oh look - an observed gene duplication....

Dear Dr Page,It was already recognised by Quetzal (although it neither falsifies nor verifies evolution), but thanks for your marvellous example demonstrating the MPG in action. All your points were predicted by the MPG. See my letter #1 mol gen evidence for a MPG thread for these predictions. And that should be expectd from a good scientific theory: it should have predictive power.The multipurpose genome (MPG) hypothesis holds that:1) DNA sequences within species —-although plastic-- are stable throughout time,
2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,
3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory],
4) the function of natural selection is to remove degenerate organisms, and
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).Predictions of the MPG hypothesis:
1) predicts that within species we do not see abundant variation with respect to genes, and usually such genetic alterations are neutral or degenerate (although distinct alleles can be expected through the principle of degeneration, which is in effect the action of entropy).
It also predicts that all organism --even the simplest-- have an elaborate and accurate mechanism to counteract mutations.
2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.
3) predicts that adaptive phenotypes of organism do never demonstrate new genes.
4) predicts that organism lacking vital DNA elements are selected against.
5) predicts that there should be organisms that have not undergone genetic changes (yet).Falsification of the MPG hypothesis:
The concept will be falsified by the observation of the evolution of new genes unrelated to preexisting genes.It will take a while before you will recognise that what you call evolution is 'differential gene expression', usually due to involvement of regulatory mechanism. I already recognised it, since I am in the field of gene regulation, and tried to share this discovery with you. You still are a bit reluctant, but here Dr PAge provides more clearcut evidence that GENE EXPRESSION DOES THE TRICK. Ever expected that? I didn't, till recently.I think Mammuthus will also like this example, since he likes to have proof for the MPG.Best wishes,
Peter[This message has been edited by peter borger, 11-20-2002]

Dear Mammuthus,In reponse to the multipurpose genome (MPG):M: Already wrong.....define the "purpose of the genome"...or by MPG do you mean miles per gallonPB: No I meant 'Mammuthus Powered Gobbledegook' 1) DNA sequences within species —-although plastic-- are stable throughout time,M: Which says absolutely nothing....and ignores hypervariable sequencesPB: Hypervariable sites can of course be explained by protein driven mechanisms. This is non-random mutations (NRM). As mentioned, the Grand Unifying Theory of Biology includes the MPG and NRM. Together they can explain all biological observations.2) organisms demonstrate genetic redundancies that reside in the genome without selective constraint,M: neutral evolution does to....duhPB: I am not going into genetic redundancies, again. You can ask almost everybody on this site how they falsify evolutionism, since I at least explained it a dozen times.3) adaptive phenotypes are due to duplication and/or shuffling of preexisting DNA elements —either genes or other non-coding elements-- that affect gene expression, or due to loss of (redundant) genes [=degeneration theory],M: Falsified by point and small and large scale deletion event mutations that also alter phenotype.PB: No, deletions are part of degeneration theory. That should have been obvious.4) the function of natural selection is to remove degenerate organisms, andM: Then why is Williams still around? ...define degeneratePB: William is apparently not selected against. Degenerate organisms have negative fitness.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: So much for your proving anything...without having a loaded crack pipe in your mouth and deeply inhaling...where can the rest of us see morphogenetic fields or creatons?PB: As long as biological phenomena are in accord with the MPG hypothesis it is correct, otherwise I will adapt it. The result of creaton-interactions in a morphogenetic field can be observed every day. Open your eyes and look around you.
BTW where can the rest of us see gravitons?Predictions of the MPG hypothesis:
1) predicts that within species we do not see abundant variation with respect to genes, and usually such genetic alterations are neutral or degenerate (although distinct alleles can be expected through the principle of degeneration, which is in effect the action of entropy).
