Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
1 online now:
Newest Member: popoi
Post Volume: Total: 915,817 Year: 3,074/9,624 Month: 919/1,588 Week: 102/223 Day: 13/17 Hour: 0/0


Thread  Details

Email This Thread
Newer Topic | Older Topic
  
Author Topic:   molecular genetic evidence for a multipurpose genome
Quetzal
Member (Idle past 5872 days)
Posts: 3228
Joined: 01-09-2002


Message 211 of 317 (22320)
11-12-2002 1:35 AM
Reply to: Message 210 by peter borger
11-12-2002 12:11 AM


quote:
PB: You are lagging behind, I responded to all Quetzal’s points. He choose not to respond to all my replies.
Given the substance-less nature of your last two replies to me, perhaps you could detail - in simpler form for those of us without your "expertise" - exactly what assertion or question I have not addressed. With 8000 plus words to wade through desperately seeking some actual argument, it is quite possible to have missed something inadvertently.
In the meantime, my previous post awaits your attention.
[This message has been edited by Quetzal, 11-12-2002]

This message is a reply to:
 Message 210 by peter borger, posted 11-12-2002 12:11 AM peter borger has replied

Replies to this message:
 Message 212 by peter borger, posted 11-12-2002 3:13 AM Quetzal has replied

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


Message 212 of 317 (22323)
11-12-2002 3:13 AM
Reply to: Message 211 by Quetzal
11-12-2002 1:35 AM


Dear Quetzal,
You write:
Given the substance-less nature of your last two replies to me, perhaps you could detail - in simpler form for those of us without your "expertise" - exactly what assertion or question I have not addressed.
I write:
If you mean by 'substance-less nature' that I addressed all your nine issues in a succinct way, I agree with you.
You write:
With 8000 plus words to wade through desperately seeking some actual argument, it is quite possible to have missed something inadvertently.
I say:
I concisely responded to your 9 issues in my previous letter.
I didn't use 8000 words in my previous mail, not even 800. What you do now is going off on a tangent. Irrelevant stuff. Even if I choose to rebut you in 8000 words, it still is a rebuttal. You choose not to reply to my responses, but rather send in 4 new issues. If these issues are your primary points --the essence to be addressed-- better prepare properly for my reply.
You say:
In the meantime, my previous post awaits your attention.
I say:
In the meantime, I am looking for Dr Peakalls email address. It seemed that you have it, and I wondered whether you could provide me with it. To find out whether or not he stands behind his words. I thank the audience will like that to. Since I am accused --and this is my last chance (before what happens? Execution?)-- I'd better call in some experts of the field. Let's get the information first hand. So, let's hear Peakall as the first witness. Thanks for your cooperation,
See you in court
Best wishes,
Peter

This message is a reply to:
 Message 211 by Quetzal, posted 11-12-2002 1:35 AM Quetzal has replied

Replies to this message:
 Message 214 by Quetzal, posted 11-12-2002 4:48 AM peter borger has replied

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


Message 213 of 317 (22327)
11-12-2002 4:46 AM
Reply to: Message 210 by peter borger
11-12-2002 12:11 AM


