Register | Sign In


Understanding through Discussion


EvC Forum active members: 65 (9162 total)
3 online now:
Newest Member: popoi
Post Volume: Total: 915,806 Year: 3,063/9,624 Month: 908/1,588 Week: 91/223 Day: 2/17 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 5871 days)
Posts: 3228
Joined: 01-09-2002


Message 16 of 317 (20671)
10-24-2002 3:20 AM
Reply to: Message 12 by peter borger
10-23-2002 9:26 PM


quote:
Q: 1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.
PB: If you know so much about this tree why don't you write a letter to Dr Peakall (University of Canberra), and explain to him how it all works. I think he will be pretty pleased, so he can publish his work --at last-- in a peer reviewed scientific journal.

Actually, I did. Dr. Peakall was quite kind enough to forward to me two of his articles:
Hogbin PM, Peakall R, Sydes MA, 2000. Achieving practical outcomes from genetic studies of rare Australian plants, Aust. J. Bot. 48, 375—382
Peakall R. 1998. Exceptionally low genetic diversity in an ancient relic, the Wollemi pine: implications for conservation theory and practice. 45th Annual meeting of the Genetics Society of Australia. Abstracts 86.
From the latter:
quote:
So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.
Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.
A point of correction: Dr. Peakall is with the Australian National University in Canberra, not the "university of Canberra".
quote:
Actually there are two populations of the tree, both were analysed and demonstrated exactly the same DNA (as mentioned in letter #1). Surviving populations with invariable DNA points in the direction of a stable multipurpose genome, not in the direction of evolution.
Actually, there are THREE populations of the tree - which of course Woodford didn't know at the time he published his book. You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...
"Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...
quote:
Q: The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.
PB: If you have your information from New Scientist december 1997 than I have to dissapoint you. Coppicing was the initial thought of Peakall but according to Woodford's book (2000) it does not coppice, but sexually reproduces (see mailing #1).

Sorry to disappoint you, but I have my info from the person who actually studied the plant. You need to reread your book, as well as my post. The plant propagates by coppicing IN THE WILD. It was found during conservation planning, however, that it quite readily reproduces sexually ex situ - making it much easier to replicate the plant in collections in multiple facilities, and giving hope to the long-term conservation of the species. IOW, the species DOES produce viable seeds and pollen. The investigation into the reasons for this is on-going - and makes for quite fascinating research in its own right.
Where you are correct is that there is no evidence yet that the three populations were connected by subterranean roots (digging up the ground between the stands could be hazardous to the trees). Given the physical separation between stands, Dr. Peakall considers it unlikely. That's why there's on-going study - to answer that question.
quote:
Q: The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.
PB: That is true. Araucariacaea demonstrate very low variability and that is in accord with the hypothesis of a multiporpose genome. Low variablity due to extremely stable DNA guarded by hundreds of DNA repair enzymes. Observed variation is due to regulatory, rather than mutational phenomena. All in accord with the multipurpose genome.

Nope, wrong again. The data indicates there are evolutionary constraints in action, not some mythical multipurpose genome. See, for example, Setoguchi, H., Osawa, T.A., Pintaud, J.C., Jaffre, T. & Veillon, J.-M. 1998. Phylogenetic relationships within Araucariaceae based on rbcL gene sequences. Amer. J. Bot. 85: 1507-1516, or Hanson, L. 2001. Chromosome number, karyotype and DNA C-value of the Wollemi Pine (Wollemia nobilis, Araucariaceae). Bot. J. Linn. Soc. 135: 271-274.
In addition, the tree isn't all that similar to the Cretaceous Araucariaceae. See, for example: Chambers, T.C., Drinnan, A.N., McLoughlin, S. 1998. Some morphological features of Wollemi Pine (Wollemia nobilis, Araucariaceae) and their comparison to Cretaceous plant fossils. Internat. J. Plant Sci. 159: 160-171.
quote:
PB: What do you mean by 'argument of journalistic sensationalism'? As far as I know nothing has been published on this tree for sensationalism. Please be specific in your statements.
Lol, almost everything published in the popular press on this tree, beginning with the first accounts of its discovery, have been sensational journalism in action. "Dinosaur tree", "living fossil", "green dinosaur", etc are all splashy, flashy journalistic bombast. Even the full title of Woodford's book which you like so much, "The Wollemi Pine. The Incredible Discovery of a Living Fossil from the Age of the Dinosaurs" lends proof to my contention. Nice try.
As to the horseshoe crab and coelocanth, please start a new thread if you want to drag out these old creationist chestnuts - more examples of "argument from journalistic sensationalism".

This message is a reply to:
 Message 12 by peter borger, posted 10-23-2002 9:26 PM peter borger has replied

Replies to this message:
 Message 24 by peter borger, posted 10-24-2002 11:03 PM Quetzal has replied

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


Message 17 of 317 (20678)
10-24-2002 5:29 AM
Reply to: Message 14 by peter borger
10-24-2002 1:04 AM


