Intelligent Design

E. coli and their evolution

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I have been thinking about E. coli and their evolution.

E. coli live in the gut. They are passed environmentally from parents to children.

When humans and baboons had their presumed common ancestor ~ 20 mill years ago, that should be the last time when E. coli in our bowel had a common ancestor with E. coli in the bowel of baboons in the wild.

The following study looked at Baboon and Human E. coli (1985).

“The biotype data indicate that the amount and distribution of genetic variation in the E. coli among free-ranging baboon troops are similar to those in isolates from humans. However, E. coli isolates from baboons are able to utilize a greater variety of sugars as their sole carbon source, possibly because of a greater variety of sugars in the baboon diet.”

If we sequence the E. coli from wild baboons and “wild” humans we should be able to see what evolution can achieve. We already know gene transfer plays a role in gut  bacteria.

As an ID supporter I predict that there will be extra genes in baboon E. coli and extra genes in human E. coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E. coli genes as there have been about 3X10^9 generations of separate development. Of special interest would be the flagellar genes.

What do you think of my predictions? Can ID make predictions? Is ID testable? Will anyone do this experiment?

91 Replies to “E. coli and their evolution

  1. 1
    Sally_T says:

    brilliant!!! I doubt that darwinist community will even acknowledge those hypotheses! i guess that is what the blinders of materialism will do for you! even if they do, its still E coli, it’s not like it sprouted wings and started living in trees or anything. I think these guys believe that Spiderman is a documentary.

  2. 2
    lars says:

    I think it’s great that you’re making true predictions (i.e. not postdictions). Follow the evidence where it leads!

    As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli

    I’m not sure I understand the prediction… When you say “extra genes in Baboon E Coli”, do you mean genes in baboon E Coli that are not in human E Coli?

    but that the origin of these functioning genes will be gene transfer.

    Sorry, I’m not a biologist… how will we know whether the origin of these (extra?) functioning genes is gene transfer?

  3. 3
    StephenA says:

    This is not a prediction! You lie! ID is not science, so it cannot make predictions! So there!
    [/sarcasm]

  4. 4
    russ says:

    lars, did you click on the link to the paper abstract?

  5. 5
    getawitness says:

    Can you help me understand this in relation to how (some) evolutionary biologists would hypothesize E.coli evolution?

  6. 6
    Nochange says:

    As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development. Of special interest would be the flagellar genes.

    Can someone please explain to me what this means?

  7. 7
    bornagain77 says:

    idnet.com.au

    As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development. Of special interest would be the flagellar genes.

    Of special note:
    “but that the origin of these functioning genes will be gene transfer.”

    From what research do you base this prediction? Genetic Similarities?

    From my reading of Dr. Behe’s work in the “Edge of Evolution” the limit (prediction) to totally random evolution is now severely constricted and estimated to be 2 novel protein/protein binding sites in an organism.
    If the e-coli is divergent, between baboons and man, by more than this limit, which you seem to be implying with gene transfer, I think we can safely assert that it did not occur by a totally RV/NS process.

    as well this other research seems to indicate a different “designed” function for gene transfer:

    http://www.pnas.org/cgi/conten.....3/40/14941

    of special note:

    Several pathogenic strains of Escherichia coli exploit type III secretion to inject “effector proteins” into human cells, which then subvert eukaryotic cell biology to the bacterium’s advantage. We have exploited bioinformatics and experimental approaches to establish that the effector repertoire in the Sakai strain of enterohemorrhagic E. coli (EHEC) O157:H7 is much larger than previously thought.

    Genes encoding proven or predicted effectors occur in >20 exchangeable effector loci scattered throughout the chromosome. Crucially, the majority of functional effector genes are encoded by nine exchangeable effector loci that lie within lambdoid prophages. Thus, type III secretion in E. coli is linked to a vast phage “metagenome,” acting as a crucible for the evolution of pathogenicity.

    Thus the main part of the genome of E-coli seems to be conserved (poly-constrained) and “all the action” seems to be occurring in a part of the genome (vast phage “metagenome) that seems to be gathering and sharing information on the environment with other e-coli.
    Kind of like a communication network among the e-coli from what I can gather.

    and then this:

    crucible for the evolution of pathogenicity.

    It seems to me that the e-coli are polluted of their primary purpose by a random variation in this “communication network”, lose their primary function, and then become pathogenic (turn on their host).

    I may be wrong, as I’m by no means an expert in this, but I feel gene transfer may not be all what you think it is , especially since Behe provided such a strict limit to what evolution can do by natural processes.

