|
Understanding through Discussion |
|
|
Register | Sign In |
|
QuickSearch
| EvC Forum active members: 63 (9162 total) |
|
| |
| popoi | |
| Total: 916,393 Year: 3,650/9,624 Month: 521/974 Week: 134/276 Day: 8/23 Hour: 0/4 |
| Thread ▼ Details |
|
|
| Author | Topic: molecular genetic evidence for a multipurpose genome | |||||||||||||||||||||||
|
Mammuthus Member (Idle past 6496 days)  Posts: 3085 From: Munich, Germany Joined: |
M: Can you give an example of diminished expression?
PB:LDH and ADH in asian populations. M: And the gene pools of Asians are poorer, better, equal to others based on this expression difference? M:However, none of this is obvious from the cheetah. There is no evidence that they lost a gene like alpha actinin 3. And again, they are not extinct so their "quality" is fine. MY RESPONSE:Non-scientific humbug. A fine quality of cheetahs? And what about the fine quality of the Allocasuarina? Also of fine quality? In a previous letter it was stated that they struggle to survive, characterised by degenerate sperm production, high newborns deathrates, etc. It demonstrates loss of genes, not monomorphism of genes. In addition, I predict that even this empoverished genepool of the cheetah will still have genetic redundancies. M: Lions which are not nearly as inbred as cheetah's also suffer from the above i.e. low sperm production etc. Which genes did the cheetah specifically lose...it should be obvious...you could try to PCR 18S rDNA and would not be there for example. Do cheetah's have more, less, equal numbers of ERVs as before? Are there chromosomes now shorter because of all this genetic loss you claim there is evidence for or do you mean genetic variation in the population? If you mean the latter it argues against multipurpose genome by the way. M: You have a knack for vaguery that makes it impossible to always know what you are talking about. "poor" genomic content is a meaningless statement. MY RESPONSE:Talking about vaguery. According to Quetzal evolutinism predicts either statics or dynamics. That's not even vague, that's nothing! It predicts nothing!!! Compared to wild types, poor genetic contents are often observed in laboratory animals. Did you know that laboratory mice can vary in genomic content between 3-3.3 billion nucleotides per diploid genome? That is 10%. M: 3.3 billion nucleotide variation in an inbred strain of mouse? Considering they have a genome similar in size to ours that is way more than 10% Peter. You sure you were looking at mouse and not C. elegans in your comparison?  As to Quetzal being vague..he has given the conditions under which one expects sequences to remain static or to vary. That you ignore it is not his problem. PB:I do not see a link between my statements and your answer. Clearly, your conclusions are base upon assumptions. That's not science, that's wishful thinking. M: As I said you did not read the papers where this is discussed..or are you now claiming that all vets are full of shit to like every other biologist besides you? MY RESPONSE:Obtuse again? It is known from elementary biological knowledge, and you also (should) know that's better to have the wild type than the mutant form for such genes. M: I'm obtuse? You might want to actually be sure your statement about mutant genes is true M: Why would we know a priori the exact number of genes? HUGO used extremely rough calculations and were wrong...and? MY RESPONSE:Are you going to say that all human subpopulation have the same genetic content (same amount of genes)? If so, you are wrong (as demonstrated in previous mails distinct subpopulation will loose distinct genes, since it is a random process). This has been sceintifically proven beyond any doubt. M: And will gain genes and will shuffle genes and will acquire mutations in genes. Show me the citation for the extreme change in number of genes in the human gene pool...I would love to see a new Hox gene in population X PB:New protein families. Although you probably doubt them, they are for sure around. For instance recombination proteins (RAG1 and RAG2)in mammals that are involved in gene rearrangemnt in B cells to optimise antigen-antibody interactions. They are found only in mammals with such adaptive immune systems, and they are new genes present in the multipurpose genome of mammals. M: How do you know they are new? Mammals by your definition only appear similar because non-random process. There is no reason for a mouse to be any more related to other mammals than to a liverwort..or are you now backing away from your illusion of descent argument? You cannot on the one hand group mammals but then claim there is only identity by descent at the subspecies level. PB:This question cannot be addressed by science (similar to the origin of gene, as discussed before). It can also not be addressed by evolutionism. It can only be speculated upon and the answer depends on the paradigms one proposes. M: That is if one just ignores the science on the subject. Considering that I, Quetzal, and others have to post links to the topics and ALWAYS find scientific citations for all of the points you claim are unknown, not thought about, or not studied your above claim is rather dubious and your scholarship is rather poor in this matter. I find that strange as you appear to be rather passionate about this subject yet refuse to inform yourself in any depth. MY RESPONSE:Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision. M: I have already provided a reference (more than once on this topic)...so go ahead..start the dicussion.... M: You still don't understand the concept of fitness do you? PB:Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness. M: I don't respond? You have left almost all of my questions hanging without answers for weeks now so you are being rather hypocritical. I have explained this point to you before and get tired of repeating it. Do you understand what fitness is? From your answer I assume no, but I am getting sick of doing your homework for you. PB:The multipurpose gene is subject to entropy. Redundant genes will get lost easily. In particular those genes not immediately required for survival and reproduction. M: Then it is pretty freaking amazing that so many redundant genes are highly conserved....or now you are going to post the exact same above sentence but just put a "not" in fron of subject in the first sentence? PB:Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied. Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG. M: Then you have failed to explain variation in the genes encoding the repair proteins, the variation in repair mechanisms, the extreme variation in repair fidelity among repair enzymes etc etc...which explains why DNA can vary as much as it does...hardly argues for your stabilizing by repair...in fact it falsifies it. MY RESPONSE:Going back in time subspecies become more and more one species. This origin-species has got the ultimate genetic variation because it still contains all preexisting genes. M: I actually asked if you think each (not the species) individual genome contains the variation of the species? That would fit with Lamarkian dynamics. MY RESPONSE:No, I already said --and this is observed in populations-- that losses are at random. So, the genepool of all populations of (sub)species contain what is left over of the original multipurpose genome. It is easy to understand (sub)speciation from this stance. Remember Occam's rasor? The easier the solution the better. M: Except that you would have to postulate that humans do not reproduce sexually and are not diploid since transfer of ALL variation from one generation to the next does not happen in a two sex diploid system...it does not work with any reproductive system known...hey, you do believe that storks bring babies M: You forgot that selection acts on the random mutation in the Darwin finches with those best adapted to the new environment surviving and reproducing. PB:Selection is not in doubt here. Random mutation is in doubt here. Studies on birds beaks demonstrate that all the variation is already within the gene pool, selection of certain characteristics of the beak can be selected against. For instance, drought will give birds with small beaks a disadvantage due to hard seeds. They will be selected against, and these genes may be removed from the gene pool if drought persists. So, here we have a nice example of reduction of genetic content. The opposite is also possible. However, the loss of such gene can be restored in the population by breeding. M: Agree with most of this paragraph...wow,imagine that..except for the part about the variation always being there..I thought you said it gets lost by entropy..now you say it has to be maintained by cross species hybridization? Where is that stabilizing of the repair system? There should be no variation at all? Selection is not in doubt??? PB::Slip of the pen. It should have read cross breeding, not inbreeding. M: Fair enough. PB:Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak. M: Why do I have to explain the origin of the beak to explain beak evolution in Galapagos finches??? We can debate the subject if you wish but it is off the topic at hand. M:Hybrids are usually less fit than either parent species and populations of such hybrids usually die out unless the two species share a hybrid zone...look it up. MY RESPONSE:What hybrids? You mean a hybrid between sheep and goat, for instance. So, please be specific and look it up. M: So yet again I have to do your freaking homework...you must be the laziest anti-science person I have ever met. Even Behe does his own background research....na ja. Take your pick... Sage RD, Heyneman D, Lim KC, Wilson AC. Related Articles, Links Wormy mice in a hybrid zone.Nature. 1986 Nov 6;324(6092):60-3. PMID: 12356091 [PubMed - indexed for MEDLINE] 2: Bridle JR, Butlin RK. Related Articles, Links Mating signal variation and bimodality in a mosaic hybrid zone between Chorthippus grasshopper species.Evolution Int J Org Evolution. 2002 Jun;56(6):1184-98. PMID: 12144019 [PubMed - in process] 3: Julian GE, Fewell JH, Gadau J, Johnson RA, Larrabee D. Related Articles, Links Genetic determination of the queen caste in an ant hybrid zone.Proc Natl Acad Sci U S A. 2002 Jun 11;99(12):8157-60. PMID: 12034873 [PubMed - indexed for MEDLINE] 4: Bierne N, David P, Boudry P, Bonhomme F. Related Articles, Links Assortative fertilization and selection at larval stage in the mussels Mytilus edulis and M. galloprovincialis.Evolution Int J Org Evolution. 2002 Feb;56(2):292-8. PMID: 11926497 [PubMed - indexed for MEDLINE] 5: Sasaki A, Kawaguchi I, Yoshimori A. Related Articles, Links Spatial mosaic and interfacial dynamics in a Mullerian mimicry system.Theor Popul Biol. 2002 Feb;61(1):49-71. PMID: 11895382 [PubMed - indexed for MEDLINE] 6: Stacy EA. Related Articles, Links Cross-fertility in two tropical tree species: evidence of inbreeding depression within populations and genetic divergence among populations.Am J Bot. 2001 Jun;88(6):1041-1051. PMID: 11410468 [PubMed - as supplied by publisher] 7: Campbell DR, Waser NM. Related Articles, Links Genotype-by-environment interaction and the fitness of plant hybrids in the wild.Evolution Int J Org Evolution. 2001 Apr;55(4):669-76. PMID: 11392384 [PubMed - indexed for MEDLINE] 8: Johnston JA, Grise DJ, Donovan LA, Arnold ML. Related Articles, Links Environment-dependent performance and fitness of Iris brevicaulis, I. fulva (Iridaceae), and hybrids.Am J Bot. 2001 May;88(5):933-938. PMID: 11353718 [PubMed - as supplied by publisher] 9: Britch SC, Cain ML, Howard DJ. Related Articles, Links Spatio-temporal dynamics of the Allonemobius fasciatus- A. socius mosaic hybrid zone: a 14-year perspective.Mol Ecol. 2001 Mar;10(3):627-38. PMID: 11298974 [PubMed - indexed for MEDLINE] 10: Good TP, Ellis JC, Annett CA, Pierotti R. Related Articles, Links Bounded hybrid superiority in an avian hybrid zone: effects of mate, diet, and habitat choice.Evolution Int J Org Evolution. 