dear mammuthus,
Thanks for your lenghty response.
M: Hi Peter..I aim to please ...I'll see if I can make this shorter but no promises..
PB:
Even if you found a new organism in your garden tomorrow and found out in your lab that the DNA is completely invariable it wouldn't refute anything, would it? Your a faithful believer. (Nothing inherently wrong with that, although not very scientific)
M: If I found an unusual finding I would actually confirm it rigorously before running around pronouncing I had discovered something spectacular. It is not faith but the wish to do proper reproducible scienc. If I found a new organism that showed no or little genetic variation I would test for a genetic bottleneck or whether the organism is clonal and not claim woo hoo! genetics is dead. (that you do that is both inherently wrong and non scientific.)
PB:
And that demonstrates that evolutionism is an outdated theory based on morphology. I think --and this will not be completely novel to you-- morphology is subject to DNA sequences and regulation of these sequences.
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
PB:
It should be clear now that I do not require deterministic mutations for this hypothesis. As demonstrated in this thread a major part of mutations are non-randomly introduced, i.e non-random with respect to nucleotide and position (see the 1G5 genes in Drosophila subpopulations, mtDNA in hominoids/human subpopulations).
M: It should be clear that unless the system is deterministic your entire hypothesis falls apart. You claim that similarity between organisms is solely due to non-random mechansim making them seemingly similar not because of common ancestry. I have asked without getting an answer before, do you believe you are related to your parents or was your DNA spontanously created and non-random giving the seeming appearance that you are related to them? In any case, as soon as you discover a mutation that occurs outside your "non-random" site your hypothesis is falsified and this has been observed in almost all instances.
PB:
I concur that deterministic mutations have not (yet) been detected. I already predicted where your mutations most likely will be introduced in your mtDNA in a previous mail. And if you currently have a C on those positions they will likely be a T when it mutates. Thus, the non-randomness I speak off is with respect to nucleotide and position (not when), but may have important implications for molecular phylogenetics.
M: This is not really a valid argument Peter. Sometimes you get C to G or C to A. Sometimes C to T. That C to T is more common is a purely chemical constraint. Which C to T mutates is random in a given generation. The only implication that it has for molecular phylogenetics is that the transition transversion ratio is taken into account as a variable.
PB:
By plastic I mean that preexisting sequences can be duplicated and/or shuffled.
M: So you don't believe there are point mutations, single base deletions, or complete changes in chromosomal content? You have some reading to do
The ZFX/ZFY paper also shows how point mutations accumulate in the ALU's...acutally when a HERV integrates the 5 and 3' LTRs diverge by point mutations and deletions etc etc etc.
MY RESPONSE:
All according to the evolutionary paradigm. Actually the ribosomal RNAs are a nice example of stability that is maintained by the hypothetical idea of 'concerted evolution'. You should be aware that is but a hypothesis. In fact, evolutionism requires this hypothesis otherwise it cannot explain the high level of stability within the rRNA genes. However, I wonder whether this hypothesis is still tenable and probably it has to be replaced by purifying selction soon (as observed for the histon H3 and H4 genes. The one story is replaced by the other story. You are free to believe them, I don't). The hypothesis of multipurpose simply holds that these rRNA genes are guarded by highly specific DNA repair mechanism.
(By the way, did you mean the "selfish meme" )
M: Ever hear of gene conversion? There are a lot of basic (and observed) methods of DNA sequence homogenization of which you seem to be completely unaware. Selection on 18S is not on one copy and by the way, there can be very different 18S copies within a single genome. There can also be rDNA pseudogenes.
PB:
If all mechanisms that induce variations --due to shuffling of preexisting DNA elements-- are already present than it advocates a multipurpose genome and not evolutionism. Nothing evolved, only the order of the DNA elemenst is different.
M: To bad that novelty and novel regulation does appear to refute this as the exclusive mechanism. Even for shuffled genes, the globin cluster of humans is exceptionally different from elephants....plenty of evolution occurring...
PB:
If a single point muations leads to a big enough degeneration (for instance members of the Src-family), it will be lethal and selected against.
M: You sure about that one? Sickle cell anemia and cystic fibrosis are both extremely fitness reducing diseases yet both persist in the population...heterozygotes get an advantage from carrying the "bad copy" thus a big degeneration is maintained. You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
PB:
The (sub)species that is not utilising an environment optimally is degenerate compared to the (sub)species that does. It will be selected against.
M: Hey, welcome our new evolutionary biologist Peter Borger
Actually, that is not necessarily correct either. Both may diverge so that they do not overlap.
PB:The creatons and the morphogenetic field can be inferred from the fossil record. You infer evolution from the fossil record and fill in the gaps between the phyla with hypothetical transition forms, also a non-falsifibale hypothesis. So, what is the difference?
M: If you find an animal fossil like say a mastodon that has many shared features with elephants but also pronounced differences, how is this evidence for creatons in a morphological field? Why would there be gaps in a morphogenetic field? How do you quantifiy a creaton? All untestable and non falsifiable.
Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
previous post M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.
MY RESPONSE:
Expand on the example please. If you mean shuffling I don't see a problem. If you mean SNPs I also don't see a problem.
M: So you have no problem with data that falisifies your premise that there is only variation due to shuffling of genes and not point mutations etc?
I SAY:
I don't see a problem here. The organism that doesn't produce sperm will not produce offspring and is therefore degenerate. Its DNA will disappear from the genepool.
M: But if it is a multipurpose genome obviously there should be a compensatory path for such mutation for such an important pathway. You are arguing from a strict selectionist point of view yet proposing a strictly Lamarkian pre-adaptation hypothesis...they are polar opposites.
PB:
How do you know that it is a captured retrovirus gene? It can be the other way around. The retrovirus captured the protein and used it for its envelope. It happend a lot in the virus world that they capture genes from their hosts. I thought you used this method to explain the IL-1beta incongruence?
M: Where did I say that about IL-1 beta? Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids.
PB:
No, it doesn't falsify anything (sounds familiar, in't it ). The multipurpose genome hypothesis hold that part of the genes is redundant, not all. In fact it holds that the part that is responsible for variations is redundant, and that are usually genes involved in regulation of gene expression. Hey, that is exactly what we see in biology: Redundant regulatory networks! In addition, there are also essential non-redundant genes.
M: This is totally inconsistent. You are constantly changing your terms and hypothesis around from selectionist to adaptationist and from here to partial redundant and multipurpose from only multipurpose. This is falsified by single copy genes involved in variation. If something is lacking in the genome your creatons should create it so that the organism can persist.
PB:
If an organism was created recently and doesn't yet have major defects (due to entropy acting on the genome) in DNA repair mechanisms, it is expected that the DNA does not change. That is what we see for the W. nobilis.
M: To bad that is not what we see for muskoxen and bears where we see past diversity is much greater than that of today (i.e. ancient DNA). Quetzal also gave examples of organisms that have suffered genetic bottlenecks and were not created recently. Quetzal already pointed out your complete and total error regarding W. nobilis.
.
PB:
Actually, molecular biology does not falsify this hypothesis. For instance, you showed me the '10.000 generations of bacteria reference' and it was demonstrated that SNPs were NOT abundant. Thus the sequences are stable and the phenotype-changes were merely due to shuffling/deletion/duplication of preexisting elements. All in accord with my hypothesis.
M: Actually, they only measured gene rearrangments as it was easier...this was not a test of the increase in SNPs. There are plenty of examples of phenotypic change due to point mutations or have you missed 50 years of genetics?
PB:
See my reponse to Quetzal. However, in a previous letter you concurred that such organism would overturn evolutionism. Can you please expand a bit on this contradiction.
M: The contradiction is as Quetzal pointed out, that you have not provided such an organism but have rather again shown a profound lack of population genetics knowledge. As a suggestion you may want to get a copy of Danial Hartl and Andrew Clark's Population Genetics. It is a bit too mathematical at times but it is a fairly comprehensive book on the genetics of populations. That is not meant as an insult Peter but if you don't have a foundation in the subject matter then you will be far less prepared to object to it.
I look forward to your response to this post and to that of Quetzal's regarding W. nobilis.
cheers,
M

This message is a reply to:
 Message 14 by peter borger, posted 10-24-2002 1:04 AM peter borger has replied

Replies to this message:
 Message 25 by peter borger, posted 10-25-2002 1:45 AM Mammuthus has replied

  
Itzpapalotl
Inactive Member


Message 18 of 317 (20683)
10-24-2002 7:47 AM
Reply to: Message 15 by peter borger
10-24-2002 1:55 AM


Hi peter B.
The papers are indeed very interesting but i don't see how they falsify evolution. They suggest that the neutral theory may be partly wrong and natural selection is very important in evolution but if anything thats going back to the very oldest darwinian ideas about evolution.
"Essential redundant genes are genes that can be knocked out with minor/no problems but point mutations in these genes are lethal) falsifies evolutionism"
There are many genes which it is better to have the gene deleted than a point mutated copy because the point mutated copy has a dominant harmful property. This can be seen in the genes for adhesion in the bacterium Helicobacter pylori. If a gene is knocked out adhesion still ocurs but it is mediated by other cell surface molecules but the mutated form of the gene gives rise to a stucture that prevents the other cell surface molecules from contacting cells therefore there is no adhesion. Other examples inlude many of the collagen related diseases in humans. This effect is often seen in genes that make subunits of protein rather like say the SRC family of nuclear receptor coactivators.
I don't know how resistance to mutation in genetic networks evolves or even if it has been selected for or is an accidental property of the organisation of genes, but that doesn't mean it can't have evolved. Before all the details of the interactions involved in the resistance to mutation of even one system is known speculating on weather it could or couldn't have evolved is futile.
Infect Immun 2002 Jun;70(6):3073-9. Helicobacter pylori does not require Lewis X or Lewis Y expression to colonize C3H/HeJ mice.Takata T, El-Omar E, Camorlinga M, Thompson SA, Minohara Y, Ernst PB, Blaser MJ.
Mol Microbiol 2000 Mar;35(6):1530-9. Lewis X structures in the O antigen side-chain promote adhesion of Helicobacter pylori to the gastric epithelium. Edwards NJ, Monteiro MA, Faller G, Walsh EJ, Moran AP, Roberts IS, High NJ.

This message is a reply to:
 Message 15 by peter borger, posted 10-24-2002 1:55 AM peter borger has replied

Replies to this message:
 Message 32 by peter borger, posted 10-25-2002 8:32 PM Itzpapalotl has replied

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


Message 19 of 317 (20686)
10-24-2002 8:18 AM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


PB:
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).
M:
According to this premise, all organisms in close proximity to one another should be genetically identical. Thus, when you were concieved Peter, you should have been most genetically similar to your mother, father, and any bacteria, viruses, and fungi that would have been present. If anyone else was in close proximity, they would be equally closely related to you as their matter would also be in the morphogenetic field. Ultimately, there should be no genetic differences among any humans and there should also be no more than one sex since this is also a genetic difference.
At the species level, all organisms that are in the same environment should be almost genetically identical not just to one another but to ALL organisms as they all reside and reproduce within the same morphogenetic field. Thus, South American monkey should in no way genetically resemble Old World monkey as they are not in the same field. If you posit that the field is world wide, then there should be absolutley no genetic differences between a tomato, person, bacteria.

