oh look - an observed gene duplication....

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]

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.M: You do know that you can actually suggest to the editors specific referees and also ask that specific reviewers be excluded due to competition? Why not ask for Behe?

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?Budikka

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

PB:
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 happen 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.andZhu P, Morelli G, Achtman M. Related Articles, LinksThe opcA and (psi)opcB regions in Neisseria: genes, pseudogenes, deletions, insertion elements and DNA islands.
Mol Microbiol. 1999 Aug;33(3):635-50.Primary literature man..primary lit

PB:
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: 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):1014-24.2: 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.Meinersmann RJ, Hiett KL.
Concerted evolution of duplicate fla genes in Campylobacter.
Microbiology. 2000 Sep;146 ( Pt 9):2283-90.

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

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+++++++++++++++LOL!!!!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.The above reference IS a functional duplicate in bacteria..you said you NEVER see duplicates..your statement is falsified. You now claim you don"t have to look at the reference however, YOU claimed you were able to see through the authors speculation and analyze the data YOURSELF...are you now claiming you can see there raw data without reading the paper? That would explain why you make so many mis-statements. Oh yeah, these references were a few of many papers on duplicated genes in bacteria...poor scholarship leads to poor thinking Peter...you really need to read up before YOU engage in Fundie-christian humbug.[This message has been edited by Adminnemooseus, 11-27-2002]

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]

"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: These constraints indicate that flaA is unlikely to have derived from flaB -or vice versa- by duplication and mutation/selection.M: Um...why?"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?"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?"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?"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?"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."..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 mind 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.You want more examples of gene duplications in bacteria that according to you NEVER occur?

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

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.M: You used a lot of words but did not say anything Peter. Your claim then is that duplicate genes should not be similar to each other and if they are it is a mere coincidence? In any case, you claimed there are NEVER duplicates in bacteria and that this is a tenet of the MPG yet there they are.PB: If these constraints are not present the genes deteriorate due to entropy.M: Funny then that in this case and many others, the genes are still there and even pseudogenes are found.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.M: Ok, yet again, which mutations are non-random specifically? You could also start by showing this with SLPx alignment
Otherwise it is an unsupported assertion.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.M: Yet duplicates are found (not just this one example) and pseudogenes are found..this is also basic microbio which falsifies your assertion.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.M: Actually niether recombination nor gene converstin is particularly specific. I have not heard that recombination is due to environmental stimuli..at least not exclusively. Gene conversion either. How is it non-random? It is completely unpredictable...this is even testable using jumping PCR methods.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?M: Yes, they are random.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?M: Um..the electron "observations" are no more direct than anything in evolution. I am surprised that this eludes you. In any case, in your model, why do you qualify it "without selective constraint"?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)M: Why is purifying selection (also called negative selection) meaningless? Define selection..define fitness. So far basic population genetics principles have been undefineable by you so it is hard to take you seriously when you claim they are meaningless. You have to understand what they intend to describe before you can make a claim that they fail. In any case who are creaton interactions in a morphogenetic field scientific? What is the testable hypothesis? Observations? Is it falsifiable? Apparently not as you NEVER responded to the thread asking you about them.M: Yes it is clear that science boggles your mind..but keep trying.PB: Logic science isn't mind boggling, illogic science is.M: Yeah, non-random mutation, MPG, creatons and morphogenetic fields are highly illogical.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.M: Ah, but I paid attention to what you said to Monkenstick which was that duplications should NEVER be observed in bacteria...that is what I have been responding to.cheers,
M