PB: By "profound misunderstanding" you must mean "comments on evolutionism just-so stories". By now you should have known that I prefer to think for myself. I can analyse the data for myself, and I can interpret the data for myself. The data that are not in accord with molecular mechanism of evolutionism, I mailed to this site. You choose to deny them. I don't mind. Deny as often as you like. It doesn't make your pet theory a better theory.
M: No, by profound misunderstandings I mean you have shown a steadfast inability to grasp concepts in developmental biology, population genetics, and evolutionary theory (which is strange if you oppose it) coupled with an unwillingness to inform yourself and then handwaving about how evolution is wrong even though you don't know what it is. That does not amke your fantasy hypothesis any better either.
PB: I mailed my comments on the ZFY region again. Maybe you can respond a bit on it, now. Haven't had any substantial responses, yet.
M: I will..but I feel that you are not giving particularly substantial responses to many posts i.e. Quetzal's either.
M: Sounds like selection not non-random evolution. As to expectations of mutations...there is a probability of mutation not an expectation that they occur. A perfectly weighted coin is expected to give heads and tails 50:50 but it seldom meets this expectation...try it and see. Erlandsson found point muations, deletions, and transpostion events throughout the ZFX/ZFY region...you can look at their raw data to...thus, the available data does not falsify evolution.
PB: Selection on neutral positions? Dear Mammuthus, at least 20% of this region is neutral. Ever heard of the neutral third codon positions of the redundant genetic code? The odds are against your simplistic presentation, as demonstrated on this site by your friend Fred. If you throw often enough the odds will be 50:50.
M: And that is where your arguement fails...if you throw often enough. How often do you think the die have been thrown here. Fred only demonstrated that he knows even less about this subject than you so I don't see your point with that comment. That is the problem for you..this is a demonstration of random mutation...not mutations where Peter wants to see them.
M: Build up as many strawmen as you like Peter. I do not believe in an accurate clock because of selective sweeps, bottlenecks, and founder events among lineages that can completely screw up the coalescence time and give an inaccurrate date. Also, since it is a random process, there is only a probability of the clock ticking, not that it actually will for a given sequence. A real clock does not have this type of statistical fluctuation as a variable. If you actually would read some literature on the subject you would see why this is the case but...you won't. Your claims as to WHAT neutral evolution says are meaningless as you have steadfastly refused to educate yourself regarding evolutionary theory or population genetics...I could do the same as what you are doing as follows..creationism posits that big hairy priests insert bananas in their rectums thus causing the creation of kinds..why do you hold to this rectal banana theory Peter? Is it your evil oppressive christian imperialism that blinds you?...(M exits creationism mode)
PB: Maybe you don’t believe in an accurate clock. But the HVR-1 mtDNA sequences presented by Adcock et al (PNAS 2001, 98:537-542) demonstrate with respect to human reference sequence 29 differences for bonobo, 24 for chimp, 27 for neanderthaler. I do not even see a RUDIMENTARY clock in these data. How about you? It should also be noted that an ancient homo sapiens (dated 62,000 BP) demonstrates 10 differences compared to reference sequence. Let me guess, bonobo/chimp and man have a common ancestor around 150.000 years ago? Nice believes you're holding to.
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. I guess since your arguments are so pathetically weak this is the only strategy left to you. Did you even read how they calculated the clock rate in the damn paper? I explained why I don't put much stock in molecular clocks, particularly recent events (last million years). You clearly did not understand it. 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: It is a 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: 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. 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: 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: So you are a neutralist?
M: What makes you say that?
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: 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. Do you beleive the environment is constant everywhere always? 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
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: The whole discussion is meaningless. If I write discussions like that, I could forget about my papers. The peer reviewers would immediately return my manuscripts with the comment: Meaningless nothingness.
M: Great clarification Peter...so I will take it to mean you could not understand Nei's papers as all.
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: 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.
cheers,
M

This message is a reply to:
 Message 210 by peter borger, posted 11-12-2002 12:11 AM peter borger has replied

Replies to this message:
 Message 234 by peter borger, posted 11-13-2002 9:57 PM Mammuthus has replied

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


Message 214 of 317 (22328)
11-12-2002 4:48 AM
Reply to: Message 212 by peter borger
11-12-2002 3:13 AM


I don't give out anyone's email address on-line, even if they are freely available. However, as was pointed out, he's at the ANU, feel free to look it up. Here's the ANU website: ANU
Oh, and btw, you appear to have misunderstood me. Although you responded to my post 171 the response can in no way be considered substantive - indeed, you merely repeated your original assertions and collected a few more ad hominems to your credit. That being the case, I tried to make it easy on you in post 205 by succinctly restating the question and the arguments I have used over the course of now 15 pages so that there could be no confusion on your part. You have not answered. Answer the specific question in post 205. Discuss the four explanations, formally and in sufficient detail to show your self-proclaimed expertise on the subject.
[This message has been edited by Quetzal, 11-12-2002]

This message is a reply to:
 Message 212 by peter borger, posted 11-12-2002 3:13 AM peter borger has replied

Replies to this message:
 Message 223 by peter borger, posted 11-12-2002 5:23 PM Quetzal has replied

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


Message 215 of 317 (22329)
11-12-2002 4:49 AM
Reply to: Message 207 by peter borger
11-11-2002 5:43 PM


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

____________________--
Hi Peter,
Thank you for the admission...but that was not acutally my point. You claimed nobody had responded to you on the issue of ZFX and ZFY and I was correcting you by saying I had posted to you on the subject.