  8. 8
    jdd says:

    I am also a little confused by this: “As an ID supporter I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer. There should be some random neutral mutations in the other E Coli genes as there have been about 730X10^6 generations of separate development.”

    Do you mean you made these predictions based on ID? If so, Could you elaborate on what aspects of ID lead to these predictions? I am very interested.

    also a small note, the divergence time between humans and baboons is suggested to be ~25 million year.

  9. 9
    getawitness says:

    BA77,

    If the e-coli is divergent, between baboons and man, by more than this limit, which you seem to be implying with gene transfer, I think we can safely assert that it did not occur by a totally RV/NS process.

    Wha???

  10. 10
    Janice says:

    idnet,

    I think there’s a problem with this:

    They are passed environmentally from parents to children.

    They’re passed environmentally but not only from parents to children.

  11. 11
    Frost122585 says:

    getawitness, i think they are talking about direct darwinian pathways or random mutation and natural selection. If it’s too complex then the random “abracadabra” of “poof” “there it is” darwinisn cant be the solution. Therefore, you need somthing guiding a new gene into the mix. My question is are all the darwinists tlaking about lateral gene transfer today? maybe someone who has read Behe’s latest could speak on LGT. I plan to read it soon though.

  12. 12
    idnet.com.au says:

    jdd
    “Do you mean you made these predictions based on ID?”

    Yes. ID predicts that RM and NS will achieve only very minor feats. This may enable processing a substrate with a slightly different side chain at most. ID theory suggests that totally new metabolic pathways and molecular machines do not arise by RM and NS. For example, most antibiotic resistance arises by Gene Transfer via plasmids.

    “also a small note, the divergence time between humans and baboons is suggested to be ~25 million year.”

    Thanks a lot. This makes the predictions even more risky as the E Coli have about 3 billion generations to evolve. I don’t speak with authority in the ID community but I stand by the predictions and think this research should be done.

  13. 13
    AussieID says:

    G’day Janice,

    Your comment: “They’re passed environmentally but not only from parents to children.”

    In this particular instance, how else are they passed? Just querying …

  14. 14
    Bob O'H says:

    idnet – it’s still unclear how this is an ID prediction. We know horizontal gene transfer occurs, so it would be a natural prediction that there would be extra genes in human E. coli, say, and that these would be associated with a fitter phenotype. One example might be antibiotic resistance.

    So, you appear to have a prediction that is in line with predictions from standard evolutionary biology. It doesn’t get you nearer to having a test of ID.

    Bob
    P.S. over the last week or so I’ve been having an intermittent problem with WordPress saying that I’m posting too quickly. Is anyone else having the same problem? It’s not that I am posting too quickly (it will happen on my first post of the day).

  15. 15
    Frost122585 says:

    Bob O’H, The Issue that ID.net is subliminally attacking and I will bring it in to he light, is that DE says that all things originate and then are selected. A transformational process of matter that has an unknown guiding force behind it according to Darwin or it just is. ID says that it is far too improbable that these thing just muted “abracadabra style” and boom you have a human out of nothing. The lateral gene transfer type processes are an even greater way of breaking down the explanatory power of “POOF IT’S A COW” into “there is an improbable chain of events that can only be explained by some form of intelligently directed process arranging the relationships between differing units into a super-highly improbable living organism that displays SC.”

  16. 16
    Frost122585 says:

    Lateral Gene Transfer brings it closer to ID then “Boom its a cow” does because you are dealing with real probabilities – “Boom its a 747” just claims that it was all mmajic ungided randomness out of nothing -per se’.

  17. 17
    bornagain77 says:

    This should be a interesting sidelight to this topic:

    http://www.biologynews.net/arc.....ation.html

    November 15, 2007

    Princeton scientists break cholera’s lines of communication.

    of special note:

    A team of Princeton scientists has discovered a key (chemical)mechanism in how bacteria communicate with each other, a pivotal breakthrough that could lead to treatments for cholera and other bacterial diseases.

    “Lots of other bugs like staph, strep and E. coli use the same general type of signaling mechanism as cholera,” said Blackwell, an assistant professor of chemistry. “Many people are looking for ways to inhibit the signaling process, and you could imagine using this process to turn off cholera. It suggests a direct pathway into the clinic.”

    This research also suggests a strong symbiotic relationship for bacteria, with their environment, that further constrains a RV/NS scenario.

