to respond to all my replies. However, talking about avoidance. You are avoiding crucial questions of my mails with increasing frequency. Why, I wonder?
M: Me? I bumped both an entire thread and multiple posts multiple times without EVER getting an answer from you other than " oh, I missed that"...you are becoming an expert at avoidance. I have responded to all of your points in all of your mails...I have even responded to mails of yours to other people. So you are either being lazy or dishonest.
PB: This thread was posted by Quetzal, not me. If time is there I will expand on this topic, but not now. I can make up my own thread, I don't need Quetzal's help.
And, it is true that I often mis reponses since I do not get a message in my postbox. If you want to have an immediate response, please send a direct mail.
Best wishes, and have a nice weekend,
[I hope you're not so prickly next week.]
Peter
[This message has been edited by peter borger, 11-14-2002]

This message is a reply to:
 Message 213 by Mammuthus, posted 11-12-2002 4:46 AM Mammuthus has replied

Replies to this message:
 Message 236 by Mammuthus, posted 11-14-2002 4:33 AM peter borger has not replied

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


Message 235 of 317 (22639)
11-14-2002 3:50 AM
Reply to: Message 227 by peter borger
11-13-2002 6:48 PM


PB:
I don not quite understand your reponses. You are attacking Svante Paabo's explanations on this region, not mine (see: REF2 in my previous mail). I was under the impression that Svante is your friend. So, please explain.
M: Friendship in drawing scientific conclusions is irrelevant. No, he is not my friend. We know each other.
M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.
PB: And that would invalidate all studies on neutral evolution, isn't it? So, you have to either deny Kimura's theory or you have to deny common descent.
M: What kind of logic is that? 1. why would conserved features in introns invalidate neutral evolution? There are conserved features of hypervariable region I as well...old hat..read up on it. And you should read Kimura...he did not state that the entire genome evolves neutrally.
PB: You mean the rape-and-run cultural practice of the Yanomami Indians? And this cultural aberration is taken as a common human trait to explain the invariable ZFY region?
M: And I see you are a racist as well..good job. Nope, this is not what I am referring to...see below.
PB:
I would call that conclusion jumping. In addition, you are talking about one Indian tribe; I was talking about the complete absence of variability throughout the human population.
M: Dominant males (whether through power, wealth, violence) in many cultures disproportionately father more children. Humans lived in smallish bands thousands of years ago. It is unlikely given current practices that all males had an equal probability of producing offspring. This is seen directly in some populations such as small nomadic groups today, and the Yanomamo (who I guess you would like to exterminate), and shows exactly the effect on the Y chromosome we observe in the broader human male population.
PB:
This is what I found in pubmed on paternity in Yanomami Indians. (I could find Jim Neel, do you have the reference? Thanks):
M: He presented the data in a seminar. I don't know if he published the data set or not...can't ask him since he is dead. But you can search medline yourself for plenty of other examples. Or do Y chromosome, Yanomamo as search terms.
M: Nope, an observation and one you could falsify Peter. Take a group of genetically diverse mice and only let one male mate for 10 generations and then measure the Y chromosome versus mtDNA variation...I can already tell you what you will see...hardly a retrospective prediction.
PB: First of all 10 generation is not 10.000 generations. You assume that the cultural thing of Yanomami Indians is representative for the entire human population. You are free to have these believes, but it is conclusion jumping. You can never present it as fact. And thirdly, what about inbreeding? Evolutionary conservationists keep stressing that small effective populations are bad for survival (ask Quetzal).
M: What's the matter Peter...hate the idea that you might be an African descendant ? Do you know what the effective population size is for humans? It is a lot smaller than you think. Conservationists stress small effective populations size is bad for survival..that is true. We are talking about the males that contribute to the next generation which does not imply the effective population size is small...or do you not count woman as human?
M: Okey....now we have gone from humans to mice...why do I expect exactly the same result?
PB: This was introduced by Svante Paboo, not me. I referred to it. (REF2).
M: No, I pointed out that you were using the mouse data as an example of human Y chromosome variation which is false.
M: So there was no selective sweep in the mice...whoo hoo!
M: Note to Peter, though you seem to not realize it...mice are not primates.
PB: According to the Science paper (REF2). All this information is from REF2. You are now doubting your evo-friends, not me.
M: Not my friends...are you in love with Spetner so you have to accept what he says..and my point was and still is that if you sequence a mouse gene and call it human you are wrong just as if you take the mouse genetical history for the Y and say that it represents humans....I may not be a primatologist like SLPx but even I know that mice are not primates.
PB: First of all, it is Svante Paabo remark in REF 2. Apparently you didn’t read REF2. What have HERV to do with the observation that no polymorphism are observed in this non-recombining region? Nothing, I know what HERV are. In the MPG hypothesis, they are (degenerate) jumping preexisting DNA elements in the genome to introduce variation due to differential regulation of gene expression.
M: Funny that you call HERV's "degenerate" since most of the ones transposing have a full complement of viral genes...not very degenerate...MPG yet again fails.
M: Well, that would be true if all of us used data from mice to determine what is happening in primates...but then you have proposed that fish should be just as genetically similar to chimps as to each other so what the hey...
PB: Again you doubt the references. Not me. It can all be found in REF2.
M: You obviously did not read any of the primary literature I posted since Svante wrote a review...and then you claim that the data from mice should be applied to humans.
PB: I do understand molecular mechanisms that should be responsible for evolutionism, apparently you don’t understand them or you deny them (Denying physics to keep the hype alive, you can't do that Mammuthus ).
M: You have actually shown complete ignorance of the fundamentals of the NDT and population genetics so your claims to understanding molecular mechanisms are highly suspect.
PB:
Read this one more time:
REFERENCE 2 says that the only way to understand the region is:
‘these regions have been retained throughout the primate lineage without any requirement for sequence conservation, implying that the SRY protein is [] the HMG box alone’ (REF2).
It immediately implies NEUTRAL EVOLUTION in the whole region, since there is NO constraint on the region. And the funny thing on the region is that there has been DIRECTED EVOLUTION. It all ends, as usual, in a PARADOX. Is't a characteristic of false paradigms.
M:
Interesting that you missed this direct comment to Svante's 1995 review
Absence of polymorphism at the ZFY locus on the human Y chromosome.
Dorit RL, Akashi H, Gilbert W.
Department of Biology, Yale University, New Haven, CT 06511, USA.
DNA polymorphism in the Y chromosome, examined at a 729-base pair intron located immediately upstream of the ZFY zinc-finger exon, revealed no sequence variation in a worldwide sample of 38 human males. This finding cannot be explained by global constraint on the intron sequence, because interspecific comparisons with other nonhuman primates revealed phylogenetically informative sequence changes. The invariance likely results from either a recent selective sweep, a recent origin for modern Homo sapiens, recurrent male population bottlenecks, or historically small effective male population sizes. A coalescence model predicts an expected time to a most recent common ancestral male lineage of 270,000 years (95 percent confidence limits: 0 to 800,000 years).
PB:
In conclusion, the falsification still stands.
M: In conclusion, you have provided nothing substantive...try again and don't beat up any of those Yanomamo on the way home...
cheers,
M