This message is a reply to:
 Message 207 by peter borger, posted 11-11-2002 5:43 PM peter borger has not replied

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


Message 216 of 317 (22332)
11-12-2002 5:17 AM
Reply to: Message 208 by peter borger
11-11-2002 8:55 PM


Thus, at least 5% variation in this region is observed between human and great apes.
The absence of variation in the ZFY region in humans is very awkward, and, according to the authors, cannot be ascribed to a chance (=random mechanism)
M: = Peter's misunderstanding of randomness not the authors.
Introns are thought to be subject to neutral evolution, and variation within the human population is predicted on neutral positions. Confronted with the peculiar situation of the absence of variation, the authors must apply statistics to define an era when the common ancestor of all males lived. They estimate that ‘Y-chromosome Adam’ lived around 270.000 (range 0-800.000) years before present (REF1).
It should be noted that the non-variant intron sequences in the ZFY region provides a severe problem for evolution biologists, since molecular rules demand some neutral evolution, and thus, variation on silent positions. But, he authors state that ‘the invariance likely may results from a selective sweep, a recent origin of modern Homo sapiens, or a historically small effective male population sizes’ (REF1).
M: 1. the entire intron is not neutral..you do know that there are conserved features of introns?..guess not.
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:
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:
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?
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!
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.
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:
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...
Do evolutionists really understand their own theories?
M: They do...you don't...to bad.
PB:
The proposal that the sequence has been retained without conservation requirement would still imply that the SRY protein is expected to evolve at a NEUTRAL rate! The peculiar thing about the SRY proteins was, however, that they are much more variable than predicted by neutral evolution. To properly understand this one has to assume SELECTION ON NEUTRAL POSITIONS!
M: Or to properly understand it one has to realize that different mammals have undergone different histories so one does not expect mice and men to be identical....nice try Peter...let's throw reptiles and Drosophila in (which have totally different sex determining mechanisms)..and maybe Daphnia which can reproduce parthenogenetically to confuse you some more.
PB:
I can imagine that evolution biologists really get frustrated solving the riddles around the SRY region. Despite several ad hoc hypotheses it all ends, again, in a paradox. Apparently, there is no evolutionary explanation for the high degree of dissimilarity of SRY region between distinct primates.
M: You mean that primate M. musculus
PB:
It points in the direction of directed, non-random mechanism. It is clear that invariability of this haploid region in humans is ensured by specific DNA guarding and stabilising proteins. All in accord with the MPG hypothesis.
M: If it is so clear, you should be able to find a citation for such a DNA repair enzyme....and since you claim you can find abstracts on your own (though ironically you seem unable in our other debates) I am sure you have read all of these papers (though it is only a small subset of the available literature of which you must clearly have read before jumping to conclusions)
Note, they are not all primates either...i.e. goats are not primates and niether are cats.
J Mol Evol 2002 Jan;54(1):54-61 Related Articles, Links
Comparison of substitution rates in ZFX and ZFY introns of sheep and goat related species supports the hypothesis of male-biased mutation rates.
Lawson LJ, Hewitt GM.
School of Biological Sciences, University of East Anglia, Norwich NR4 7TJ, UK. lori.lawson@ebc.uu.se