This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has replied

Replies to this message:
 Message 20 by Quetzal, posted 10-24-2002 9:18 AM Mammuthus has not replied
 Message 23 by peter borger, posted 10-24-2002 9:02 PM Mammuthus has replied
 Message 48 by Mammuthus, posted 10-29-2002 10:09 AM Mammuthus has not replied

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


Message 20 of 317 (20697)
10-24-2002 9:18 AM
Reply to: Message 19 by Mammuthus
10-24-2002 8:18 AM


Mammuthus: I hadn't thought about that. I wonder how Peter's morphogenetic field "hypothesis" explains continuous gradations in populations of the same species over the full geographic extent of its range. One sterling example is the red-backed salamander of the eastern US (Plethodon cinereus). There is significant phenotypical variation in a gradual blending of characteristics from the southern to the northern end of the range, as well as east-west, northeast-northwest, etc. Taxonomists only divide the species into subspecies using a suite of average traits at the extreme ends of the range (and because taxonomists always want to pigeonhole organisms into neat categories). However, the geographic divisions are not only arbitrary but pretty near meaningless.
How about it Peter? Want to try and answer M's question?

This message is a reply to:
 Message 19 by Mammuthus, posted 10-24-2002 8:18 AM Mammuthus has not replied

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


Message 21 of 317 (20708)
10-24-2002 12:13 PM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


Here is another one
If genomes are multipurpose and pre-adaptive, why are most species that ever lived extinct? Mammoths and elephants are extremely similar genetically yet mammoths are extinct...surely their multipurpose genome would have rearranged to adapt to new environment? Actually, mammoths went extinct in multiple different environments so in multiple morphogenetic fields, the same result occurred...why did creatons and the morphogenetic field stop functioning worldwide at the end Pleistocene for some animals but not others in exactly the same regions i.e. mammoths, American horses, camels, giant ground sloths, cave bears, several species of birds etc. etc., but not bison, deer, wolves, etc.? Same problem for neanderthals...besides having been in the same morphogenetic field as humans they had very distinct mtDNA genomes...but why did their multipurpose redundant genomes fail to "create" more individuals or adapt to whatever the change was that caused them to become extinct?

This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has not replied

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


Message 22 of 317 (20709)
10-24-2002 12:14 PM
Reply to: Message 1 by peter borger
10-23-2002 1:57 AM


deleted by Mammuthus due to duplication of message
[This message has been edited by Mammuthus, 10-24-2002]

This message is a reply to:
 Message 1 by peter borger, posted 10-23-2002 1:57 AM peter borger has not replied

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


Message 23 of 317 (20749)
10-24-2002 9:02 PM
Reply to: Message 19 by Mammuthus
10-24-2002 8:18 AM


Dear mammuthus,
You say:
M:
According to this premise, all organisms in close proximity to one another should be genetically identical. Thus, when you were concieved Peter, you should have been most genetically similar to your mother, father, and any bacteria, viruses, and fungi that would have been present. If anyone else was in close proximity, they would be equally closely related to you as their matter would also be in the morphogenetic field. Ultimately, there should be no genetic differences among any humans and there should also be no more than one sex since this is also a genetic difference.
My comments:
"You've watched too many movies" .
Will respond in more detail on your comments, but I can already reveal that the concept of a multipurpose genome --although it is a fact-- is not easy to understand.
I will elaborate on it soon.
Best wishes,
Peter

This message is a reply to:
 Message 19 by Mammuthus, posted 10-24-2002 8:18 AM Mammuthus has replied

Replies to this message:
 Message 31 by Mammuthus, posted 10-25-2002 9:24 AM peter borger has not replied

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


Message 24 of 317 (20755)
10-24-2002 11:03 PM
Reply to: Message 16 by Quetzal
10-24-2002 3:20 AM