This message is a reply to:
 Message 227 by peter borger, posted 11-13-2002 6:48 PM peter borger has not replied

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


Message 236 of 317 (22640)
11-14-2002 4:33 AM
Reply to: Message 234 by peter borger
11-13-2002 9:57 PM


PB: A bit prickly today? However, I am not putting words in your mouth, I was drawing a conclusion from the data in the PNAS paper. These data are a clearcut falsification of common descent and the molecular clock.
M: Nope not prickly but if your tactic is to attribute statements to me that I did not make then it is clear that you have completely lost this debate. Other than your offhand remark about the data being a clearcut falsification, you will have to actually explain why...you avoided this issue completely when SLPx presented raw data (which you claim to prefer) and asked you to point out the non-random mutation. So go for it...we have all only been waiting for about half a year for this.
PB: Please mind your words, Mammuthus. "Pathetically weak... left to you" does not sound like an argument. Better explain how you see the molecular clock, and convince me with scientific arguments that your visions are right.
M: Pathetically weak is an apt characterization as you have not yet again attributed to me, the polar opposite of what I initially stated..I claimed I do NOT see why evolution, even neutral evolution should provide a reliable clock. Do your homework and you might even find out why yourself.
PB: All the paper showed are the polymorphisms in the HVR-1 region of mtDNA and according to these data there is NO molecular clock.
M: How perceptive of you...the paper was just a picture of the sequence I take it? And all those funny little objects around the figures..most of us call them words...what did they say about it?
PB: Are you a bit prickly today? However, although it is not compulsory to addressing questions I would appreciate it. The EXTRAORDINARY evolutionary claims require EXTRAORDINARY scientific evidence.
If you don't want to discuss evolutionary topics, why did you register to this board? I am under the impression that you registered to educate me on evolutionism (remember your first letter?). So, here is an excellent challenge to help me understand evolutionism. Please explain how you see it. [Or, maybe you could recommend a review on the controversy. Thanks.]
M: Wow are you one heck of a megalomaniac...you think I registered on EvC to educate you...yes I have been searching the internet all my life for Peter Borger to bring him out of the dark ages of ignorance that he is clinging to...LOL!!!! You are so freaking lazy Pete. You want to claim you have easily refuted evolution yet you are unable to even find references on your own...I really hope your scholarship is many orders of magnitude more thorough for your asthma research.
My claims are completely mainstream Peter...you are the one making claims to morphogenetic fields, creatons, and non-random mutations. The first two you have refused to even debate much less provide support for and the last you have been unable to support since your entry on this board...I suggest YOU support your claims with a nice big post full of citations (not reviews not novels) from primary literature supporting each one of your thus far unsupported claims.
Well..here is Mommy to spoon feed Petey Wetey again...
Ayala FJ. Related Articles, Links
Molecular clock mirages.
Bioessays. 1999 Jan;21(1):71-5. Review.
M: And I see you had no answer to my question. My understanding is fine. That you do not is obvious.
PB: If it is not difficult to understand, please explain the PNAS data to me.
M: And I see you still have no answer to my question...I know Peter, science is tough..maybe you will get it some day.
PB: A nice flame War? Who are you really Mammuthus? A deep dark inside? Keep it scientific please. Besided, you claimed selection so proof it!
M: What is a deep dark inside? Anyway, you are accusing me of not answering questions that You did not answer and attributing positions to me that I did not take...so you keep it scientific...and answer the question. I will then gladly answer.....and who I am would not really be so unbelievably difficult to figure out
PB: Your friend Wagner, among others. Evolutionary theorists on genetic redundancies introduced this concept. I introduced the concept of neutral seletion for the alpha actinin genes. You need this concept to explain these redundant genes. If you don't need this concept, please explain.
M: Not sure what you are talking about here...I posted papers from Nei not Gunther Wagner. You also seem to find some need to attribute lots of friends to me....I mean, I am a popular guy but hey..not that popular.
PB: Your remark on stuff residing in the genome waiting for someting.
M: Oh, that remark that I never made..I see.