There is a growing body of evidence that males serve as the major generators of mutations, due to the larger number of cell divisions involved in sperm compared to egg production. In mammals, this hypothesis (referred to as "male-driven evolution") has been tested by comparison of nucleotide substitution rates on the X and Y sex chromosomes in a limited number of taxa, predominantly primates and rodents. This study asks whether male-driven evolution is a more general phenomenon among mammals, by comparison of paralogous ZFX and ZFY intron sequences in sheep and goat species (the tribe Caprini). The male-to-female mutation ratio, alpha(m), was estimated to be between 2.93 (95% CI, 1.51-8.61) and 3.94 (95% CI, 1.25-32.29) when calculated using pairwise distance and branch length, respectively, suggesting that the Caprini are subject to weak, male-driven evolution. Comparison to published values for primates, felids, and rodents implies that there may be some correlation with reproductive life span. However, this is difficult to test with current data because confidence intervals are large and overlapping. Nonindependent evolution of paralogous sequences and/or the presence of selective constraints could lead to inaccurate estimates of alpha(m). No evidence for gene conversion between the ZFX and the ZFY introns was found, and this suggests that they have evolved independently during the radiation of the Caprini. Finally, there was no apparent evidence that these introns are subject to selective constraints, although low levels of intraspecific polymorphism reduce the power of neutrality tests.
Mamm Genome 2001 Jan;12(1):17-21 Related Articles, Links
Sex determination without the Y chromosome in two Japanese rodents Tokudaia osimensis osimensis and Tokudaia osimensis spp.
Sutou S, Mitsui Y, Tsuchiya K.
National Institute of Bioscience and Human-Technology, Tsukuba, Ibaraki, Japan. sutou@nibh.go.jp
Both males and females of the species of spinous country-rats (Tokudaia osimensis osimensis, T.o.o., Rodentia: Muridae), which live on Amami Oshima Island, a southern Japanese island, have 25 chromosomes. Another species of spinous country-rats (Tokudaia osimensis spp., T.o. spp., which live on Tokunoshima Island 40 km south of Amami Oshima Island, also have an odd number of chromosomes, 45. Karyotypes of males and females by the G-band method were indistinguishable in both populations. The lesser number of chromosomes (25) of T.o.o. is likely to be a result of Robertsonian fusions of 45 chromosomes of T.o. spp. that seem to be the offspring of another spinous country-rat Tokudaia osimensis muenninki (T.o.m.), which live on Okinawa Island and have 44 chromosomes including the X and Y Chrs. The lengths of the non-paired, putative X-Chr of T.o.o. and T.o. spp. occupied roughly 3.2% and 1.7% of the total lengths, respectively, hinting at translocation or exchange of a part of the X Chr and thus in violation of Ohno's Law. Southern blot analysis with murine Sry as a probe indicated that these two animals do not have Sry. When Zfx from T.o. spp. was used as a probe, both males and females of T.o.o. and T.o. spp. showed two bands, suggesting possible translocation of Zfy from the Y Chr. Comparison of physical characteristics, constituents of chromosomes, and sex-determination methods of these three Tokudaia country-rat populations suggests that each is endemic to each island and constitutes an independent species. These specialized species would provide us with clues to elucidate the mechanisms of primary sex determination and karyotype evolution in mammals.
Proc Natl Acad Sci U S A 2000 May 9;97(10):5307-12 Related Articles, Links
Novel gene conversion between X-Y homologues located in the nonrecombining region of the Y chromosome in Felidae (Mammalia).
Pecon Slattery J, Sanner-Wachter L, O'Brien SJ.
Laboratory of Genomic Diversity, National Cancer Institute, Frederick Cancer Research and Development Center, Frederick, MD 21702, USA. Slattery@mail.ncifcrf.gov