Dear Quetzal,
First of all thanks for your scrutiny and your refernces. I missed them during my search, so I had to focus on Woodford's book, that is far from 'journalistic sensationalism' as you like to call it.
YOU WRITE:
--------------------------------------------------------------------------------
quote:
--------------------------------------------------------------------------------
Q: 1. The species is clonal. (I thought you said your magic organism wasn't a clone?) The miniscule population (39 individuals) represents the descendents of a single tree - the ultimate in population bottlenecks, hence refuting your #5 - the very point you thought it proved.
PB: If you know so much about this tree why don't you write a letter to Dr Peakall (University of Canberra), and explain to him how it all works. I think he will be pretty pleased, so he can publish his work --at last-- in a peer reviewed scientific journal.
--------------------------------------------------------------------------------
YOUR RESPONSE:
Actually, I did. Dr. Peakall was quite kind enough to forward to me two of his articles:
Hogbin PM, Peakall R, Sydes MA, 2000. Achieving practical outcomes from genetic studies of rare Australian plants, Aust. J. Bot. 48, 375—382
Peakall R. 1998. Exceptionally low genetic diversity in an ancient relic, the Wollemi pine: implications for conservation theory and practice. 45th Annual meeting of the Genetics Society of Australia. Abstracts 86.
From the latter:
quote:
--------------------------------------------------------------------------------
So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.
--------------------------------------------------------------------------------
MY RESPONSE:
And if you paid attention to what you read you would have noticed that the title is a misrepresentaion of the content. They didn't find LOW varibility, they found NO variablity at all. In my opinion that is something completely different, and if it would have been LOW --instead of NO-- variability I wouldn't have shown it as an example!! You may think I am, but I'm not stupid!!
YOU SAY:
Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.
MY RESPONSE:
To judge from your intonation I hit a raw nerve. Well, at last you met somebody who checks all evo-claims and it may hurt a bit that I already overturned several claims. So, I can imagine that it not so funny. Sorry for that.
And apparently, you --like Dr Page-- seem to find it pleasing to be condescending. As soon as you are able to nitpick your so eager, it shows. I really feel sorry for that and if it demonstrates something: defence of your beliefs.
If you can send me a copy of the Peakall's articles as soon as you have them in, I would be very grateful.
Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.
YOU SAY:
A point of correction: Dr. Peakall is with the Australian National University in Canberra, not the "university of Canberra".
I SAY:
Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Actually there are two populations of the tree, both were analysed and demonstrated exactly the same DNA (as mentioned in letter #1). Surviving populations with invariable DNA points in the direction of a stable multipurpose genome, not in the direction of evolution.
--------------------------------------------------------------------------------
Actually, there are THREE populations of the tree - which of course Woodford didn't know at the time he published his book.
MY RESPONSE:
Actually there are already SEVERAL populations of the tree. I've seen them in the Botanic Gardens in Sydney, the Botanic Gardens of St Thomas, the Zoo, etcetera.
YOU WRITE:
You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...
MY RESPONSE:
O yes since I am not in evolutionisms I am not a scientist. I almost laugh my pants off.
(By the way, Dawkins is a zoologist trying to get a bit of understanding of genes. I could educate him in this topic, and I wouldn't let you get away with qouting him, that's for sure).
YOU SAY:
"Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...
MY RESPONSE:
I notice that you are perfectly able to copy opinions of evolutionary biologists. I am not impressed by their opinions and you should know that by now. Did you ever ponder these evolutionary riddles youself? Do you have a personal opinion/explanation on these observations? I would really like to know about it.
Furthermore, if it is so well understood explain it to me.
And, it doesn't explain the invariable DNA between the two (or three, or more) stands in the wild.
Please explain to me why it is a misstatement. The trees survive wonderfully, and their DNA is unvariable. I don't see a misstatement here. How can their DNA be so stable? No somatic mutations? Ever thought about that?
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Q: The species propagates by coppicing - roots grow out from the main tree, then send up shoots. IOW, it isn't a sexually reproducing organism in the wild. Interestingly enough, it was discovered during planning for conservation of this unique species that it DOES produce viable seeds like other conifers. Why it clones itself in the wild is unknown at this time.
PB: If you have your information from New Scientist december 1997 than I have to dissapoint you. Coppicing was the initial thought of Peakall but according to Woodford's book (2000) it does not coppice, but sexually reproduces (see mailing #1).
--------------------------------------------------------------------------------
Sorry to disappoint you, but I have my info from the person who actually studied the plant. You need to reread your book, as well as my post. The plant propagates by coppicing IN THE WILD. It was found during conservation planning, however, that it quite readily reproduces sexually ex situ - making it much easier to replicate the plant in collections in multiple facilities, and giving hope to the long-term conservation of the species. IOW, the species DOES produce viable seeds and pollen. The investigation into the reasons for this is on-going - and makes for quite fascinating research in its own right.
MY RESPONSE:
So it is able to copice and also to reproduce sexually. Sounds pretty redundant to me. Multipurpose genome?
YOU SAY:
Where you are correct is that there is no evidence yet that the three populations were connected by subterranean roots (digging up the ground between the stands could be hazardous to the trees). Given the physical separation between stands, Dr. Peakall considers it unlikely. That's why there's on-going study - to answer that question.
MY RESPONSE:
I was not only correct in this statement, all my claims on the tree's DNA are correct and you didn't show otherwise. Do you really think that I am presenting this site with disinformation? Of course not, I show all examples that violate evolutionism, including the Wollemia nobilis. I know the answer to their questions: multipurpose genome, no explanation in the evolutionary paradigm. And Peakall knows, since he talked about an ALL-PURPOSE genome regarding the W. nobilis.
YOU WRITE:
quote:
--------------------------------------------------------------------------------
Q: The entire family Araucariaceae, of which W. nobilis is a member, shows low genetic variability.
PB: That is true. Araucariacaea demonstrate very low variability and that is in accord with the hypothesis of a multiporpose genome. Low variablity due to extremely stable DNA guarded by hundreds of DNA repair enzymes. Observed variation is due to regulatory, rather than mutational phenomena. All in accord with the multipurpose genome.
--------------------------------------------------------------------------------
Nope, wrong again. The data indicates there are evolutionary constraints in action, not some mythical multipurpose genome.
MY RESPONSE:
Evolutionary constraints??? Come on Quetzal, don't fool yourself with these meaningless words. What are evolutinary constraints? That the 'DNA isn't plastic anymore', 'evolution ceased in this tree', 'Evolution slow-down' or other humbug.
Actually this all is exactly what the multipurpose genome predicts: "endstations of 'evolutinism'"
YOU WRITE:
See, for example, Setoguchi, H., Osawa, T.A., Pintaud, J.C., Jaffre, T. & Veillon, J.-M. 1998. Phylogenetic relationships within Araucariaceae based on rbcL gene sequences. Amer. J. Bot. 85: 1507-1516, or Hanson, L. 2001. Chromosome number, karyotype and DNA C-value of the Wollemi Pine (Wollemia nobilis, Araucariaceae). Bot. J. Linn. Soc. 135: 271-274.
In addition, the tree isn't all that similar to the Cretaceous Araucariaceae. See, for example: Chambers, T.C., Drinnan, A.N., McLoughlin, S. 1998. Some morphological features of Wollemi Pine (Wollemia nobilis, Araucariaceae) and their comparison to Cretaceous plant fossils. Internat. J. Plant Sci. 159: 160-171.
MY COMMENTS:
I've had a close-up look at all families of the Araucariacaea --the can all be found in Australia-- and I agree with you that I do not understand that Wollemia, Agathis and Araucaria are classified as Araucariacaea. They don't even resemble each other and are also highly distinct from fossilised Araucaria. (Never understood classifications beyond (sub)species anyway).
YOU WRITE:
quote:
--------------------------------------------------------------------------------
PB: What do you mean by 'argument of journalistic sensationalism'? As far as I know nothing has been published on this tree for sensationalism. Please be specific in your statements.
--------------------------------------------------------------------------------
Lol, almost everything published in the popular press on this tree, beginning with the first accounts of its discovery, have been sensational journalism in action. "Dinosaur tree", "living fossil", "green dinosaur", etc are all splashy, flashy journalistic bombast. Even the full title of Woodford's book which you like so much, "The Wollemi Pine. The Incredible Discovery of a Living Fossil from the Age of the Dinosaurs" lends proof to my contention. Nice try.
As to the horseshoe crab and coelocanth, please start a new thread if you want to drag out these old creationist chestnuts - more examples of "argument from journalistic sensationalism".
MY RESPONSE:
Dear Quetzal you really don't understand what I am trying to convey, is it? For your understanding: Between two isolated populations (like two or three isolated stands of trees) of 'living fossils' molecular evolutionism expects to find loads of variablity with respect to neutral positions, redundant genes, 'junk' DNA etcetera. If we don't find it, than I rest my case: multipurpose genome. We didn't observe it for the first organism analysed in this way, the W. nobilis. The other studies have not yet been carried out. I wait for them and I have a close eye on it, since I am almost certain that it will provide more falsification of evolutionism.
Best wishes,
Peter
[This message has been edited by peter borger, 10-24-2002]

This message is a reply to:
 Message 16 by Quetzal, posted 10-24-2002 3:20 AM Quetzal has replied

Replies to this message:
 Message 28 by Quetzal, posted 10-25-2002 6:57 AM peter borger has replied
 Message 29 by Quetzal, posted 10-25-2002 8:32 AM peter borger has not replied

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


Message 25 of 317 (20763)
10-25-2002 1:45 AM
Reply to: Message 17 by Mammuthus
10-24-2002 5:29 AM