PB: I am rather curious about how much selection purification of redundant genes require. You are the proponent of an extraordinary claim....
M: As much as they need ....wow Peter...it so much easier if I just make my posts like yours.
PB: Dim? I'd rather call it bright.
M: I don't think the tactic is particularly bright (note: I am not calling you generally dim or claiming that you are otherwise not bright)
PB: Usually the environment does not change a lot. Sometimes, environments change overnight. For instance after meteor impacts, ice ages, total earth crust crushes, etc. Fortunately organisms have a multipurpose genome that interacts with creatons, so they can immediately adapt.
M: You think the environment does not change a lot and that ice ages are overnight?? LOL!!!!!!!!!!!!!!!!!
As to the second part...show us the evidence.
PB: Of course! There is always selection. Selection AGAINST. The issue here is, since I reason from a distinct paradigm, we can never come to the same conlusions.
M: No wonder you have so much trouble with understanding population genetics and evolution...you think selection is constant...well, that explains a lot of the conceptual problems you have...it also is the underpining of your strawman arguments.
PB: Dear mammuthus, it is elementary that stable DNA sequences can't reside in the genome longer than one generation without repair mechanism. Even the simplest organisms have a complete set of repair enzymes. It is a prediction of MPG hypothesis. I checked it and it is true (PNAS 2002, 99:9509).
M: Do a PCR with a repair deficient Taq, clone the product and sequence the clones....after multiple replication cycles the sequence will remain stable without repair and with accumulation of RANDOM mutations in some individual clones...your claim is false. You claim that the appearance of identitiy of descent is due to non-random processes yet all data sets you have seen you claim are random mutations masking non-random...thus, no evidence for your model. In addition, there is no such thing as a "complete" set of repair enzymes...bacteria have different repair mechanisms from humans...which one of us is complete?
PB: I have the feeling that you don't understand the concept of the MPG. Maybe, you don't want to understand or you cannot think beyond the paradigm of evolutionism.
M: I understand that you are proposing a hypothesis with several non-testable components (creatons etc), that is internally inconsistent (non-random with random, stable yet plastic), with several of the initial claims falsified...it needs a lot of work Peter.
PB: The whole discussion is meaningless (Nei's paper). If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.
M: Great clarification Peter...so I will take it to mean you could not understand Nei's papers as all.
PB: Only just-so statements. Not much of a discussion. So, meaningless.
M: Great further clarification Peter...not much of a discussion...so meaningless
PB: Apparently these experiments have never been published. Or do you mean the reference below? If so, than I have to disappoint you. It is NOT an experiment it is interpretations of data. You know the difference, I hope. (If not, it explains a lot ).
M: So I guess you are willing to retract all of your papers now to Peter..I mean you did not actually see the change in gene expression..you inferred it from your experiments..I look forward to the retraction letter...
PB: If I have to retract, all inferred papers have to be retracted.
M: So you mean now that it is ok for YOU to do inferrential work but not Caroll et al.? Interesting....peer review Tuesday, Peter review Thursday?
M: Me? I bumped both an entire thread and multiple posts multiple times without EVER getting an answer from you other than " oh, I missed that"...you are becoming an expert at avoidance. I have responded to all of your points in all of your mails...I have even responded to mails of yours to other people. So you are either being lazy or dishonest.
PB: This thread was posted by Quetzal, not me. If time is there I will expand on this topic, but not now. I can make up my own thread, I don't need Quetzal's help.
M: The thread was unanswered, bottom line...I bumped it repeatedly..and this does not address the other posts that I made that went to this day unanswered.
PB:
And, it is true that I often mis reponses since I do not get a message in my postbox. If you want to have an immediate response, please send a direct mail.
M: I prefer to have the debate on the public forum where others can contribute to both our sides....though given the length of our posts to each other, I find it hard to imagine anybody reads them but the two of us.
PB:
Best wishes, and have a nice weekend,
[I hope you're not so prickly next week.]
M: Have a nice weekend to....no promises about being prickly (I see you liked that word)
How do you say ciao in Dutch?
ciao
Mammuthus