Genes located on the mammalian Y chromosome outside of the pseudoautosomal region do not recombine with those on the X and are predicted to either undergo selection for male function or gradually degenerate because of an accumulation of deleterious mutations. Here, phylogenetic analyses of X-Y homologues, Zfx and Zfy, among 26 felid species indicate two ancestral episodes of directed genetic exchange (ectopic gene conversion) from X to Y: once during the evolution of pallas cat and once in a common predecessor of ocelot lineage species. Replacement of the more rapidly evolving Y homologue with the evolutionarily constrained X copy may represent a mechanism for adaptive editing of functional genes on the nonrecombining region of the mammalian Y chromosome.
Mol Biol Evol 1999 Nov;16(11):1633-40 Related Articles, Links
Is selection responsible for the low level of variation in the last intron of the ZFY locus?
Jaruzelska J, Zietkiewicz E, Labuda D.
Institute of Human Genetics, Polish Academy of Sciences, Strzeszynska, Poland.
DNA variability was investigated in the last intron of the Y-chromosome-specific zinc finger gene, ZFY, and its X homolog on Xp21.3, ZFX. No polymorphisms were found in the 676-bp ZFY segment in a sample of 205 world-wide-distributed Y chromosomes, other than a solitary nucleotide variant in one individual (nucleotide diversity pi = 0.0014%). In contrast, 10 segregating sites (pi = 0.082%) were identified within 1,089 bp of the ZFX sequence in a sample of 336 X chromosomes. Four of these polymorphisms, which contributed most of the diversity, were located within an Alu insert disrupting the ZFY-ZFX homology (pi Alu = 0.24%). The diversity in the homologous portion of the ZFX intron, although higher than that in ZFY, was lower than that found in genomic segments believed to evolve neutrally; interspecies divergence in both segments was also reduced. Although this suggests that the evolution of both ZFY and ZFX homologs may not be entirely neutral, both Tajima and HKA tests did not reject neutrality. The lack of statistical significance may be attributed to a lack of power in these tests (the low divergence and variability values reduce the power of the HKA and Tajima tests, respectively); furthermore, Homo sapiens has recently undergone a rapid population growth, and selection is more difficult to detect in an expanding population. Therefore, the failure to reject neutrality does not necessarily indicate the absence of selection. In this context, the phylogenetic argument was given more weight in out interpretations. The high level of sequence identity in ZFY and ZFX segments, in spite of their separation 80-130 MYA, reflects a lower mutation rate as compared with other segments believed to undergo unconstrained evolution. Thus, the possibility of weak selection contributing to the low level of nucleotide diversity in the last ZFY intron cannot be excluded and should be kept in mind in the population genetics studies based on Y chromosome variability.
Mol Biol Evol 1993 Mar;10(2):271-81 Related Articles, Links
Evolution of the Zfx and Zfy genes: rates and interdependence between the genes.
Pamilo P, Bianchi NO.
Department of Genetics, Uppsala University, Sweden.
A phylogenetic analysis of sex-chromosomal zinc-finger genes (Zfx and Zfy) indicates that the genes have not evolved completely independently since their initial separation. The sequence similarities suggest gene conversion in the last exon between the duplicated Y-chromosomal genes Zfy-1 and Zfy-2 in the mouse. There are also indications of conversion (or recombination) between the X- and Y-chromosomal genes in the crab-eating fox and in the mouse. The method for estimating synonymous and nonsynonymous substitutions is modified by incorporating the substitutions in the twofold-degenerate sites in a novel way. The estimates of synonymous substitutions support the generation-time hypothesis in that the obtained rates are higher in mice (by a factor of 4.7) than in humans and higher in the Y-chromosomal genes (by a factor of 1.9) than in the X-chromosomal genes.