Dear Mammuthus,
You write:
PB:
Even if you found a new organism in your garden tomorrow and found out in your lab that the DNA is completely invariable it wouldn't refute anything, would it? Your a faithful believer. (Nothing inherently wrong with that, although not very scientific)
M: If I found an unusual finding I would actually confirm it rigorously before running around pronouncing I had discovered something spectacular. It is not faith but the wish to do proper reproducible scienc. If I found a new organism that showed no or little genetic variation I would test for a genetic bottleneck or whether the organism is clonal and not claim woo hoo! genetics is dead. (that you do that is both inherently wrong and non scientific.)
MY RESPONSE:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.
PB:
And that demonstrates that evolutionism is an outdated theory based on morphology. I think --and this will not be completely novel to you-- morphology is subject to DNA sequences and regulation of these sequences.
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
MY RESPONSE:
Indeed, and how do you think this works?
PB:
It should be clear now that I do not require deterministic mutations for this hypothesis. As demonstrated in this thread a major part of mutations are non-randomly introduced, i.e non-random with respect to nucleotide and position (see the 1G5 genes in Drosophila subpopulations, mtDNA in hominoids/human subpopulations).
M: It should be clear that unless the system is deterministic your entire hypothesis falls apart. You claim that similarity between organisms is solely due to non-random mechansim making them seemingly similar not because of common ancestry.
I have asked without getting an answer before, do you believe you are related to your parents or was your DNA spontanously created and non-random giving the seeming appearance that you are related to them? In any case, as soon as you discover a mutation that occurs outside your "non-random" site your hypothesis is falsified and this has been observed in almost all instances.
MY RESPONSE:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.
PB:
I concur that deterministic mutations have not (yet) been detected. I already predicted where your mutations most likely will be introduced in your mtDNA in a previous mail. And if you currently have a C on those positions they will likely be a T when it mutates. Thus, the non-randomness I speak off is with respect to nucleotide and position (not when), but may have important implications for molecular phylogenetics.
M: This is not really a valid argument Peter. Sometimes you get C to G or C to A. Sometimes C to T. That C to T is more common is a purely chemical constraint. Which C to T mutates is random in a given generation. The only implication that it has for molecular phylogenetics is that the transition transversion ratio is taken into account as a variable.
MY RESPONSE:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)
PB:
By plastic I mean that preexisting sequences can be duplicated and/or shuffled.
M: So you don't believe there are point mutations, single base deletions, or complete changes in chromosomal content? You have some reading to do.
MY RESPONSE:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.
M: The ZFX/ZFY paper also shows how point mutations accumulate in the ALU's...acutally when a HERV integrates the 5 and 3' LTRs diverge by point mutations and deletions etc etc etc.
MY RESPONSE:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?
PB: All according to the evolutionary paradigm. Actually the ribosomal RNAs are a nice example of stability that is maintained by the hypothetical idea of 'concerted evolution'. You should be aware that is but a hypothesis. In fact, evolutionism requires this hypothesis otherwise it cannot explain the high level of stability within the rRNA genes. However, I wonder whether this hypothesis is still tenable and probably it has to be replaced by purifying selction soon (as observed for the histon H3 and H4 genes. The one story is replaced by the other story. You are free to believe them, I don't). The hypothesis of multipurpose simply holds that these rRNA genes are guarded by highly specific DNA repair mechanism.
(By the way, did you mean the "selfish meme" )
M: Ever hear of gene conversion? There are a lot of basic (and observed) methods of DNA sequence homogenization of which you seem to be completely unaware. Selection on 18S is not on one copy and by the way, there can be very different 18S copies within a single genome. There can also be rDNA pseudogenes.
MY RESPONSE:
No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?
PB:
If all mechanisms that induce variations --due to shuffling of preexisting DNA elements-- are already present than it advocates a multipurpose genome and not evolutionism. Nothing evolved, only the order of the DNA elemenst is different.
M: To bad that novelty and novel regulation does appear to refute this as the exclusive mechanism. Even for shuffled genes, the globin cluster of humans is exceptionally different from elephants....plenty of evolution occurring...
MY RESPONSE:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.
PB:
If a single point muations leads to a big enough degeneration (for instance members of the Src-family), it will be lethal and selected against.
M: You sure about that one? Sickle cell anemia and cystic fibrosis are both extremely fitness reducing diseases yet both persist in the population...heterozygotes get an advantage from carrying the "bad copy" thus a big degeneration is maintained.
MY RESPONSE:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.
Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
MY RESPONSE:
Nice example of redundancy. I see no problems here.
PB:
The (sub)species that is not utilising an environment optimally is degenerate compared to the (sub)species that does. It will be selected against.
M: Hey, welcome our new evolutionary biologist Peter Borger
Actually, that is not necessarily correct either. Both may diverge so that they do not overlap.
MY RESPONSE:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.
PB:The creatons and the morphogenetic field can be inferred from the fossil record. You infer evolution from the fossil record and fill in the gaps between the phyla with hypothetical transition forms, also a non-falsifibale hypothesis. So, what is the difference?
M: If you find an animal fossil like say a mastodon that has many shared features with elephants but also pronounced differences, how is this evidence for creatons in a morphological field?
MY RESPONSE:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.
M:Why would there be gaps in a morphogenetic field? How do you quantifiy a creaton? All untestable and non falsifiable.
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.
M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
MY RESPONSE:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.
M: previous post M: This absolutely does not follow from your statement that DNA is plastic and stable (polar opposites). Acutally nothing follows from premise 1. However, this is also falsified as some species do have abundant variation in some genes and others not. If your prediction is that all organisms have elaborate and accurate mechanisms to counteract mutation it does not fit with the observations that even related species have tremendous variation in genetic variability i.e. Homo sapiens and Pan troglodytes for example.
PB: Expand on the example please. If you mean shuffling I don't see a problem. If you mean SNPs I also don't see a problem.
M: So you have no problem with data that falisifies your premise that there is only variation due to shuffling of genes and not point mutations etc?
MY RESPONSE:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.
PB: I don't see a problem here. The organism that doesn't produce sperm will not produce offspring and is therefore degenerate. Its DNA will disappear from the genepool.
M: But if it is a multipurpose genome obviously there should be a compensatory path for such mutation for such an important pathway. You are arguing from a strict selectionist point of view yet proposing a strictly Lamarkian pre-adaptation hypothesis...they are polar opposites.
MY RESPONSE:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.
PB: How do you know that it is a captured retrovirus gene? It can be the other way around. The retrovirus captured the protein and used it for its envelope. It happend a lot in the virus world that they capture genes from their hosts. I thought you used this method to explain the IL-1beta incongruence?
M: Where did I say that about IL-1 beta? Syncytin is an envelope protein common to all retroviruses both exogenous and endogenous. The direction of capture is clear from the lack of such a viral gene outside of old world monkeys and hominids.
MY RESPONSE:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get his protein?
PB: No, it doesn't falsify anything (sounds familiar, in't it ). The multipurpose genome hypothesis hold that part of the genes is redundant, not all. In fact it holds that the part that is responsible for variations is redundant, and that are usually genes involved in regulation of gene expression. Hey, that is exactly what we see in biology: Redundant regulatory networks! In addition, there are also essential non-redundant genes.
M: This is totally inconsistent. You are constantly changing your terms and hypothesis around from selectionist to adaptationist and from here to partial redundant and multipurpose from only multipurpose. This is falsified by single copy genes involved in variation. If something is lacking in the genome your creatons should create it so that the organism can persist.
MY RESPONSE:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).
PB: If an organism was created recently and doesn't yet have major defects (due to entropy acting on the genome) in DNA repair mechanisms, it is expected that the DNA does not change. That is what we see for the W. nobilis.
M: To bad that is not what we see for muskoxen and bears where we see past diversity is much greater than that of today (i.e. ancient DNA). Quetzal also gave examples of organisms that have suffered genetic bottlenecks and were not created recently. Quetzal already pointed out your complete and total error regarding W. nobilis.
MY RESPONSE:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.
PB: Actually, molecular biology does not falsify this hypothesis. For instance, you showed me the '10.000 generations of bacteria reference' and it was demonstrated that SNPs were NOT abundant. Thus the sequences are stable and the phenotype-changes were merely due to shuffling/deletion/duplication of preexisting elements. All in accord with my hypothesis.
M: Actually, they only measured gene rearrangments as it was easier...this was not a test of the increase in SNPs. There are plenty of examples of phenotypic change due to point mutations or have you missed 50 years of genetics?
MY RESPONSE:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.
PB: See my reponse to Quetzal. However, in a previous letter you concurred that such organism would overturn evolutionism. Can you please expand a bit on this contradiction.
M: The contradiction is as Quetzal pointed out, that you have not provided such an organism but have rather again shown a profound lack of population genetics knowledge.
As a suggestion you may want to get a copy of Danial Hartl and Andrew Clark's Population Genetics. It is a bit too mathematical at times but it is a fairly comprehensive book on the genetics of populations. That is not meant as an insult Peter but if you don't have a foundation in the subject matter then you will be far less prepared to object to it.
MY RESPONSE:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.
M: I look forward to your response to this post and to that of Quetzal's regarding W. nobilis.
MY RESPONSE:
Gleichfalls.
best wishes,
Peter
[This message has been edited by peter borger, 10-25-2002]

This message is a reply to:
 Message 17 by Mammuthus, posted 10-24-2002 5:29 AM Mammuthus has replied

Replies to this message:
 Message 26 by Mammuthus, posted 10-25-2002 5:06 AM peter borger has replied

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


Message 26 of 317 (20771)
10-25-2002 5:06 AM
Reply to: Message 25 by peter borger
10-25-2002 1:45 AM