2000 Oct;54(5):1774-83. PMID: 11108604 [PubMed - indexed for MEDLINE] 11: Fritsche F, Kaltz O. Related Articles, Links Is the Prunella (Lamiaceae) hybrid zone structured by an environmental gradient? Evidence from a reciprocaltransplant experiment.Am J Bot. 2000 Jul;87(7):995-1003. PMID: 10898777 [PubMed - as supplied by publisher] 12: Alarcon R, Campbell DR. Related Articles, Links Absence of conspecific pollen advantage in the dynamics of an Ipomopsis (Polemoniaceae) hybrid zone.Am J Bot. 2000 Jun;87(6):819-824. PMID: 10860912 [PubMed - as supplied by publisher] 13: Castiglia R, Capanna E. Related Articles, Links Contact zones between chromosomal races of Mus musculus domesticus. 1. Temporal analysis of a hybrid zone between the CD chromosomal race (2n=22) and populations with the standard karyotype.Heredity. 1999 Sep;83 ( Pt 3):319-26. PMID: 10504430 [PubMed - indexed for MEDLINE] 14: Alibert P, Renaud S, Dod B, Bonhomme F, Auffray JC. Related Articles, Links Fluctuating asymmetry in the Mus musculus hybrid zone: a heterotic effect in disrupted co-adapted genomes.Proc R Soc Lond B Biol Sci. 1994 Oct 22;258(1351):53-9. PMID: 7997458 [PubMed - indexed for MEDLINE] 15: Barton NH. Related Articles, Links The effects of linkage and density-dependent regulation on gene flow.Heredity. 1986 Dec;57 ( Pt 3):415-26. PMID: 3804768 [PubMed - indexed for MEDLINE] 16: Shaw DD, Wilkinson P, Moran C. Related Articles, Links A comparison of chromosomal and allozymal variation across a narrow hybrid zone in the grasshopper Caledia captiva.Chromosoma. 1979;75(3):333-51. PMID: 535498 [PubMed - indexed for MEDLINE] PB:Thus, the more variability is inbred the closer the organism will resemble the original 'kind' containing all original genetic info. M:Inbreeding reduces variability. More inbred individuals do not look like the last common ancestor or do you think the Amish are more genetically similar to Homo erectus because they are more inbred than the average human population? MY RESPONSE:Here I also meant crossbreeding. M: Ok, so if I cross two species or subspecies, they should be genetically more similar to their ancestor?....care to show some evidence that donkeys or wolf-dog hybrids are more like their last common ancestor? If an Asian and an African have a kid, are you saying the genotype will be closer to cro magnon? What about all the stabilizing repair enzymes preventing any change backwards or forwards..so much for your hypothesis being the easiest answer to everything. MY RESPONSE:I already explained how the multipurpose genome works. Preexisting DNA elements induce variability due to differential regulation, and is probably partially irreversibel due to the character of these elements. I guess you would call these elements retroviroids, or LINE's or SINE's. Or whatever you call them. M: Does not look like this holds up either....BMC Evol Biol 2002 Sep 10;2(1):16 Related Articles, Links Little qualitative RNA misexpression in sterile male F1 hybrids of Drosophila pseudoobscura and D. persimilis. Reiland J, Noor MA. Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. mnoor@lsu.edu BACKGROUND: Although the genetics of hybrid sterility has been the subject of evolutionary studies for over sixty years, no one has shown the reason(s) why alleles that operate normally within species fail to function in another genetic background. Several lines of evidence suggest that failures in normal gene transcription contribute to hybrid dysfunctions, but genome-wide studies of gene expression in pure-species and hybrids have not been undertaken. Here, we study genome-wide patterns of expression in Drosophila pseudoobscura, D. persimilis, and their sterile F1 hybrid males using differential display. RESULTS: Over five thousand amplifications were analyzed, and 3312 were present in amplifications from both of the pure species. Of these, 28 (0.5%) were not present in amplifications from adult F1 hybrid males. Using product-specific primers, we were able to confirm one of nine of the transcripts putatively misexpressed in hybrids. This transcript was shown to be male-specific, but without detectable homology to D. melanogaster sequence. CONCLUSION: We tentatively conclude that hybrid sterility can evolve without widespread, qualitative misexpression of transcripts in species hybrids. We suggest that, if more misexpression exists in sterile hybrids, it is likely to be quantitative, tissue-specific, and/ or limited to earlier developmental stages. Although several caveats apply, this study was a first attempt to determine the mechanistic basis of hybrid sterility, and one potential candidate gene has been identified for further study. PB:Whether the original kind can ever be backcrossed remains to be established. My guess is NOT, since regulatory elements like retroviruses may have an irreversible effect on gene expression. So, in my opinion, the original genome is plastic within preset limits. M: To bad this is not a testable hypothesis...preset by whom? PB:As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over. Preset by the multipurpose genome, of course. The Creator if you like. M: Besides your desperate attack on evolution you did not answer actually respond to this...what is the testable hypothesis? But thanks for your candor in eliminating the multipurpose genome from the realms of science and properly designating it as a religion (an interesting one granted). PB:Alleles of what? Regulatory networks? Immunogenes? Genes coding metabolism proteins? It all depends on the alleles you are referring to. Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles. M: Hmmmm have you ever studied genetics? Are you really really sure that "Monomorphic alleles are only detrimental to the organism if the monomorphic alleles are bot mutant alleles"? Ever hear of dominant mutants? Partial dominance? Penetrance? Genetics 101 Peter. MY RESPONSE:Yep, any idea about the mechanisms underlying dominant mutations, and penetrance? M: Yes I do...you going to answer my question first? PB:Your explanation does not account for wild type alleles. You also have to consider the fact that monomorphic alleles (homozygous) genes is the rule rather than the exception in any organism studied. So, in my opinion, monomorphic genes cannot be the culprit. Loss of genes can be. M: Funny then that for many genes heterozygosity is very high. MY RESPONSE:That point in the direction of non-random mecahnisms. All in accord with the multipurpose genome. M: Funny that there is no evidence for it...yet Monkenstick could easily find evidence for random mutations...show us your data. PB:The Wollemi pine doesn't demonstrate very little, it demonstrates NO variation. Wanna play the same game as Quetzal, with his distortion of scientific observations? M: I sequenced two mammoths for 350 bp of cytb and they were identical...Oh, I believe in god/Elvis resurrected/creator...my belief in evolution is shattered! Dolly the clone is identical to the animal she was cloned from...Oh no...I have to go re-evaluate everything I ever did...thanks for the eye opener PB:No, it is an evolutionary problem. It cannot be explained by NDT, or the gain of new genes. It can be explained by the multipurpose genome: differntial loss and differential regulation of preexisting genes. M: Okay, then you finally have a testable hypothesis. You can isolate a group of poodles like Fred says and you should get St. Bernards if you agree with his prediction..this is not a predicition of evolutionary theory but obviously one of multipurpose-ism. MY RESPONSE:No, it is YOUR prediction and based upon lack of understanding of the hypothesis of the MG. The actual prediction made by the MG is that due to lost genetic sensible-sequences --not due to genetic monomorphism as you may think-- it is impossible to get St Bernards, or backcross a wolflike animal. However, if you artificially select certain dogs you will be able to generate a wolflike animal from the complete gene pool of the subspecies of dogs. Thus, you bring together all genes that are still present in the gene pool in one organism. Next, you can start breeding with this 'restored multipurpose genome' and you can get the St Bernard, the poodle, the dachshund, the chihuahua, etc. M: Ah, so you don't think dogs are diploid either..or sexually reproducing. Storks bring them to? Earlier you said you could cross breed animals to get an ancestor..now you say you cannot. Interesting that suddenly your entire theory needs natural selection whereas beforer it was pure non-random pre adaptation... PB:Non-random mutations have been demonstrated but every time evolutionist provide fallacies to overcome them. M: If by demonstrating you are wrong is how you define fallacy then so be it. Monkenstick at least provided a graph..let's see yours. MY RESPONSE:I commented on his graph. What I meant is the comments of evolutionists in response to the adaptive mutations of Raddman (mail#52 mol. gen. ev. against random mut. thread). It demonstrates that evolutionists overbluff Raddman (a molecular biologist) by their assertions that "..the error prone polymerase has been selected for their ability to allow cell to cope with damage; the generation of variability [in the genome due to this error prone polymerase] may simply a non-selected byproduct". Well, dear evolutionists, do you really understand biology? I have the feeling that they don't, since it makes the polymerase redundant and since they are not under selective constraint evolutionism predicts highly variable DNA sequences with respect to redundant gene. Based on the MG, I predict that knocking out the errorprone polymerase doesn't effect the organism at all. So here you have another problem. Contrary what evolutionists believe and propagate as fact, molecular biology is not in accord with evolutionism. M: Um, so now you think that if you remove DNA polymerases from an organism it will survive? Have fun trying to generate that mutant strain And please list the full quote and context for the quote you have posted. As you have it written it really does not make much of a point...and if non-random mutation is so obvious why can't you provide just simply something equivalent to Monkenstick's post? PB:This is also clear from the Cairns excerpt in letter #52 in the "mol gen evidence against random mutaion thread" (Dr Page response to Fred). Let's have a look at this paper again and I will demonstrate where the evolutionist's reasoning goes wrong. I don't understand that it is not seen through by the molecular biologists involved. M: Let's have a look at some of my and Quetzal's unanswered questions to while we are at it. MY RESPONSE:As mentioned before, I will answer (and rebut) all your questions. Easy, since evolutionism is false. M: It does not appear to be so easy since you have not convinced any of the evolutionists on this board of anything...but keep trying. best wishes,M
|
|||||||||||||||||||||||
|
Mammuthus Member (Idle past 6496 days) Posts: 3085 From: Munich, Germany Joined: |
|
|||||||||||||||||||||||
|
Mammuthus Member (Idle past 6496 days) Posts: 3085 From: Munich, Germany Joined: |
|
|||||||||||||||||||||||
|
mark24 Member (Idle past 5216 days)  Posts: 3857 From: UK Joined: |
|
|||||||||||||||||||||||
|
Mammuthus Member (Idle past 6496 days) Posts: 3085 From: Munich, Germany Joined: |
|
|||||||||||||||||||||||
|
Quetzal Member (Idle past 5893 days)  Posts: 3228 Joined: |
|
|||||||||||||||||||||||
|
derwood Member (Idle past 1897 days) Posts: 1457 Joined: |
|
|||||||||||||||||||||||
|
peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
|
|||||||||||||||||||||||
|
peter borger Member (Idle past 7686 days) Posts: 965 From: australia Joined: |
|
|||||||||||||||||||||||
|
Quetzal Member (Idle past 5893 days) Posts: 3228 Joined: |
|
|||||||||||||||||||||||
|
Mammuthus Member (Idle past 6496 days) Posts: 3085 From: Munich, Germany Joined: |
Hi Peter