It also predicts that all organism --even the simplest-- have an elaborate and accurate mechanism to counteract mutations.M: This hardly follows from anything in the above tenets you posted...in addition, you have previously claimed that all identity by descent is an illusion so there can be no species...each genome has to be an entity in iteself indepenedent of all others...which falsifies you miles per gallon theory.PB: It follows from point 1-4.2) predicts that a considerable part of the genes of any organism can be knocked out without being lethal.M: And when you put them back in the wild, do thay do better, worse, the same as organisms with the genes?PB: Knockouts can be oberved in the wild to. The human alpha actinin is knocked out in 18% of caucasians, without any effect on reproductive succes (reference is somewhere on this site).3) predicts that adaptive phenotypes of organism do never demonstrate new genes.Falsified..even in primates...syscytin...you are the weakest link..goodbyePB: No, you say that the syncytin gene has been tranferred by a virus into primates and adopted a new function. I say, the virus arose from the primate genome and captured the protein and uses it in the capsid. My vision is probably correct, since viruses have their origin in the genome. Viruses do not drop out of the sky, that's for sure. In fact your syncytin is an example of a new gene in primates that doesn't have an origin. I take it as evidence for creaton interactions in a morphogenetic field. Thanks for the example.4) predicts that organism lacking vital DNA elements are selected against.M: What is a "vital" element? Or do you mean that when an organism has disruption of say the developmental pathway that leads to heart development this is selected against? Wow..what a novel discovery...PB: An element that negatively affects reproductivity.5) predicts that there should be organisms that have not undergone genetic changes (yet).M: I have not changed genetically in 34 years...wow!PB: So, you will live for ever? Dear Mammuthus, in 34 years you have lost a lot of sensible DNA sequences already. Ever cell division will at least change these sequences at certain spots (due to entropy) and will decrease the length of telomeres. So, your assertion is non-sense.Falsification of the MPG hypothesis:
The concept will be falsified by the observation of the evolution of new genes unrelated to preexisting genes.M: And by all the rest of the data against almost every one of the hypothesis put forward..PB: Like what? Till know it hasn't been falsified.PB:
It will take a while before you will recognise that what you call evolution is 'differential gene expression', usually due to involvement of regulatory mechanism. I already recognised it, since I am in the field of gene regulation, and tried to share this discovery with you. You still are a bit reluctant, but here Dr PAge provides more clearcut evidence that GENE EXPRESSION DOES THE TRICK. Ever expected that? I didn't, till recently.M: I knew that drugs were freely available in the Netherlands but really Peter..you need to cut back.PB: I almost laugh my pants off!! Seriously. Now and then, you really are a comediant. You could perform and make money out of it. Did, you know that The Netherlands have a lot of German Drugs Tourists? I am sure you know. PB:
I think Mammuthus will also like this example, since he likes to have proof for the MPG.M: Then the other half of your post where you actually provide this "proof" must have been cut off from your message..care to re-post it?PB: Reread all my 500 -or so- mails. Including at least 10 falsifications of evolutionism and the introduction of a new theory that explains all biology. Frankly, your questioning and scepticism contributed to the improvement of the initial hypothesis. Thanks for the discussions.
BTW, you were the one that stressed I had to introduce such theory and now you are still not contents. What's the matter with you?Best wishes,
Peter

Dear Monkenstick,MS: the GUToB and MPG theories will never see the light of publication because they rely on invisible undetectable particles, processes which haven't been observed..PB: That can hardly be the problem. Evolutionism also relies on processes that haven't been observed. The real problem is that it will never be published in PEER reviewed scientific jounals, since the PEERS are evolutionists themselves.MS: ..or described and they stem from a egomaniacal nutcase who formulated his theory because he "objects to the nihilism of NDT" rather than because he is in any way interested in the truthPB: You are always so flattering
As mentioned before, a scientific theory has to explain observations and to do risky predictions. Evolutionism doesn't either of them, while the MPG hypothesis is explanatory and risky predictions turn out right. Draw your conclusions.Best wishes,
Peter[This message has been edited by peter borger, 11-24-2002]

Dear Buddika,Buddika says:
That's a fine comment coming from someone who, in the Bohar thread, had this to say in response to a comment of mine also quoted:Buddika "Novel genes arise through duplication and mutation."Borger: "...Novel genes do not arise by duplication and mutation..."So are you now prepared to admit that you told a big fat whopping great lie in the other thread and correct it (as well as get back on topic), or are you going to find some other cheap, weaselly excuse? I know, you are going to weasel. You're a creationist loser. How can you do anything other than weasel?I say:My 'weasily' excuse is the observation that you are unable to read.