  18. 18
    Joseph says:

    When Humans and Baboons had their presumed common ancestor ~ 6 mill years ago, that should be the last time when E Coli in our bowel had a common ancestor with E coli in the bowel of Baboons in the wild.

    1- Humans and baboons did not share a common ancestor ~ 6mya. I don’t know of anyone who claims that. Humans and chimps (not baboons) allegedly share a common ancestor ~ 7mya. (anti-IDists will shred someone for that mistake)

    2- Symbiotes do NOT get passed on from generation to generation. Meaning the e. coli in your parents’ guts are not passed on to your gut, they are not inherited (hat tip to Janice comment 10)

    Bugs in the News:

    The fetus of any animal is completely sterile. Immediately after birth however, the newborn acquires all kinds of different bacteria which live symbiotically (we help them to live, and they help us to live) with the newborn and throughout the individual’s life.

    To Bob OH-

    The standard theory of evolution doesn’t make any predictions based on the proposed mechanisms.

    As for testing ID- CSI & IC suffice.

    1- We only have experience with CSI & IC arising from agency involvement.

    2- There isn’t any data, evidence nor observation that demonstrates that either (CSI or IC) can arise

    And yes I am having the same issue with WordPress. It is very frustrating but it has taught me to first save my comment before posting.

  19. 19
    russ says:

    same problem with wordpress.

  20. 20
    jerry says:

    I have found that the problem with word press is browser dependent. We have several different Mac computers in our business and there seems to be a problem with Safari but not Firefox. I got three straight “posting too fast” comments using Safari then took the comment and pasted it into Firefox and it posted immediately. I also found that just repeating the post gets it accepted sometimes almost immediately.

    By the way if your post is long, select it and copy it so if it dissapears you have a copy of what you wrote.

  21. 21
    jerry says:

    I am also having a hard time understanding the point of this post. Bacteria are everywhere and I assume that the bacteria that a baby is born with comes somehow from the mother during the gestation process.

    But the chance that a bacteria could have been introduced from outside seems immense since bacteria are everywhere in cluding humans eating baboon innards. So what is the big deal here? It seems reasonable that the bacteria could have changed somehow along the way for a variety of reasons.

  22. 22
    bornagain77 says:

    Thanks Joseph for bringing a little clarity.

    I’m still wondering. “What study do you base this prediction on idnet.com.au.?”

    “I predict that there will be extra genes in Baboon E Coli and extra genes in Human E Coli but that the origin of these functioning genes will be gene transfer.”

    I dug out Dr. Behe’s EOE book and found what he had to say about E-coli.

    pg. 141-142

    In the early 1990’s Lenski and coworkers began to grow E.coli in flasks; the flasks reached their capacity of bacteria after about 6 or 7 doublings. Everyday he transferred a portion of the bugs to a fresh flask. By now over thirty thousand generations of E. coli, roughly the equivalent of a million years in the (supposed) history of humans, have been born and died in Lenski’s lab. In each flask the bacteria would grow to a population size of five hundred million. Over the whole course of the experiment, perhaps ten trillion, 10^13, E coli. have been produced. Although ten trillion sounds like a lot(it’s probably more than the number of primates on the (supposed) line from chimp to human), it’s viryually nothing compared to the number of malaria cells that have infested the earth. In the past fifty years there have been about a billion times as many of those as E. coli in the Michigan lab, which makes the study less valuable than our data on malaria.
    Nonetheless, the E coli. work has pointed in the same general direction. The lab bacteria performed much like the wild pathogens: A host of incoherent cahnges have slightly altered pre-existing systems. Nothing fundamentally new has been produced. No new protein-protein interactions, no new molecular machines. As with thalasswemia in humans, some large evolutionary advantages have been conferred by breaking things. Several populations of bacteria lost their ability to repair DNA. One of the most beneficial mutations, seen repeatidly in separate cultures, was the bacterium’s loss of the ability to make a sugar called ribose, which is a component of RNA. Another was a change in a regulatory gene called spoT, which affected in masse how fifty-nine other genes work, either increasing or decreasing their activity. One likely explanation for the net good effect of this very blunt mutation is that it turned off the energetically costly genes that make bacterial flagellum, saving the cell some energy. Breaking some genes and turning others off, however, won’t make much of anything. After a while, beneficial changes from the experiment petered out. The fact that malaria, with a billion fold more chances gave a pattern very similar to the more modest studies on E. coli strongly suggests that’s all Darwinism can do.