thanks for your response, here is my reply: My pleasure..here we go. M: And the gene pools of Asians are poorer, better, equal to others based on this expression difference? PB: To my knowledge, no studies on this topic, yet. Considering the LDH and ADH genes, they are present in the gene pool but less expressed. A more obvious example is melanin in African and European population. The gene is present in both gene pools but differentially expressed. M: I think you missed my point on this. I am not arguing that there are no expression differences among populations. There are large differences among members of the same population. My question was related to the "quality" of the genomes by your definition. Are they better, worse, or equal? M: Lions which are not nearly as inbred as cheetah's also suffer from the above i.e. low sperm production etc. Which genes did the cheetah specifically lose...it should be obvious...you could try to PCR 18S rDNA and would not be there for example. Do cheetah's have more, less, equal numbers of ERVs as before? Are there chromosomes now shorter because of all this genetic loss you claim there is evidence for or do you mean genetic variation in the population? If you mean the latter it argues against multipurpose genome by the way. PB: 18S? Why 18S? It is an essential gene, so losing it will immediately be selected against. Why not tRNA genes? They are abundantly present, and can to a certain extent be lost. M: Why? In a multipurpose genome why wouldnt actin just take over the function of 18S? Why do you need selection in your hypothesis? And by the way, 18S is multicopy i.e. redundant. M: 3.3 billion nucleotide variation in an inbred strain of mouse? Considering they have a genome similar in size to ours that is way more than 10% Peter. You sure you were looking at mouse and not C. elegans in your comparison? As to Quetzal being vague..he has given the conditions under which one expects sequences to remain static or to vary. That you ignore it is not his problem. PB: the genomic content of mice varies between 3 +/- 0.3 billion nucleotides per diploid genome. M: This is then a completely different statement than the one before. You said laboratory (inbred) mice differ from one another by an amount an order of magnitude larger than what you are posting now. Or do you mean all lab mice in which case the number you post here is hardly surprising. M. musculus is at least 1 or 2 million years separated from M. spretus for example. PB: Explain, I don’t get it. M: Here is some homework : O'Brien SJ, Yuhki N. Related Articles, Links Comparative genome organization of the major histocompatibility complex: lessons from the Felidae.Immunol Rev. 1999 Feb;167:133-44. Review. PMID: 10319256 [PubMed - indexed for MEDLINE] 3: Spencer JA. Related Articles, Links Lymphocyte blast transformation responses and restriction fragment length analysis in the cheetah.Onderstepoort J Vet Res. 1993 Sep;60(3):211-7. PMID: 7970577 [PubMed - indexed for MEDLINE] 4: Miller-Edge MA, Worley MB. Related Articles, Links In vitro responses of cheetah mononuclear cells to feline herpesvirus-1 and Cryptococcus neoformans.Vet Immunol Immunopathol. 1992 Jan 15;30(2-3):261-74. PMID: 1317618 [PubMed - indexed for MEDLINE] 5: Miller-Edge M, Worley M. Related Articles, Links In vitro mitogen responses and lymphocyte subpopulations in cheetahs.Vet Immunol Immunopathol. 1991 Jul;28(3-4):337-49. PMID: 1835214 [PubMed - indexed for MEDLINE] 6: Yuhki N, O'Brien SJ. Related Articles, Links DNA variation of the mammalian major histocompatibility complex reflects genomic diversity and population history.Proc Natl Acad Sci U S A. 1990 Jan;87(2):836-40. PMID: 1967831 [PubMed - indexed for MEDLINE] PB: It is elementary that the wild type gene is superior to a mutant gene in the genetic background of that gene. Denying that is denying biology. M: It is elementary that mutations can be beneficial...denying that is denying biology and common sense. PB: Due to such mechanism the genetic content of seperated population will not be the same. Soon, the differences between human subpopulation will be elucidated. It is already known that different subpopulations lost distinct genes. I already mentioned the alpha actin gene: completely lost in 18% of the Caucasian population. The CFTR gene: 1 in 25 are carrier of the inactivated (=loss) gene in Caucasian population, etc. Easy to understand from MG stance.I also would like to see a completely new gene in a human subpopulation. M: Though what your saying would be easily latched on to by racists as a genetic basis for descrimination, the problem with this is there is more variation within human populations than between them..thus concepts like Caucasian, etc. are moot...one big happy species. M: How do you know they are new? Mammals by your definition only appear similar because non-random process. There is no reason for a mouse to be any more related to other mammals than to a liverwort. Or are you now backing away from your illusion of descent argument? You cannot on the one hand group mammals but then claim there is only identity by descent at the subspecies level. PB: Novel systems need novel genes and gene programs. The RAG2 doesn’t demonstrate homology with other known protein. M: And you did not answer the question. M: That is if one just ignores the science on the subject. Considering that I, Quetzal, and others have to post links to the topics and ALWAYS find scientific citations for all of the points you claim are unknown, not thought about, or not studied your above claim is rather dubious and your scholarship is rather poor in this matter. I find that strange as you appear to be rather passionate about this subject yet refuse to inform yourself in any depth. PB: I can find these references myself. I can read them myself, and discover that all data are discussed subject to evolutionism. Next, I object to the just so stories presented by the authors, post my comments here, provide another solution to the data, usually an equal solution