This message is a reply to:
 Message 208 by peter borger, posted 11-11-2002 8:55 PM peter borger has replied

Replies to this message:
 Message 227 by peter borger, posted 11-13-2002 6:48 PM Mammuthus has replied

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


Message 217 of 317 (22348)
11-12-2002 10:30 AM
Reply to: Message 209 by peter borger
11-11-2002 10:17 PM


Everything, it seems, can be used by the creationist as 'evidence' for their preferred hocus pocus...
That you do not accept the valid explanations presented for the lack of polymorphism in a ZFY intron in humans is your issue. You can claim that you have one 'example' of your 'non-Darwinian' beliefs, sadly, one such anomoly, if we are kind enough to grant it to you in the hopes of going on, is hardly sufficient to topple NDT or 'prove' whatever it is you believe in.
quote:
Originally posted by peter borger:
Dear Dr Page,
Your examples are all in accord with the multipurpose genome. Lets start with your reference:
From the abstract:
"Transgenic analysis of Cyp6 1 shows that overtranscription
of this gene alone is both necessary and sufficient for resistance. Resistance and up-regulation in Drosophila populations are associated wit a single Cyp6 1 allele that has spread globally. The allele is characterized by the insertion of an Accord transposable element into the 5' end of the Cyp6 1 gene."
What does the MPG hypothesis predict (see mail #1):
The concept 'multipurpose genome' holds that:
1) DNA sequences —although plastic-- are stable throughout time,
Amazingly, that is what NDT says!
quote:
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
Amazingly, that is what NDT says!
quote:
3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory],
Amazingly, that is what NDT says!
Well, accept for this 'degenration theory' - since this is labelled a 'theory', perhaps you can point in the direction wherein I can read for myself what must be voluminous documentation for this theory.
Of course, adaptive evolution results in an accumulation of new genetic information. But you knew that....
quote:
4) the function of natural selection is to remove degenerate organisms, and
Amazingly, that is what NDT says! Of course, the "non-degenrate" or better adapted organisms are selected for. So far, all I see is a co-option of NDT .
quote:
5) there is/has been creation (=creaton interactions with matter in a morphogenetic field giving rise to genes and genetic programs in preexisting genetic programs).
Now here is where you go off the deep end.
Evidence for "creatons" please.
Evidence for morphogenic fields, please.
Evidence that you are refilling your prescriptions, please.
quote:
Point #3 predicted your observation.
It did? Can I see the documentation for this? Hindsight is, afterall, 20/20. I would like to see the paper outlining the likely pesticide resistence strategies encumbent upon mosquitos having a multipurpose genome.
Thanks.
quote:
So, I do not see a problem for the MPG hypothesis here. The other examples are similar. They all involve differential gene regulation. As predicted by the MPG hypothesis.
Yeah, I guess no evolutionary biologist/geneticist had ever even thought about differential gene expressions.
Wow. I guess NDT is all wrong...
So, how does that fare for the creationist information arguments?
quote:
The ball is back in 'your' ZFY region.
Best wishes,
Peter
Already addressed. You have taken the "fingers in ears shouting LALALALAL" approach. What could I possibly add?
[Fixed quoting. --Admin]
[This message has been edited by Admin, 11-12-2002]

This message is a reply to:
 Message 209 by peter borger, posted 11-11-2002 10:17 PM peter borger has replied

Replies to this message:
 Message 222 by peter borger, posted 11-12-2002 4:53 PM derwood has replied

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


Message 218 of 317 (22349)
11-12-2002 10:38 AM


quote:
PB: 5) Is evolution a phenomenon driven by random mutation?
YES
PB: Apparently NOT, judging from examples like the alpha actinin genes, the ZFY region, the 1G5 gene, etcetera.
Here is your big chance, Pete.
I have offered it to you before, and like all creationists before and likely all that will follow, you simply ignored it.
Go here:
http://www2.norwich.edu/spage/alignmentgam.htm
Apply your amazing scientific insights as they pertain to MPG.
Analyze the sequence data there, and tell us all:
Which of those nucleotide sites represent non-random changes.
Which are evidence for MPG.
Which are anomolous for MPG.
Surely, you can do this.

Replies to this message:
 Message 221 by peter borger, posted 11-12-2002 4:48 PM derwood has replied

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


Message 219 of 317 (22350)
11-12-2002 10:42 AM
Reply to: Message 207 by peter borger
11-11-2002 5:43 PM


duplicate
[This message has been edited by SLPx, 11-12-2002]

This message is a reply to:
 Message 207 by peter borger, posted 11-11-2002 5:43 PM peter borger has not replied

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


Message 220 of 317 (22351)
11-12-2002 10:42 AM
Reply to: Message 207 by peter borger
11-11-2002 5:43 PM


quote:
Originally posted by peter borger:
However, are you a neutralist or a selectionist?
Best wishes,
Peter
Informed scientists understand that the two are not mutually exclusive.