This message is a reply to:
 Message 234 by peter borger, posted 11-13-2002 9:57 PM peter borger has not replied

  
Itzpapalotl
Inactive Member


Message 237 of 317 (22646)
11-14-2002 6:32 AM
Reply to: Message 227 by peter borger
11-13-2002 6:48 PM


Hi peter B.
I thought you might be interested in some references on selection at 'silent' loci:
L. D. Hurst and C. Pal. Evidence for purifying selection acting on silent sites in BRCA1. Trends Genet. 17 (2):62-65, 2001.
T. I. Orban and E. Olah. Purifying selection on silent sites -- a constraint from splicing regulation? Trends Genet. 17 (5):252-253, 2001.
L. Cartegni, S. L. Chew, and A. R. Krainer. Listening to silence and understanding nonsense: exonic mutations that affect splicing. Nat.Rev.Genet. 3 (4):285-298, 2002.
The reason selection can act at these 'silent' sites is that mutations in them affect the final protein so although they are silent with respect to the amino acids they code for they are not with respect to splicing factors. What you end up with is selection against mutations that grossly alter protein structure. Most silent mutations do not affect protein structure so there is still room for neutral evolution its just something that must be considered when examining patterns of mutation and drawing concluions from that.

This message is a reply to:
 Message 227 by peter borger, posted 11-13-2002 6:48 PM peter borger has replied

Replies to this message:
 Message 259 by peter borger, posted 11-15-2002 5:07 PM Itzpapalotl has not replied

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


Message 238 of 317 (22660)
11-14-2002 8:34 AM
Reply to: Message 221 by peter borger
11-12-2002 4:48 PM


quote:
Originally posted by peter borger:
Dear Dr Page,
I had a look at the sequences.
Easy to explain. Non-random in conjunction with random mechanisms give the illusion of common descent. I will study these sequences in detail, and respond to it next month (or so).
Best wishes,
Peter

Great deduction.
Now tell us all which ones are which.
You must be able to do this, lest your 'theory' be vacuous.