PB:
What I understand from Quetzals mailing is that genetic variability hasn't been found between the trees in two (or three, now) seperated stands. That has been scientifically demonstrated in Peakall's lab. So, my claims on this tree are still standing. And, also my assertion that it violates molecular evolution still stands. Even the assertion that 'neither geneticist, paleontologist, dendrologist nor C14 expert would be able to disproof that the organism had been created a century ago' still stands.
M: First off, you can sequence the mtDNA of 3 cheetahs and find no genetic variation to. It is historically known that they went through a bottleneck (perhaps down to a single breeding pair) and they are still today extremely genetically uniform. All as predicted by population genetics much less evolution. Same goes for the musk oxen. The entire population of musk oxen in Greenland were a transplant of a few from Alaska...thus, they are identical in the sequences thus far studied. Of 37 modern muskoxen only 8 very similar haplotypes were found...though I have some upcoming surprises about 15 thousand year old muskoxen
Very few W. nobilis exist so it would have been a much greater surprise if the 3 stands demonstrated genetic variability as that would be inconsistent with a bottleneck. Bottlencks can be observed expreimentally and in the wild. Your concept of morphogenetic fields cannot so is thus unsupported.
As to your arguement that no one could "prove" that W. nobilis was not created 100 years ago...(you don't prove in science which you obviously do not know)...Find the closest relative of W. nobilis and you can determine how long ago it separated from that relative..thus much evolution has occurred and had to occur before the trees present as the genome does not spontaneously change after the organism is present, except for a few loci
M: I was correcting your mistatement as to the origins of the theory not desputing regulation of morphology. By the way, environment can have a tremendous impact on morphology regardless of sequence i.e. phenocopies or if you have ever seen a victim of thalidomide with limb reduction.
PB:
Indeed, and how do you think this works?
M: Are you being serious or joking? Are you really unaware of why thalidomide is a mutagen? Before I go into this I need to know if you have any knowledge of developmental biology.
PB:
I not only claimed that, but also provided scientific evidence for that. I already mentioned that there are two types of mutations: random and non-random. The latter is non-random with respect to nucleotide and position, and will give the illusion of common descent if one compares between species. I expect to find more evidence if we look within subpopulations instead of looking between distinct species.
M: And again, you have not provided any evidence for non-random mutation except for your poor tactic of redefining random to suit your purpose though it is not correct. There are lots of papers on subpopulation variation and they don't show non-random mutation. You still cannot tell me for the hottest of hotspots if a mutation will occur there in the next generation or not.
PB:
That is what YOU expect. And I also expected to find this, untill I discovered that mutations can be non-random. As mentioned in the mtDNA example where subspecies are compared several observations can be made that are not in accord with molecular evolutionism. I already pointed it out in another thread and we could continue there if you like. (Observations: fast evolutionary clock, no common descent, non-random nucleotide substitutions)
M: We can continue as you like. Your repeating non-random mutation is not making it any more valid....so please continue but actually supply something substantive.
PB:
Of course, I acknowledge all these forms of mutations. They all have their place in the hypothesis of the multipurpose genome. Usually they are neutral or degenerate. Changes in chromosomal content I am not yet sure off. How? deletions? rearrangements? additions from other sources? However, I guess, they all fit the multipurpose genome. Will think about it if you elaborate on it.
M: Actually, you have previously denied other forms of mutation contribute to variation. However, you stated multipurpose genome was all about shuffling of existing sequences only with no acknowledgement of point mutations etc...do you wish to revise your premise?
As to your questions, I think we may be talking past each other. I am not sure what you are asking me. I can give you examples of close species with different chromsomal content but I am not sure if that is what you are asking for.
PB:
Did the sequence divergence start after integration or did they already diverge before integration? How do you assess this?
M: That is an easy one. Novel integration events have been observed including with HIV when the virus integrates into the genome of its host. The LTRs are identical..the divergence is post integration.
MY RESPONSE:
No, I know of these mechanisms. I only wondered where the other copies go? They seem to disappear from the genome without a trace since otherwise we would observe them as junk DNA and we would be able to track them back in time. In fact such mechanisms predict that a considerable amount of pseudogenes must exist that vary in sequence from 0-100 %. For histon H4 we don't find them. Why, I wonder?
M: Please read any basic chapter on recombination and you should be able in 2 seconds to see why the reciprocal recombinant is lost.
PB:
And who says that they derived through evolution? You see novelty and novel regulation and you say that evolution did it. It is but a plain statement. I do not negate that mutations occur. I negate that elephants and human have a common ancestor linked by a Darwinian mechanism.
M: actually you deny that you are linked to your parents by common ancestry as well. It is not a plain statement but one supported by paleontology, morphology, biochemistry, and genetics....what have you got?
PB:
Apparently, the diploid genome allows this bit of degeneracy. However, it is loss of a diploid redundancy. So, I see no problem.
Talking about anemia. Did you know that the hemoglobin gene is an apparent "hot gene". I propose there is some kind of mechanism that prefers this gene above --say-- the ZFX gene. Over 250 mutations in the hemoglobin gene are known, while the ZFX gene is completely stable for 20.000.000 years [as discussed]. Directed mutations? Yes, I keep trying it!).
M: Ah, so now the mutlipurpose is now only semi-multipurpose on certain occasions? As to ZFX..you are not helping your case by posting this fallacy again (as discussed)
M:
You remove the mitochondira in its entirety from yeast and they survive by switching to fermentation i.e. the petite mutant lines. If what you said were true we would not have such a large genetic load.
PB:
Nice example of redundancy. I see no problems here.
M: Except that in almost all other organisms such a loss is lethal? Selective redundancy? Redundancies on Tuesdays but not Thursdays? I see big problems for your hypothesis with the redundancy argument.
PB:
There is a big difference between selection against, and natural selection as driving force of evolutionism. You need the genes first and than you can select on these genes. So, the genes have to be derived from some other gene (duplication is the favourite, I guess) and than they have to evolve into another gene without selective constraint (the duplictated genes demonstrate redundancy after duplication) that gives selective advantage. Prediction: we should oberve redundancy correlated to duplication in any genome. Fact: we don't see it. Clear case.
M: Clear to you but that is not a prediction of any evolutionary biologist. Some cases do operate as you have said. In other cases a gene involved in one function takes on a new function i.e. homoglobins in bacteria versus multicellular organisms. And you the need organism to be selected on by its environment at the phenotypic level, not the gene to be selected for to pre adapt the organism to something..get it?
PB:
It isn't. However, if you find a manatee and an elephant and you claim (as evolutionism does) that the are linked by Darwinian principles, than I like to have evidence for that.
Otherwise, I claim that the genomes have been created through creaton-matter-interactions.
M: There is a lot of evidence for a manatee-elephant association..you up for reading it?
PB:
Maybe there ar gaps in the creatons. Maybe we pass through an interstellar creaton wave every 26.000.000 years or so. This vision would also nicely fit extinctions (anti-creatons?) and sudden appearance of species.
M: Except that it is a non-testable hypothesis just like plain old biblical creationism.
M: Find me a mastodon fossil that is older than a T.rex and evolution is in trouble.
PB:
There have been books published on this topic. If I recall properly by Michael Cremo. Never read it though.
M: LOL!!!!!!!!!!!!!!!!!!!!
PB:
I do not have objections to observations like point mutations. They have their place in the hypothesis of the multipurpose genome. Point mutations due to inefficient repair of DNA and this may be due to a degenerate loss of repair genes. Shared point mutations in related genomes may be due to non-random mechanism as previously explained.
M: Glad you don't object to point mutations as that would make for some very strange demonstrations in front of the White House
You have falsified your own hypothesis. Two humans have the same repair mechanism (as do chimps and humans)yet any two individuals have different amounts and locations of mutations so it cannot be due to loss of repair genes.
PB:
As mentioned before the multipurpose genome also includes essential genes. Not only redundancies. The Lamarkian adaptation hypothesis coud be revisited, but has to be adapted to current understanding of (epi)genetics.
M: Go ahead an revisit Lamark and tell me what our current understanding is of epigenetics and how it relates to evolution and then how it relates to your hypothesis.
PB:
In a previous letter. I was going to check out viral sequences in this region of chromoseme 2. Didn't find them yet. Where did the virus get his protein?
M: 8% of the human genome is composed of HERVs so there are plenty of options...you have a lot of work cut out to support your assumption
PB:
Do you think it a simple task to set up a new hypothesis that covers all biological phenomena? It takes a lot of effort, but luckily you and other biologists already provided some good comments.
Creatons are not omnipresent, so the phenomena we observe in the genome are usually the result of entropy, or preexisting mechanisms (shuffling, duplications, etc).
M: You have claimed multiple times that it was easy to support your hypothesis and very easy to refute evolution based on your hypothesis. Suddenly it is hard? How do you know if creatons are omnipresent or not since you have never measured one or observed one? How will you go about identifying such a particle?
PB:
Apparently, these muskusoxes and bears have lost a lot of redundant gentic information that used to be present in their multipurpose genome. That happens a lot. It is predicted by the hypothesis.
M: Then the hypothesis is falsified as the ancient and modern muskoxen and bears have the same genetic content as modern representatives.
PB:
Sometimes a point mutation in a PREEXISTING gene occurs and leads to phenotypic change. Either through inactivation of the gene (=degeneracy of the genome) or through a slight decrease of specificity. Spetner wrote a book on this topic. According to him none of the examples added information to the genome. Maybe you have such examples. I would be pleased to know about it.
M: Syncytin for one.
PB:
First of all, you are unable to insult me even if you wanted to. I'm always open for critique and completely stoic to insults.
M: You often seem rather prickly these days. However, you did not deny your lack of knowledge of the fields you are criticizing and have not indicated a willingness to inform yourself. If you did so you might bolster your credibility and not make so many errors.
PB:
However, I have provided such an organism. The three seperated populations of W. nobilis did not derive from cloning, still they were not able to demonstrate genetic differences. That's what I promissed and that is what you get. Maybe population genetics has something to do with it, since it says that low genetic variablity may be expected in small population (due to losses ). However, this example violates molecular evolution. You know that and I know that. Although the Wollemia nobilis may be an evolutionary riddle, it is not a riddle to me.
M: On the one hand you say that population genetics predicts this and thus it falsifies evolution...evolution is population genetics...again Daniel Hartl and Andrew Clark Principles of Population Genetics..there is even a "Cliffs Notes" version with less of the mathematical derivations for some of the equations they present.
PB:
Gleichfalls.
Tschuss,
Mammuthus