The MPG says that adaptive phenotypes can involve gene duplications, but novel genes are never the result of duplications and mutations. An example is chemotherapy resistance, or duplications observed under strong selective pressure in bacteria. As soon as the pressure is reduced the duplicated DNA region will recombine out and get lost. That's the reason why wildtype bacteria never demonstrate duplicated genes. I recommend you to read pages 200-202 in Molecular biology of the gene. (Watson JD, et al, ISBN 0-8053-9614-4).Best wishes,
Peter

dear Mammuthus,As soon as the pressure is reduced the duplicated DNA region will recombine out and get lost. That's the reason why wildtype bacteria never demonstrate duplicated genes. I recommend you to read pages 200-202 in Molecular biology of the gene. (Watson JD, et al, ISBN 0-8053-9614-4).M: Except when it does not happenPB: Maybe I should have written:
"As soon as the pressure is reduced the duplicated DNA region will recombine out and/OR get lost. That's the reason why wildtype bacteria never demonstrate FUNCTIONAL duplicated genes. I recommend you to read pages 200-202 in Molecular biology of the gene. (Watson JD, et al, ISBN 0-8053-9614-4).Gene 2002 Jul 10;294(1-2):25 Related Articles, LinksA systematic investigation identifies a significant number of probable pseudogenes in the Escherichia coli genome.Homma K, Fukuchi S, Kawabata T, Ota M, Nishikawa K.Laboratory of Gene-Product Informatics, Center for Information Biology-DNA Data Bank of Japan, National Institute of Genetics, 1111 Yata, Mishima, 411-8540, Shizuoka, JapanPseudogenes are open reading frames (ORFs) encoding dysfunctional proteins with high homology to known protein-coding genes. Although pseudogenes were reported to exist in the genomes of many eukaryotes and bacteria, no systematic search for pseudogenes in the Escherichia coli genome has been carried out. Genome comparisons of E. coli strains K-12 and O157 revealed that many protein-coding sequences have prematurely terminated orthologs encoding unstable proteins. To systematically screen for pseudogenes, we selected ORFs generated by premature termination of the orthologous protein-coding genes and subsequently excluded those possibly arising from sequence errors. Lastly we eliminated those with close homologs in this and other species, as these shortened ORFs may actually have functions. The process produced 95 and 101 pseudogene candidates in K-12 and O157, respectively. The assigned three-dimensional structures suggest that most of the encoded proteins cannot fold properly and thus are dysfunctional, indicating that they are probably pseudogenes. Therefore, the existence of a significant number of probable pseudogenes in E. coli is predicted, awaiting experimental verification. Most of them were found to be genes with paralogs or horizontally transferred genes or both. We suggest that pseudogenes constitute a small fraction of the genomes of free-living bacteria in general, reflecting the faster elimination than production of pseudogenes.PB: "As soon as the pressure is reduced the duplicated DNA region will recombine out and/OR get lost. That's the reason why wildtype bacteria never demonstrate FUNCTIONAL duplicated genes."best wishes,
Peter

Dear Mammuthus,M: Oh looky..duplicated genes in bacteria...LOL!Badel JL, Charkowski AO, Deng WL, Collmer A.
A gene in the Pseudomonas syringae pv. tomato Hrp pathogenicity island conserved effector locus, hopPtoA1, contributes to efficient formation of bacterial colonies in planta and is duplicated elsewhere in the genome.
Mol Plant Microbe Interact. 2002 Oct;15(10):1014-24.PB: The abstract reads:"The ability of Pseudomonas syringae to grow in planta is thought to be dependent upon the Hrp (type III secretion) system and multiple effector proteins that this system injects into plant cells. ORF5 in the conserved effector locus of the P. syringae pv. tomato DC3000 Hrp pathogenicity island was shown to encode a Hrp-secreted protein and to have a similarly secreted homolog encoded in an effector-rich pathogenicity island located elsewhere in the genome. These putative effector genes were designated hopPtoA1 and hopPtoA2, respectively. DNA gel blot analysis revealed that sequences hybridizing with hopPtoA1 were widespread among P. syringae pathovars, and some strains, like DC3000, appear to have two copies of the gene. uidA transcriptional fusions revealed that expression of hopPtoA1 and hopPtoA2 can be activated by the HrpL alternative sigma factor. hopPtoA1 and hopPtoA1/hopPtoA2 double mutants were not obviously different from wild-type P. syringae pv. tomato DC3000 in their ability to produce symptoms or to increase their total population size in host tomato and Arabidopsis leaves. However, confocal laser-scanning microscopy of GFP (green fluorescent protein)-labeled bacteria in Arabidopsis leaves 2 days after inoculation revealed that the frequency of undeveloped individual colonies was higher in the hopPtoA1 mutant and even higher in the hopPtoA1/hopPtoA2 double mutant. These results suggest that hopPtoA1 and hopPtoA2 contribute redundantly to the formation of P. syringae pv. tomato DC3000 colonies in Arabidopsis leaves."PB: According to the MPG genetic redundancies can be expected, although not compulsary, upon stringent selection. The prediction is that the duplicated gene is lost after selection. Only certain strains have the copy, indictaing that they have recently duplicatd it or that all other strains lost it already. In con, I do not see a problem here for the MPG.2: Jordan IK, Makarova KS, Spouge JL, Wolf YI, Koonin EV.
Lineage-specific gene expansions in bacterial and archaeal genomes.