This message is a reply to:
 Message 207 by peter borger, posted 11-11-2002 5:43 PM peter borger has replied

Replies to this message:
 Message 233 by peter borger, posted 11-13-2002 8:29 PM derwood has replied

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


Message 221 of 317 (22378)
11-12-2002 4:48 PM
Reply to: Message 218 by derwood
11-12-2002 10:38 AM


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

This message is a reply to:
 Message 218 by derwood, posted 11-12-2002 10:38 AM derwood has replied

Replies to this message:
 Message 238 by derwood, posted 11-14-2002 8:34 AM peter borger has not replied

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


Message 222 of 317 (22380)
11-12-2002 4:53 PM
Reply to: Message 217 by derwood
11-12-2002 10:30 AM


Dear Dr Page,
At least the MPG hypothesis predicts properly. Something NDT/evolutiomnism lacks completely.
best wishes,
Peter

This message is a reply to:
 Message 217 by derwood, posted 11-12-2002 10:30 AM derwood has replied

Replies to this message:
 Message 242 by derwood, posted 11-14-2002 2:16 PM peter borger has not replied

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


Message 223 of 317 (22383)
11-12-2002 5:23 PM
Reply to: Message 214 by Quetzal
11-12-2002 4:48 AM


Dear Quetzal,
You say:
--------------------------------------------------------------------------------
I don't give out anyone's email address on-line, even if they are freely available. However, as was pointed out, he's at the ANU, feel free to look it up. Here's the ANU website: ANU
I say:
Thanks I will look it up and write him a letter.
You say:
Oh, and btw, you appear to have misunderstood me. Although you responded to my post 171 the response can in no way be considered substantive - indeed, you merely repeated your original assertions and collected a few more ad hominems to your credit.
I say:
That is what you do too. What's the difference?
You:
That being the case, I tried to make it easy on you in post 205 by succinctly restating the question and the arguments I have used over the course of now 15 pages so that there could be no confusion on your part. You have not answered. Answer the specific question in post 205. Discuss the four explanations, formally and in sufficient detail to show your self-proclaimed expertise on the subject.
I say:
Understanding biology is not as hard as you think it is. It depends on the paradigm. If one tries to explain things subject to a false paradigm things get hard indeed. That's the is the isue here. However, I will answer your 4 points as soon as I got Dr Peakall's response.
Best wishes,
Peter

This message is a reply to:
 Message 214 by Quetzal, posted 11-12-2002 4:48 AM Quetzal has replied

Replies to this message:
 Message 225 by Quetzal, posted 11-13-2002 2:53 AM peter borger has not replied

  
Fred Williams
Member (Idle past 4856 days)
Posts: 310
From: Broomfield
Joined: 12-17-2001


Message 224 of 317 (22394)
11-12-2002 7:12 PM
Reply to: Message 206 by derwood
11-11-2002 2:07 PM


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!
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!
(BTW, your fallacious reasoning, globin and all, was also committed by Richard Dawkins)
(Helpful clue for Scott can be found here: Page not found - Nizkor)
(I’m swamped, but will try to get to FK’s strawman and other replies tomorrow)

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

Replies to this message:
 Message 239 by derwood, posted 11-14-2002 11:08 AM Fred Williams has not replied

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


Message 225 of 317 (22438)
11-13-2002 2:53 AM
Reply to: Message 223 by peter borger
11-12-2002 5:23 PM


quote:
Q: That being the case, I tried to make it easy on you in post 205 by succinctly restating the question and the arguments I have used over the course of now 15 pages so that there could be no confusion on your part. You have not answered. Answer the specific question in post 205. Discuss the four explanations, formally and in sufficient detail to show your self-proclaimed expertise on the subject.
PB: Understanding biology is not as hard as you think it is. It depends on the paradigm. If one tries to explain things subject to a false paradigm things get hard indeed. That's the is the isue here. However, I will answer your 4 points as soon as I got Dr Peakall's response.
I'm glad you consider biology so simple. I'm looking forward to hearing your discussion. Out of curiosity, if it's so easy, why do you need to wait for Dr. Peakall to answer (which may or may not happen, depending on how you ask the question)? It doesn't even have to be the case of Wollemia specifically - just discuss why any or a combination of the four explanations I provided are NOT valid for describing an observation such as "lack of or limited variation in an isolated population".

This message is a reply to:
 Message 223 by peter borger, posted 11-12-2002 5:23 PM peter borger has not replied

  
Newer Topic | Older Topic
Jump to:


Copyright 2001-2023 by EvC Forum, All Rights Reserved

™ Version 4.2
Innovative software from Qwixotic © 2024