This message is a reply to:
 Message 25 by peter borger, posted 10-25-2002 1:45 AM peter borger has replied

Replies to this message:
 Message 34 by peter borger, posted 10-25-2002 11:44 PM Mammuthus has replied

  
Andya Primanda
Inactive Member


Message 27 of 317 (20776)
10-25-2002 5:49 AM
Reply to: Message 11 by peter borger
10-23-2002 8:31 PM


Cool! Anyway, their studies demonstrate that up to 9,3 percent of the E.coli genome is irrelevant junk. How about knocking out introns? Or maybe using mice / Drosophila. These experiments might be off topic but they can answer other questions i.e. how much of the genome is junk, and how much are supposed to be junk/selfish but actually not.

This message is a reply to:
 Message 11 by peter borger, posted 10-23-2002 8:31 PM peter borger has not replied

Replies to this message:
 Message 30 by Syamsu, posted 10-25-2002 8:43 AM Andya Primanda has not replied

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


Message 28 of 317 (20777)
10-25-2002 6:57 AM
Reply to: Message 24 by peter borger
10-24-2002 11:03 PM


quote:
Quoted from Peakall 1998: So far, within the Wollemi Pine no allozyme variability has been found at 13 allozyme loci. Furthermore, no variability has been detected at more than 800 loci, visualised by the AFLP method. While the absence of allozyme variability is know for other rare species, the lack of AFLP variation is unexpected, since this method normally reveals polymorphic loci, even when allozyme variation is absent. This suggests exceptionally low genetic diversity in the Wollemi Pine. Long term isolation, small population size and clonality may have contributed to this pattern.
PB: And if you paid attention to what you read you would have noticed that the title is a misrepresentaion of the content. They didn't find LOW varibility, they found NO variablity at all. In my opinion that is something completely different, and if it would have been LOW --instead of NO-- variability I wouldn't have shown it as an example!! You may think I am, but I'm not stupid!!

Actually, the abstract states exceptionally low genetic diversity, not no variability. To be fair, it also states that the loci examined to date don’t show variation where expected (or where found in other organisms) — the key word being to date. Talk about nitpicking — if you’d like, you can always email Dr. Peakall yourself and ask for a clarification. I’m going by what the man wrote — not what I want it to be.
quote:
Q: Ya see, Peter, I don't get my info from popular science books written by journalists. You ought to try it some time. BTW: Dr. Peakall also told me that a detailed genetics paper is now in preparation, and promised to forward a copy when it is submitted.
PB: To judge from your intonation I hit a raw nerve. Well, at last you met somebody who checks all evo-claims and it may hurt a bit that I already overturned several claims. So, I can imagine that it not so funny. Sorry for that.
And apparently, you --like Dr Page-- seem to find it pleasing to be condescending. As soon as you are able to nitpick your so eager, it shows. I really feel sorry for that and if it demonstrates something: defence of your beliefs.

Nitpicking? I certainly don’t consider it nitpicking to contrast a popular press book written by a journalist with the scientific, peer-reviewed papers published by the researchers who are actually studying the organism. Not my fault you can’t find more reliable data to back up your claims. Also, feel free to point out specifically where you think I was condescending so I’ll know what to avoid in the future. Although, to be honest, I feel flattered to be compared favorably to Dr. Page.
quote:
If you can send me a copy of the Peakall's articles as soon as you have them in, I would be very grateful.
Feel free to get them the same way I did — or use a university lending library. I provided the references, you’re quite capable of digging them out. You can even take the opportunity to explain to Dr. Peakall why he’s got it all wrong. I’ll be fascinated to see his response.
quote:
Furthermore, as stated the tree doesn't demonstrate variation in the expected regions, so where exactly do my claims fail. I simply give it another interpretation. By the way, if I recall properly, it was you who claimed in a previous letter (on mtDNA) not to be a molecular biologist so you were not able to interpret the data on this topic. And now suddenly you are able to interpret these molecular data? Very confusing.
Your claims fail because there are alternate, mainstream explanations for the preliminary data. It’s YOUR responsibility, as the claimant in this case, to provide testable, replicatable reasons why the mainstream explanations are in error. So far, all you’ve done is hand-wave away anything that contradicts you. As to your little ad hominem aside, it appears I struck a nerve. If you feel I’m unqualified to discuss the issue with you, then you are free to ignore anything I post. That won’t, of course, help your case, but perhaps it will make you feel better. As a clarification — I forbore to challenge your sequence data on that one issue. Doesn’t mean even someone as ignorant as I apparently am can’t see the flaws in your arguments.
quote:
Thanks for that, I knew he was in Canberra, but as usual I recalled by head (almost photographic memory, I presume). Nitpicking again. You just earned yourself 100 points.
If you’ll reread the sentence you were responding to, you’ll note I prefaced it with the phrase a point of correction. That doesn’t equate to nitpicking. Now if I’d said, Peter’s ignorant because he doesn’t know that; now THAT would be nitpicking in some ridiculous attempt to score points as you seem to suggest was my intent.
quote:
Actually there are already SEVERAL populations of the tree. I've seen them in the Botanic Gardens in Sydney, the Botanic Gardens of St Thomas, the Zoo, etcetera.
Okay, allow me to clarify: there are three populations IN THE WILD. Your statement is, as you’ve accused me, nitpicking.
quote:
Q: You really should look into some of the original sources rather than relying on a popular press book - no matter how good it might be. Would you let me get away with quoting Dawkins in a scientific argument? At least he's a scientist...
PB: O yes since I am not in evolutionisms I am not a scientist. I almost laugh my pants off.

The statement was a contrast between Dawkins and Woodford. Getting a little shrill, here, Peter. You appear to be LOOKING for some kind of personal attack. Good luck.
quote:
Q: "Surviving populations with invariable DNA" is a serious misstatement. Lack of genetic variability due to long-term isolation and/or severe genetic bottleneck is a relatively well-understood phenomenon. There are numerous examples, from cheetahs to elephant seals. It doesn't, however, imply that the DNA can't vary - simply that it hasn't for the reasons noted. Throw in clonality, and you'd almost expect it...
PB: I notice that you are perfectly able to copy opinions of evolutionary biologists. I am not impressed by their opinions and you should know that by now. Did you ever ponder these evolutionary riddles youself? Do you have a personal opinion/explanation on these observations? I would really like to know about it.
Furthermore, if it is so well understood explain it to me.
And, it doesn't explain the invariable DNA between the two (or three, or more) stands in the wild.
Please explain to me why it is a misstatement. The trees survive wonderfully, and their DNA is unvariable. I don't see a misstatement here. How can their DNA be so stable? No somatic mutations? Ever thought about that?