This message is a reply to:
 Message 221 by peter borger, posted 11-12-2002 4:48 PM peter borger has not replied

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


Message 239 of 317 (22687)
11-14-2002 11:08 AM
Reply to: Message 224 by Fred Williams
11-12-2002 7:12 PM


[QUOTE]Originally posted by Fred Williams:
[B]
quote:
What example? Oh yes - an example of a gene duplication and subsequent mutation that conferred a benefit to the population. The series of gene duplications in what we now call the beta globin gene cluster, a group of 5 genes and a pseudogene. Epsilon-globin,
MEGAROTFL! I must say you are consistent! Perhaps you should let me write your posts for you, I know what you are going to say before you say it! [/quote]
Oh, you are so clever Fred! You knew I was going to write this? Why didn't you pre-resond, then?
quote:
Following is an important question for Scott to answer for the audience.
Scott, please tell the audience when you believe this duplication + subsequent mutation event occurred? Thanks!
I will go with the evidence. You will go with your fairy tale protection.
http://opbs.okstate.edu/~melcher/PE/PE41.html
"The phylogenetic distribution of globin genes is consistent with their degrees of divergence."
There is lots more, of course, but most is farily technical and I know that it is over your head.
No time line is mentioned there - but the time does not really matter, does it? You are just producing your usual red herrings, or is it double standards? For do you not assume a priori that the earth is no more than 10,000 years old (talk about megaROFTLMAO!) whenever you engage in your little ego-stroking fests?
The difference is, Williams, I can actually produce evidence supportive of my claims.
You produce accusations, repeated assertions, and bombast.
What Williams the creationist does not understand is that there are valid reasons for accepting the time frame.
As I indicated before - let the hand-waving and dodging begin.
No legitimate rebuttal? Insult insult insult! Accuse of 'fallacious reasoning'! Yeah, thats the ticket to Heaven!
quote:
(I’m swamped, but will try to get to FK’s strawman and other replies tomorrow)
I take it then that you are just going to ignore the other aspects of my post?
Perhaps you are not the genetics and information theory expert that you tell everyone you are...
So, were you ever planning to support your claims?
Or are you content to just do your little flame dance?

This message is a reply to:
 Message 224 by Fred Williams, posted 11-12-2002 7:12 PM Fred Williams has not replied

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


Message 240 of 317 (22703)
11-14-2002 11:46 AM
Reply to: Message 229 by Itzpapalotl
11-13-2002 7:24 PM


quote:
Originally posted by Itzpapalotl:
quote:
here’s the target: gene duplication followed by subsequent mutation that provides a new benefit to the population as a whole. Find this, and you have a BINGO.
How about this:
L. Chen, A. L. DeVries, and C. H. Cheng. Evolution of antifreeze glycoprotein gene from a trypsinogen gene in Antarctic notothenioid fish. Proc.Natl.Acad.Sci.U.S.A 94 (8):3811-3816, 1997.
Trypsinogen duplicated (clear molecular relics of origin) then mutated to give new benefit (resistance to freezing) to the population of these antarctic fish.
You might also want to read: M. Long. Evolution of novel genes. Curr.Opin.Genet.Dev. 11 (6):673-680, 2001.

LOL! Come on guys, you're killing me!
Itzpapa, please tell us when this event was observed in the lab. Tanks a bunch!
It looks like you missed my helpful hint to Scott:
Page not found - Nizkor
What is ironic about your citation is that it is actually evidence for adaptive mutation. Of course the NDT die-hards will dismiss this!
"New research shows that fish in the Antarctic and Arctic oceans, at opposite ends of the earth, independently evolved nearly identical antifreeze glycoproteins."

This message is a reply to:
 Message 229 by Itzpapalotl, posted 11-13-2002 7:24 PM Itzpapalotl has replied

Replies to this message:
 Message 241 by Itzpapalotl, posted 11-14-2002 1:27 PM Fred Williams has not replied
 Message 246 by derwood, posted 11-14-2002 2:59 PM Fred Williams has replied

  
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