Genome Res. 2001 Apr;11(4):555-65.PB: The abstract says:"Gene duplication is an important mechanistic antecedent to the evolution of new genes and novel biochemical functions. In an attempt to assess the contribution of gene duplication to genome evolution in archaea and bacteria, clusters of related genes that appear to have expanded subsequent to the diversification of the major prokaryotic lineages (lineage-specific expansions) were analyzed. Analysis of 21 completely sequenced prokaryotic genomes shows that lineage-specific expansions comprise a substantial fraction (approximately 5%-33%) of their coding capacities. A positive correlation exists between the fraction of the genes taken up by lineage-specific expansions and the total number of genes in a genome. Consistent with the notion that lineage-specific expansions are made up of relatively recently duplicated genes, >90% of the detected clusters consists of only two to four genes. The more common smaller clusters tend to include genes with higher pairwise similarity (as reflected by average score density) than larger clusters. Regardless of size, cluster members tend to be located more closely on bacterial chromosomes than expected by chance, which could reflect a history of tandem gene duplication. In addition to the small clusters, almost all genomes also contain rare large clusters of size > or =20. Several examples of the potential adaptive significance of these large clusters are explored. The presence or absence of clusters and their related genes was used as the basis for the construction of a similarity graph for completely sequenced prokaryotic genomes. The topology of the resulting graph seems to reflect a combined effect of common ancestry, horizontal transfer, and lineage-specific gene loss."PB: Evo-humbug and Retro-speculation.Meinersmann RJ, Hiett KL.
Concerted evolution of duplicate fla genes in Campylobacter.
Microbiology. 2000 Sep;146 ( Pt 9):2283-90.PB: Don't have to look up the paper. Concerted evolution = retro-speculation. I predict that if one does a proper study on these genes, it has to be replaced by purifying selection. Probably: neutral purifying selection.Best wishes,
Peter

Dear Mammuthus,Here is the abstract and my comments:"Campylobacters have two similar copies (flaA and flaB) of their flagellin gene."PB: They already HAVE two similar genes."It has been hypothesized that the two copies can serve for antigenic phase variation. Analysis of polymorphisms within aligned multiple DNA sequences of the Campylobacter flagellin genes revealed high pairwise homoplasy indexes between flaB/flaB pairs that were not observed between any flaA/flaA pairings or flaA/flaB pairings. Thus it seems there are constraints on the sequence of flaB that distinguish it from flaA."PB: These constraints indicate that flaA is unlikely to have derived from flaB -or vice versa- by duplication and mutation/selection."Nevertheless, segments of the two genes that are highly variable between strains are conserved between the flaA and flaB copies of the genes within a strain."PB: Conserved regions taken as proof for duplication? Conserved regions implicate a highly specific function, that's all."The patterns of synonymous and non-synonymous differences suggest that one segment of the flagellin sequence is under selective pressure at the amino acid sequence level."PB: This is evolutionary interpretation. It can also suggest special design in this region. Besides selective pressure of duplicated genes? After duplication the gene is redundant. It will get lost easily, unless the direction of evolution is known."Another segment of the protein is maintained within a strain by conversion or recombination."PB: Maintained by conversion or recombination? It has been demonstrated for several genes that were said to be in the genome by concerted evolution that gene conversion has to be replaced by purifying selection. However, the MPG says that the genome is maintained by DNA repair mechanism. Even the simplest organism have (unexpectedly) a complete and eleborate DNA repair mecahnism (Eisen et al, PNAS 2002, 99;9509-9514)."Comparisons of strict consensus amino acid sequences did not reveal any motifs that are uniquely FlaA or FlaB, but there are differences between FlaA and FlaB in those amino acids available for post-translational modification."PB: A mechanism preexistent in the genome that contributes to phenotypic variation after genes have been transcribed. It is MPG."The observed pattern of concerted evolution.."PB Observed (????) concerted evolution. Nothing was observed here, it is inferred from the data. It IS retro-speculation."..of portions of a structural gene is an unusual finding in bacteria and should be searched for with other duplicated genes. Concerted evolution was unexpected for genes involved in phase variation since it minimizes the antigenic repertoire that can be expressed by a single clone in the face of the host immune response."PB: Of course it was UNEXPECTED. A careful look will reveal that it is purifying selection. In other words: creation."I really don't understand the evolutionist's logic. Their conclusions are mind-boggling.Best wishes,
Peter[This message has been edited by peter borger, 11-27-2002]