Uhh, that was my opinion. Unlike you, I HAVE studied wild populations with a eye towards developing conservation strategies — that used to be my profession, and is still my avocation. Although not a genetics researcher, I do understand the use of genetics studies in this context. One of the reasons I got (vaguely) interested in Wollemia in the first place — it presented an interesting conservation management challenge. So yeah, in answer to your further condescension, because I’ve personally seen the results in the wild I agree with the findings of the ecologists that small, isolated in-bred populations which have undergone severe population bottlenecks tend to homogenize their genotypes — in the case of cheetahs, for example, to the point where they can accept skin grafts from each other. The specifics of Wollemia, and particularly why it seems to be an extreme case of this, haven’t yet been published. I’m content to wait for an explanation — from the people actually doing the studies. However, I’m willing to bet that in a few generations those specimens that have been transplanted in the various institutes and botanical gardens around Australia WILL begin to significantly diverge unless very stringent controls are put in place.
As far as your misstatement goes — you state the DNA is unvariable. I call into question your assertion. Show from ANY available data that the DNA of Wollemia is incapable of variation. In fact, from the available published information there is no way you can even infer that the stands are 100% identical genetically. The full study hasn’t been published yet. Can you show me there are NO mutations at all anywhere in the genome of Wollemia? Also, can you show that there was NO variation in the modern organism compared with the fossils (hint — look up the Chambers 1998 article I referenced)? If you can’t your assertion stands as falsified: the DNA of Wollemia nobilis is not incapable of variation.
quote:
So it is able to copice and also to reproduce sexually. Sounds pretty redundant to me. Multipurpose genome?
Nope. Sounds like we need more information.
quote:
1. I was not only correct in this statement, all my claims on the tree's DNA are correct and you didn't show otherwise. 2. Do you really think that I am presenting this site with disinformation? 3. Of course not, I show all examples that violate evolutionism, including the Wollemia nobilis. I know the answer to their questions: multipurpose genome, no explanation in the evolutionary paradigm. 4. And Peakall knows, since he talked about an ALL-PURPOSE genome regarding the W. nobilis. (Numbers added to make response clear)
1. NONE of your claims about the tree’s DNA are correct, as I have shown, using the papers referenced. Look ‘em up.
2. Disinformation? Not really. Deliberate, skewed interpretation coupled with misunderstanding and a weak argument from personal incredulity, usually.
3. You haven’t shown a single concrete example of anything that falsifies evolution. Every example, argument, quibble, etc, that you’ve produced has been shown to be in error by one person or another here. Mere repeated assertion doesn’t prove your case.
4. Now I insist you email him. Where in ANY his articles does Dr. Peakall talk about an all-purpose genome?
quote:
Evolutionary constraints??? Come on Quetzal, don't fool yourself with these meaningless words. What are evolutinary constraints? That the 'DNA isn't plastic anymore', 'evolution ceased in this tree', 'Evolution slow-down' or other humbug.
Actually this all is exactly what the multipurpose genome predicts: "endstations of 'evolutinism'"

Now THAT’S condescending. Meaningless words? Are you denying that organisms are constrained by their natural history (genetics, ecology, ancestry)? I gave you several reasons why your favorite organism may have been constrained — clonality in the wild, miniscule in-bred population (bottleneck), etc. You’re waaaayyy out there on this one, Peter. Nothing in the concept states that evolution ceased or any of the other strawmen you’re arguing here. What is an endstation of evolution? Can you even conceive of any possible way of falsifying or providing evidence for the existence of any single species of any organism of any kind anywhere on the planet outside of a strictly controlled lab lineage has ceased to evolve? It’s certain as taxes that Wollemia hasn’t stopped (or somehow is no longer capable of) evolving — one of the key issues dealt with by the conservation biology people is how to prevent hybridization. If you don’t think this is a problem, I suggest you look up the stringent efforts being used with the Catalina mahogany (Cercocarpus traskiae) conservation efforts.
quote:
I've had a close-up look at all families of the Araucariacaea --the can all be found in Australia-- and I agree with you that I do not understand that Wollemia, Agathis and Araucaria are classified as Araucariacaea. They don't even resemble each other and are also highly distinct from fossilised Araucaria. (Never understood classifications beyond (sub)species anyway).
Really? This is fascinating. Please reference the articles you published on the phylogeny of the Araucariacea. (Hint: Agathis and Wollemia are sister clades based on both 18s and rbcL data — of course, you knew that).
Just for fun — how do you personally classify subspecies? How have you gone about identifying specific demes in a wild population? And why do you always put sub in parentheses?
quote:
Dear Quetzal you really don't understand what I am trying to convey, is it? For your understanding: Between two isolated populations (like two or three isolated stands of trees) of 'living fossils' molecular evolutionism expects to find loads of variablity with respect to neutral positions, redundant genes, 'junk' DNA etcetera. If we don't find it, than I rest my case: multipurpose genome. We didn't observe it for the first organism analysed in this way, the W. nobilis. The other studies have not yet been carried out. I wait for them and I have a close eye on it, since I am almost certain that it will provide more falsification of evolutionism.
Condescending again, Peter? Actually, the truth of it is the studies haven’t even been carried out on W. nobilis yet. Your statement is trivially true — two populations WOULD be expected to diverge, all other things being equal — not because it’s predicted, but rather because it’s been observed. However, you’re ignoring a few inconvenient facts again.
1. With your extensive knowledge of population genetics, I’m sure you know that inbreeding depression and mutational load can counteract each other in very small populations. Although possibly an extreme example of this, the observation that Wollemia shows negligible variation at the loci thus far compared between stands could be related to this. In other words, there may not be significant change due to mutation because, if two of the stands were originally seeded from one tree (which hasn’t been shown one way or the other), under even theoretically ideal conditions, the divergence would possibly be minimal over several generations.
2. Somatic mutations were NOT tested for — merely 18s and rcbL divergence, which would only be detectable through inheritance of different (i.e., mutated) genes. Somatic mutations are generally not considered during these types of analyses because they are usually limited to a single cell of a single individual in a single generation, and hence are useless for comparative genomics. Somatic mutations are not inherited.
3. Wollemia is a very long-lived organism. Several of the oldest trees are tentatively dated to ~1000 years of age. There has been no data published indicating how long ago the three populations separated. If the stands represent first generations, especially if from a single parent plant, there would NO variation between stands — as observed. I think Dr. Peakall contends that each STAND was produced by coppicing from a single original seed — which would mean within the stands all the growth represents the same plant, so again would not show any variation (see also #2 above).
4. All of your junk DNA, redundancies, etc, would only appear/accumulate in separated populations of multiple organisms over many generations. With Wollemia we are essentially dealing with three organisms only (although that may change with more data), not three populations. That’s the implication of the coppicing growth pattern from an original seeding.
Try again, Peter.

This message is a reply to:
 Message 24 by peter borger, posted 10-24-2002 11:03 PM peter borger has replied

Replies to this message:
 Message 47 by Mammuthus, posted 10-29-2002 10:00 AM Quetzal has not replied
 Message 52 by peter borger, posted 10-29-2002 10:59 PM Quetzal has replied

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


Message 29 of 317 (20779)
10-25-2002 8:32 AM
Reply to: Message 24 by peter borger
10-24-2002 11:03 PM


Actually, there was another bit that I forgot to address in your post, Peter.
quote:
(By the way, Dawkins is a zoologist trying to get a bit of understanding of genes. I could educate him in this topic, and I wouldn't let you get away with qouting him, that's for sure).
And yet, Dawkins IS a zoologist and actually knows something about morphology, anatomy, and evolution. Nonetheless, I would never quote one of his popular books in a scientific discussion. Your ENTIRE argument rests on one popular press book written by a JOURNALIST! Can you say, "double standard"?
Tell you what, Peter, I won't use Dawkins if you don't use Woodford. Fair deal?

This message is a reply to:
 Message 24 by peter borger, posted 10-24-2002 11:03 PM peter borger has not replied

  
Syamsu 
Suspended Member (Idle past 5589 days)
Posts: 1914
From: amsterdam
Joined: 05-19-2002


Message 30 of 317 (20780)
10-25-2002 8:43 AM
Reply to: Message 27 by Andya Primanda
10-25-2002 5:49 AM


It's not ethical to knock out genes genes in mice and see what happens! I wouldn't use drosophila either, but organisms which have no nervous system whatsoever, like plants.
regards,
Mohammad Nor Syamsu

This message is a reply to:
 Message 27 by Andya Primanda, posted 10-25-2002 5:49 AM Andya Primanda 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