    One of the studies of Lenski:

    Long-term experimental evolution in Escherichia coli. XI. Rejection of non-transitive interactions as cause of declining rate of adaptation

    J Arjan GM de Visser and Richard E Lenski

    http://www.pubmedcentral.nih.g.....tid=134600

    “Experimental populations of Escherichia coli have evolved for 20,000 generations in a uniform environment. Their rate of improvement, as measured in competitions with the ancestor in that environment, has declined substantially over this period…..Therefore, this and the other evolving populations must have fairly quickly incorporated mutations that provided the greatest gains, and their slower subsequent adaptation reflects beneficial mutations that are fewer in number, smaller in effect, or both.”

    me again:

    Reading the preceding study on E.coli by J Arjan GM de Visser and Richard E Lenski, and seeing them trying, desperately, to fit the clear evidence for ID/Genetic Entropy into some type of evolutionary framework made me remember this quote.

    ” The final result of all my researches and discussions is that the theory of evolution should be discarded in its entirety, because it always leads to extreme contradictions and confusing consequences when tested against the empirical results of research on the formation of different kinds of living forms and related fields. This assertion would agitate many people. Moreover: my next conclusion is that, far from a benign natural philosophical school of thought, the theory of evolution is a severe obstacle for biological research. As many examples show (this study of Lenski’s, being a prime example), it actually prevents the drawing of logical conclusions from even one set of experimental material. Because everything must be bent to fit this speculative theory (evolution), an exact biology cannot develop.” Prof. Dr. Heribert Nilsson Lund University Sweden

    Kudos Dr. Nilsson, Kudos.

  23. 23
    Collin says:

    I have wordpress problems with internet explorer and copying and pasting does not work.

  24. 24
    Hu says:

    I see two potential problems with these predictions, although they may simply stem from my ignorance. My knowledge of biology is quite limited.

    One of them is that, as pointed out by Bob O’H above, it isn’t entirely clear how the predictions contradict those of the theory of evolution. If the two strains of bacteria live in reasonably stable and similar (albeit not identical) environments, they presumably don’t face particularly strong evolutionary pressures.

    The second problem concerns the verification of the prediction about horizontal gene transfer. Supposing some new genes are found in the E. coli bacteria and some unrelated ones, how can one rule out the possibility that at least some of the genes evolved in the E. coli and spread to the others, without begging the question?

    I’ll be thankful for any clarifications.

    Frost122585:

    How does horizontal gene transfer bring us any closer to “real probabilities”? As far as I know, HGT is less well understood than mutations, which makes it harder to estimate the probabilities. Am I missing something obvious?

  25. 25
    Q says:

    Is it reasonable to predict that the e coli genes would still be the same?

  26. 26
    Janice says:

    AussieID,

    They don’t so much get passed as get swallowed. Transmission is faecal/oral.

  27. 27
    lars says:

    OK, I think I’m getting it now… I believe idnet is predicting that (a) the different E. coli genomes will each have some functional genes unshared with the other genome, but that (b) these genes will be shown to have originated via gene transfer as opposed to RM+NS. How does the latter prediction arise from ID? IDnet explained above that ID says undirected RM+NS is not capable of much; so any new, functional genes must have arrived some other way. Hence, gene transfer (if we exclude new intelligent input … so this prediction assumes not only ID, but also assumes that intelligent input stopped before baboons and humans diverged… which I guess is basically Common Descent, but goes farther than Behe, who argues for intelligent input throughout the evolutionary process).

    Be that as it may, it’s not obvious to me how you would test this prediction — how do you know if a gene came about by gene transfer? Do you check other genomes for similar genes? Whose genomes do you check – the hosts’?

  28. 28
    Nochange says:

    Janice,

    So for those of us who *don’t* eat poop, would that mean that we don’t have E. coli? (I would expect E. coli to be more common among Darwinists than among IDists – how’s that for a prediction?).

    I mean, I could understand if there are still some weird tribes that carry E. coli, but wouldn’t E. coli have gotten wiped out in modern society if it’s all gotten through eating poop? Either that, or there’s another way to get it? In the womb?

  29. 29
    Janice says:

    Nochange,

    Strictly speaking, you don’t have to eat poop – just the E.coli that was in it.

    So how do you know you don’t eat or drink E. coli?

    Do you subject everything you plan to swallow to microbiological testing beforehand?

    Ever watched a cooking show and seen those celebrity chefs using their bare hands to mix a salad or taste a sauce or test a steak for how well done it is? Does everybody working in food preparation always wash their hands properly after using the toilet? Obviously not or there wouldn’t be outbreaks of Hep A.