and often a better solution. What happens? You deny it, Quetzals denies it, Dr Page denies it, and he scoffs it. So, what is the use of reading these severely biased evo-stories. I know the content already. There is nothing new in it for science, no challenge, nothing! And nothing at all for mankind. Meaningless nothingness. M: How convenient for you Peter. Just ignore everything everyone else writes or says and then claim that you are misunderstood and that there is a global conspiracy...megalomania would be an apt description. You have shown an almost exclusive inability to find articles on the subjects you debate and now claim that all scientist that publish are evil evolutionist trying to hold you down personally. At least I, Quetzal, and Page read what the other side has to say rather than using your "ignorance is bliss" argument. MY RESPONSE:Novel genes is primates doesn't make it easier for evolutionists. Now you have to explain them. Duplication and random mutaion would be my guess. If so, let's discuss the redundant alpha actinin genes. It immediately falsifies this vision. M: I have already provided a reference (more than once on this topic)...so go ahead..start the dicussion.... PB: Refernce? Where can I find it, I will discuss it with you. M: Since you keep making me do your homework I will make you do some of your own...it is in two of the posts that I bumped and you ignored...have fun looking. M: You still don't understand the concept of fitness do you? PB: Again, you do not respond to my statements. You are starting to behave like Dr Page. He's got a degree in elusiveness. M: I don't respond? You have left almost all of my questions hanging without answers for weeks now so you are being rather hypocritical. I have explained this point to you before and get tired of repeating it. Do you understand what fitness is? From your answer I assume no, but I am getting sick of doing your homework for you. PB: If you mean the letters 94-96, I missed them, but will repond to them soon. Sick of doing my home work? If you wanna back up your assertions you have to do your homework. M: I do my homework but end up having to provide YOU with references you cannot seem to find for yourself in addtion to having to hunt down posts you ignore repeatedly. If you want to make up silly hypothesis to defend why is it that I have to support all the data for it exactly? PB:It is you who claims that all life we observe came about by pure coincidence and randomness, so you better provide me with compelling evidence, instead of the stuff usually provided by evo’s. As demonstrated these data can be explained according to the multipurpose genome equally well or better. M: Well then get started explaining including all the posts you ignored. And why should I provide you with any more refrerences? Above you claimed you refuse to read anything by anyone who actually studies the subject as they are all conspiring against your non-existent god? PB:Back to start, Mammuthus. You didn't read or didn't understand, what I wrote in mail #1. If you reread it you will notice that stability of DNA sequences is secured by DNA stabilising and repair proteins. That's a prediction of the hypothesis of multipurpose genome and it has been demonstrated to be correct in even the simplest organisms studied. Why would I post exactly the same sentence? I know what I am talking about and I can explain all biological phenomena with the hypothesis of the MG. M: Then you have failed to explain variation in the genes encoding the repair proteins, the variation in repair mechanisms, the extreme variation in repair fidelity among repair enzymes etc etc...which explains why DNA can vary as much as it does...hardly argues for your stabilizing by repair...in fact it falsifies it. PB: Ever heard of entropy? Differential regulation of gene expression due to Shuffling DNA elements? All provided by the MPG hypothesis. Yes, Mammuthus, it explains all biological observations. M: First, you did not answer the question, second you abandoned your repair enzyme fantasy and came up with a new argument..guess you must have also realized how uncompelling an argument it was....interesting that you think "DNA element" shuffling explains all biological phenomenon..please explain genomic imprinting of the H19 locus using genomic shuffling and entropy M: Except that you would have to postulate that humans do not reproduce sexually and are not diploid since transfer of ALL variation from one generation to the next does not happen in a two sex diploid system...it does not work with any reproductive system known...hey, you do believe that storks bring babies PB: Why would I have to postulate non-sexual reproduction of humans? Why would it be necessary to transfer ALL variation at once? It is merely your introduction of a straw man. M: How so? You claim that there was a multipurpose genome with all variation and since that point there has been no more variation only loss (though ironically you also say that variation is generated by shuffling and entropy). How many genomes were there? How much was lost? How do you distinguish gain then loss then gain of variation?Why do ancient DNA studies of Native Americans show haplotypes that exist today? Shouldn't they all be novel entropy lost? Where did the variation in the original population come from? M: Agree with most of this paragraph...wow,imagine that..except for the part about the variation always being there..I thought you said it gets lost by entropy..now you say it has to be maintained by cross species hybridization? Where is that stabilizing of the repair system? There should be no variation at all? Selection is not in doubt??? M: No answer here? PB:Cross breeding will restore genetic variability. In addition, you have to explain the beak in the first place. I mean an evolutionary explanation for the genetic program that gave rise to the first beak. M: Why do I have to explain the origin of the beak to explain beak evolution in