Dear Mammuthus,"Campylobacters have two similar copies (flaA and flaB) of their flagellin gene."PB: They already HAVE two similar genes.M: So duplicates have to be dis-similar? What kind of sense does that make?PB: duplicates --the word already spells it-- are the same, otherwise they wouldn't have been called duplicates. It is your hypothesis that similar genes have arisen from duplicates. I don't mind that you believe this but a duplicate is a redundant gene and will get lost if no selective constraint are applied. An increase in DNA content that doesn't convey improved fitness will be selected against. MPG, you know. The fla genes are alternately expressed every ten generations or so. The mechanism of switching from flaA to flaB is unclear, but it is clear that it is the only way to keep the two genes in the bacteria's genome.PB: These constraints indicate that flaA is unlikely to have derived from flaB -or vice versa- by duplication and mutation/selection.M: Um...why?PB: If these constraints are not present the genes deteriorate due to entropy."Nevertheless, segments of the two genes that are highly variable between strains are conserved between the flaA and flaB copies of the genes within a strain."PB: Conserved regions taken as proof for duplication? Conserved regions implicate a highly specific function, that's all.M: Then why are they "highly variable" between strains?PB: Non-random mutations within strains."The patterns of synonymous and non-synonymous differences suggest that one segment of the flagellin sequence is under selective pressure at the amino acid sequence level."PB: This is evolutionary interpretation. It can also suggest special design in this region. Besides selective pressure of duplicated genes? After duplication the gene is redundant. It will get lost easily, unless the direction of evolution is known.M: So your argument is that duplications will NEVER be observed in bacteria is now that when found they just have not been removed yet?PB: It can be observed, but it is expected that in the course of time the duplication will get lost. As long as selective constraints favor the duplication it will be part of the genome. As soon as selective constraints are relieved, the duplication is embellishment and will be selected against. Bacteria are able to divide every 20 minutes, Even a slight delay results in the overgrow of the mutant by the wildtype. This is elementary microbiology."Another segment of the protein is maintained within a strain by conversion or recombination."PB: Maintained by conversion or recombination? It has been demonstrated for several genes that were said to be in the genome by concerted evolution that gene conversion has to be replaced by purifying selection. However, the MPG says that the genome is maintained by DNA repair mechanism. Even the simplest organism have (unexpectedly) a complete and eleborate DNA repair mecahnism (Eisen et al, PNAS 2002, 99;9509-9514).M: Actually they said nothing about concerted evolution. Gene conversion is an observed fact as is recombination or do you deny that those processes exist to? Why is it unexpected that simple organisms have DNA repair?PB: Here I am wrong. Skimmed the abstract to quickly. However, conversion and recombination are highly specific event involving several proteins that are preexisting in the genome. Probably triggered by the environment. It is a non-random 'mutation' event guided by preexisting DNA sequences and proteins. So, it is MPG."Comparisons of strict consensus amino acid sequences did not reveal any motifs that are uniquely FlaA or FlaB, but there are differences between FlaA and FlaB in those amino acids available for post-translational modification."PB: A mechanism preexistent in the genome that contributes to phenotypic variation after genes have been transcribed. It is MPG.M: It is fantasy land...pre-existent?PB: How do you think conversions and recombination events are carried out? Utterly at random?"The observed pattern of concerted evolution.."PB Observed (????) concerted evolution. Nothing was observed here, it is inferred from the data. It IS retro-speculation.M: An electron has never been observed I guess you don't believe in them either...I guess you are going to retract your papers on gene expression to since you only INFERRED that there were changes and did not observe them.PB: 'Observed' suggests 'fact'. However, it has never been observed and will never be observed. In contrast, electrons have been observed as particles and waves. I suggest the following experiment. Take a gene, duplicate it, grow the culture with and without selective constraints, wait for 10000 generations and have a look at the sequences. I predict neutral mutations, duplications and shuffling and no novel genes. What do you predict?"..of portions of a structural gene is an unusual finding in bacteria and should be searched for with other duplicated genes. Concerted evolution was unexpected for genes involved in phase variation since it minimizes the antigenic repertoire that can be expressed by a single clone in the face of the host immune response."PB: Of course it was UNEXPECTED. A careful look will reveal that it is purifying selection. In other words: creation."M: So now you equate purifying selection with creation? That is indeed strange...what religious fanaticism does to a mindPB: You know what I mean. Purifying selection is another meaningless term to save evolutionism. Why don't the call it 'creation' (meaning: creaton interactions in a morphogenetic field. Sounds very scientific)PB: I really don't understand the evolutionist's logic. Their conclusions are mind-boggling.M: Yes it is clear that science boggles your mind..but keep trying.PB: Logic science isn't mind boggling, illogic science is.M: You want more examples of gene duplications in bacteria that according to you NEVER occur?PB: Actually, if you had paid attention to what I write (letter #1, mol gen evidence for the MPG), than you should know that gene duplications are part of the MPG, and are expected to take place upon severe selective constraints.best wishes,
peter