    Ever eaten an apple before washing it thoroughly? I could go on but I think that’s enough.

  30. 30
    russ says:

    This is a bit off topic, but this molecular biologist says [his strawman version of] ID is dumb.

    http://www.humanevents.com/article.php?id=23404

    AIDS was unknown just thirty years ago. HIV, the virus that causes AIDS, did not exist fifty years ago. It evolved from a relatively harmless virus of lower primates. A new species evolved within our own lifetimes, before our own eyes. We developed drugs to combat it. It then went on to evolve drug resistance, again while we actually watched it happen and documented the timelines and intermediate forms.

    I haven’t finished “The Edge of Evolution”, so I haven’t gotten to the HIV discussion (I think there is one). This guy implies he’s observed macroevolution. What gives?

  31. 31
    idnet.com.au says:

    lars. You get it.

    First, I am a doctor. I know babies are born without bacteria. I know also where they come out and that the area is rife with E Coli and other bugs. You don’t have to eat faeces to get E Coli. Has anyone ever had the runs? That was from part of someone’s faeces ending up in your mouth.

    The quoted paper demonstrates that these populations of E Coli have been separated for a long time.

    If E Coli over 3 billion generations can engineer new systems from RM and NS then ID is unlikely to stand. Until we do the research, how will we know?

    It is not hard to determine which genes are from LGT.

  32. 32
    bornagain77 says:

    Russ,
    HIV demonstrated a trivial gain in complexity, but destroyed more complexity from its host life form (us) than it gained.

    as put by Dr. Behe:

    Second, the viroporin (of HIV) is not some new molecular machine. There is no evidence that it exerts its effect in, say, an ATP- or energy-dependent manner. Rather, similar to other viroporins, the protein simply forms a passive leaky pore or weak channel. (4,5) This situation is probably best viewed as a foreign protein degrading the integrity of a membrane, rather than performing some positive function.

    Thus, Since the non-living HIV destroyed more complexity than it gained, The HIV stayed within, what is termed “the principle of Genetic Entropy”.

    As well all other mutations, to living organisms, that are claimed to be beneficial, always “break” something or turn something off (see post 22) to get their so called beneficial adaptation. Thus in truth “Genetic Entropy” is the foundational rule of biology for all advantageous adaptations. That is to say all advantageous adaptations of a sub-species from a parent species to new environment will be found to come at a cost of information from the parent species.

  33. 33
    idnet.com.au says:

    “The cost of CGS resequencing services from Nimblegen Systems is currently $7500 per clone for E. coli.”

    Sounds cheap to me.

  34. 34
    idnet.com.au says:

    “Comparison of E. coli O157’s sequence, the pathogenic bacteria that often infects ground beef, with that of its harmless E. coli cousin revealed 1,387 new genes in the virulent version. There are ‘DNA islands’ of sequences unique to 0157 scattered throughout the genome. Conversely, there are islands in the laboratory E-coli strain containing 530 genes that are not found in 0157. Many of the genes in the 0157-specific islands are thought to have arisen through cross-species transfer from other bacteria. “The sheer magnitude of the differences was totally shocking to us,” says Perna. Though the 0157 strain was recognized only in the last 20 years, it is thought to have diverged from the harmless version some 4.5 million years ago.

    GENOMICS: E-coli Sequence Holds Surprises; Applied Genetics News, Feb, 2001

    http://findarticles.com/p/arti.....i_70907653

  35. 35
    bornagain77 says:

    Slightly Off Topic:
    I thought this was interesting:

    New Stem Cell Technique Effects Cure

    http://www.philly.com/philly/w.....scure.html

    Scientists have the first evidence that those “reprogrammed stem cells” that made headlines last month really have the potential to treat disease: They used skin from the tails of sick mice to cure the rodents of sickle cell anemia.

    …The study, published in the journal Science, doesn’t bring this potential therapy closer to people just yet. Big hurdles remain, including a risk of cancer from the reprogramming method.

    ….The researchers converted those skin cells into iPS (Induced Pluripotent stem) cells by infecting them with viruses engineered to change the skin cell’s gene activity so they would resemble embryonic cells.

    Using DNA splicing techniques in those cells, the researchers then snipped out the small mutated stretches of DNA that cause sickle cell anemia and filled those gaps with bits of DNA bearing the proper genetic code.

    Next the researchers treated the corrected iPS cells with another kind of virus – this time one “designed” to induce genetic change the cells to mature into bone marrow cells.