Galapagos finches??? We can debate the subject if you wish but it is off the topic at hand. PB: If you want to discuss minor beak variations between subpopulations of finches, you first have to explain the beak, since the beak has an evolutionary origin too, according to your worldview. So, please explain. Other wise we simply discuss population genetics and that’s NO evolution. That is frequency changes of preexisting DNA elements over time. M: LOL! You claim refuse to read anything about evolution because it is against your worldview but then claim you can define evolution as not being population genetics? Wake up Peter...evolution is population genetics over long periods of time....ok, if I have to explain the beak before we can talk about Galapagos finch beak evolution then you have to show me a picture of god poof banging the entire human gene pool into existence...fair enough?...Hartl and Clark...use the eyes, flip the pages, learn M: So yet again I have to do your freaking homework...you must be the laziest anti-science person I have ever met. Even Behe does his own background research....na ja. PB: No, you have to back up your extraordinary claim that all life evolved from nothing through randomness and selection. I will look up your references. Probablyy, the reduced fitness is related to an incompatible secondary DNA code, or maybe incompatible transcriptional code. Will read them. Thanks. M: Oh, so now you will read references? Which is it? Deny all the biological sciences or actually inform youself whether you agree with the authors or not...up to you. M: Ok, so if I cross two species or subspecies, they should be genetically more similar to their ancestor?....care to show some evidence that donkeys or wolf-dog hybrids are more like their last common ancestor? If an Asian and an African have a kid, are you saying the genotype will be closer to cro magnon? What about all the stabilizing repair enzymes preventing any change backwards or forwards..so much for your hypothesis being the easiest answer to everything. PB: Cro magnon was probably already another subspecies of the human archetype. But, anyway, you show that you are beginning to understand the MPG hypothesis. Your idea is okay. M: Actually I was joking...Kind of scary that you think this is how genetics works...how about this, Finnish man has a child with a Chinese woman...will the mtDNA look more like cro magnon, Finnish haplotype, Chinese? M: Does not look like this holds up either....BMC Evol Biol 2002 Sep 10;2(1):16 Related Articles, Links Little qualitative RNA misexpression in sterile male F1 hybrids of Drosophila pseudoobscura and D. persimilis. Reiland J, Noor MA. Department of Biological Sciences, Louisiana State University, Baton Rouge, LA 70803, USA. mnoor@lsu.edu BACKGROUND: Although the genetics of hybrid sterility has been the subject of evolutionary studies for over sixty years, no one has shown the reason(s) why alleles that operate normally within species fail to function in another genetic background. Several lines of evidence suggest that failures in normal gene transcription contribute to hybrid dysfunctions, but genome-wide studies of gene expression in pure-species and hybrids have not been undertaken. Here, we study genome-wide patterns of expression in Drosophila pseudoobscura, D. persimilis, and their sterile F1 hybrid males using differential display. RESULTS: Over five thousand amplifications were analyzed, and 3312 were present in amplifications from both of the pure species. Of these, 28 (0.5%) were not present in amplifications from adult F1 hybrid males. Using product-specific primers, we were able to confirm one of nine of the transcripts putatively misexpressed in hybrids. This transcript was shown to be male-specific, but without detectable homology to D. melanogaster sequence. CONCLUSION: We tentatively conclude that hybrid sterility can evolve without widespread, qualitative misexpression of transcripts in species hybrids. We suggest that, if more misexpression exists in sterile hybrids, it is likely to be quantitative, tissue-specific, and/ or limited to earlier developmental stages. Although several caveats apply, this study was a first attempt to determine the mechanistic basis of hybrid sterility, and one potential candidate gene has been identified for further study. PB: I will spell this paper out. At fisrt sight I don’t see a problem here for the MPG hypothesis. M: Except that it falsifies most of the tenets. PB:As if evolutionism is a testable hypothesis. It has been tested and falsifies over and over. Preset by the multipurpose genome, of course. The Creator if you like. M: Besides your desperate attack on evolution you did not answer actually respond to this...what is the testable hypothesis? But thanks for your candor in eliminating the multipurpose genome from the realms of science and properly designating it as a religion (an interesting one granted). PB: The predictions made by the MPG hype can be tested. See mail #1 for predictions and falsifications. M: See all my immediate responses following mail 1. M: Yes I do...you going to answer my question first? PB: Wildtype genes are usually better than mutant genes. The major part of the genes is homozygously present, and reflects this observation. So this statement is not so farfetched. For instance, for Drosophila only approximately 30 % of the D. melanogaster genes is polymorph and only 11 % is heterozygous (Page, D.M, and Holmes, E.C. Molecular evolution. A phylogenetic approach. 1998. Blackwell Science Inc. ISBN 0-86542-889-1, p231). M: Better? How? Plenty of slightly deleterious alleles are stable in the population...plenty of lethal alleles also. Better than what? 30% is a huge amount of variation! What happened to your poor stablizing enzymes? M: Funny that there is no evidence for it...yet Monkenstick could easily find evidence for random mutations...show us your data. PB: Monkenstick’s graph showed nothing related to this subject. M: Sure, he provided evidence for random mutation...you have not provided evidence for non-random...why is this so difficult? Make a graph from a published data set or genbank showing non-random mutation...I want to know where and when my next P53 mutation will occur so that I can cut off any cancer before it can take hold... M: I sequenced two mammoths for 350 bp of cytb and they were identical...Oh, I believe in god/Elvis resurrected/creator...my belief in evolution is shattered! Dolly the clone is identical to the animal she was cloned from...Oh no...I have to go re-evaluate everything I ever did...thanks for the eye opener PB: Pretty stable DNA. Guarded by stability ensuring proteins I guess. It is a prediction of MPG hypothesis. Did you also determine the age of the samples? Same location finds? M: Oops addendum...found several more mammoths with differences in cytb and several nuclear genes...evolution safe again...whew Assuming the last part of your question is honest curiosity, I have about 100 mammoth samples I am working on. 40 or so are dated, locality varies. A large collection comes from the Taimyr peninsula and another group from Wrangel Island. Some are from Alaska. The rest are from all over the place in Siberia. M: Ah, so you don't think dogs are diploid either..or sexually reproducing. Storks bring them to? Earlier you said you could cross breed animals to get an ancestor..now you say you cannot. Interesting that suddenly your entire theory needs natural selection whereas beforer it was pure non-random pre adaptation... PB: Yeah the stork is also included in the multipurpose genome. Not as baby deliverer, however. No, it does NOT require natural selection. Here you refer to artificial selection. As should be obvious, artificial selection can not be compared to natural selection, since it involves intelligence (human intelligence). M: Read the Origin of species....dog and pigeon breeding were one of the key influences on Darwin's thinking about natural selection. How do you distinguish natural and artificial selection? Is selection due to industrial waste output natural or artificial?...by the way, where does the stork fit in the MG? PB: How can I back up my new hypothesis with peer reviewed science papers that are always discussed subject to evolutionism. As soon as I start to explain the data subject to another paradigm, you start to object. However, I already discussed the ZFX region in this forum with NO response at all. To explain the data between the specis it absolutely requires NON-RANDOM mutations. M: No response at all??? I freakin posted in response to your ZFX nonesense mutliple times with references!!!! So did SLPx. Let's stay honest here. PB:None of the evo-explanations can hold (as discussed). Likewise, the redundant alpha actinin genes. (I will respond to your comments in mail 64-96 soon) M: OK, look forward to it. M: Um, so now you think that if you remove DNA polymerases from an organism it will survive? Have fun trying to generate that mutant strain. And please list the full quote and context for the quote you have posted. As you have it written it really does not make much of a point...and if non-random mutation is so obvious why can't you provide just simply something equivalent to Monkenstick's post? PB: I am talking about the alternative error prone polymerase. I am sure that it can be removed without affecting the organism. I guess, it is a redundant gene. M: Which one is it? Where is the evidence for it? What about the non error prone (less error prone I should say) polymerases? Repair enzymes? M: It does not appear to be so easy since you have not convinced any of the evolutionists on this board of anything...but keep trying. PB: Paradigms shifts do not come overnight. M: No they don't, and when they do come they require a lot of consistency in the new paradigm and reams of supporting data. Best wishes,M
|
|||||||||||||||||||||||
|
derwood Member (Idle past 1897 days) Posts: 1457 Joined: |
|
|||||||||||||||||||||||
|
Fred Williams Member (Idle past 4876 days) Posts: 310 From: Broomfield Joined: |
|
|||||||||||||||||||||||
|
Fred Williams Member (Idle past 4876 days) Posts: 310 From: Broomfield Joined: |
quote: Good post. I agree cheetahs may be in error catastrophe, but genomes have proven to be amazingly resilient (due to an incredible design, of course! ) I'll have to search for a paper (I think it's at home), that provides an excellent example of a bottlenecked organism that showed reslience far beyond what was expected; that is, it could not be explained via NDT. BTW, my question can be answered, as I indicated to Page. I'm still waiting for his "example".
|
|||||||||||||||||||||||
|
Fred Williams Member (Idle past 4876 days) Posts: 310 From: Broomfield Joined: |
quote: Actually, I never went to grad school because of all things I wanted to play in a band (which I did for 17 years, then I grew up  ). After graduating at 21 years of age with a BSEE (from Univ Missouri-Rolla), I decided that in order to support the expensive hobby of keyboardist, I figured getting a job was a better option than becoming a full-time student! Some people like to go make money and have fun in other ways than staying in school.
quote: Baloney. I have not caved on anything, I merely point out that even if I did cave, it doesn’t help your argument on iota. I could admit to martians creating non-random genome or to a flat earth influence on the genome, and your argument would *still* be bogus.
quote: Good, now that we got possibility #1 out of the way, this leaves us with possibility #2: a strawman. As I said before, and you seem to be the only one here who doesn’t understand this, your argument is a classic strawman since Peter and I never questioned the existence of random mutations. [This message has been edited by Fred Williams, 11-08-2002]
|
|||||||||||||||||||||||
|
|
Do Nothing Button
Copyright 2001-2023 by EvC Forum, All Rights Reserved
™ Version 4.2
Innovative software from Qwixotic © 2024