    Finally,, each mouse was given an infusion with the corrected marrow cells created from its own skin cells.

    Those cells set up permanent residence in the animals bones and began producing blood cells – the major function of marrow cells – and releasing them by the millions into the animals circulatory system.

    But now the blood cells being produced were free of the sickle cell mutation.

  36. 36
    bornagain77 says:

    ellazimm,

    The principle of Genetic Entropy remains intact and robust, even for HIV’s trivial gain in complexity. This is because HIV is a non-living “hijacker” into each and every person it infects. HIV trivial gain in complexity destroys far more tremendous complexity each and every time it infects a person.
    Is complexity in the whole human race lost to HIV’s trivial gain in complexity? NO, for HIV has not infected the entire population of humans. Yet Genetic Entropy still remains intact because each and every human being, the HIV interacts with and infects with its new trivial gain in complexity, suffers a severe loss in the integrated complexity necessary for life.
    I stress that this tremendous complexity is clearly lost, and Genetic Entropy is clearly payed for in infected Humans EACH and EVERY time HIV interacts with a specific infected human.
    As well, I don’t see how HIV is demonstratively any closer to the very tremendous and very specific complexity, that is absolutely necessary to be accomplished, to actually become “alive” and self-sustaining. Unless you can prove how a “passive” ring structure will lead to the very specific complexity necessary for life, I think HIV’s perceived violation of Genetic Entropy will be falsified on this front as well.

    Thus the seeming violation of “Genetic Entropy” in HIV is, when viewed soberly, clearly payed for by the tremendous complexity that is lost in each and every individual infected, each and every time infection occurs.

  37. 37
    bornagain77 says:

    idnet.com.au,

    I’m still trying to figure out how this prediction fits into the current ID/Genetic Entropy Mo^del:

    “I predict that there will be extra genes in baboon E. coli and extra genes in human E. coli but that the origin of these functioning genes will be gene transfer.”

    Which particular gene transfer study are you basing this prediction on? Is not this a sub-section of the symbiotic evolution that Dr. Lynn Margulis was trying to popularize in her book “Acquiring Genomes”: A Theory of the Origins of Species,

    I went to the study you cited and found this:

    “Comparison of O157’s sequence with that of its harmless E. coli cousin revealed 1,387 new genes in the virulent version. There are ‘DNA islands’ of sequences unique to 0157 scattered throughout the genome. Conversely, there are islands in the laboratory E-coli strain containing 530 genes that are not found in 0157.”

    Then I found the total number of genes for E-coli:

    E. coli 4,639,221 base pairs: 4,377 genes: 4,290 of these genes encode proteins; the rest RNAs.

    530+1387= 1917 gene difference of 44.6% between the two different E-coli’s

    That’s quite a lot of difference to attribute to solely to “gene transfer”.

    As well, In the ENCODE studies we are finding that a large portion of genomes (at least for higher life forms) appear to be poly-functional thus poly-constrained to this type of radical change you seem to be stipulating for E-coli (Sanford Genetic Entropy pg. 141). I believe that much of the E-coli genome will be also found to be similarly poly-functional and thus poly-constrained to this type of radical change you seem to be predicting for ID.

    These following articles will give you an indication where I am having problems with your gene transference prediction for ID.

    http://www.genome.gov/25521554

    BETHESDA, Md., Wed., June 13, 2007 – An international research consortium today published a set of papers that promise to reshape our understanding of how the human genome functions. The findings challenge the traditional view of our genetic blueprint as a tidy collection of independent genes, pointing instead to a complex network in which genes, along with regulatory elements and other types of DNA sequences that do not code for proteins, interact in overlapping ways not yet fully understood.

    http://www.boston.com/news/glo.....ed/?page=1

    “The science of life is undergoing changes so jolting that even its top researchers are feeling something akin to shell-shock. Just four years after scientists finished mapping the human genome – the full sequence of 3 billion DNA “letters” folded within every cell – they find themselves confronted by a biological jungle deeper, denser, and more difficult to penetrate than anyone imagined.

    “Science is just starting to probe the wilderness between genes,” said John M. Greally, molecular biologist at New York’s Albert Einstein School of Medicine. “Already we’re surprised and confounded by a lot of what we’re seeing.”

    A slew of recent but unrelated studies of everything from human disease to the workings of yeast suggest that mysterious swaths of molecules – long dismissed as “junk DNA” – may be more important to health and evolution than genes themselves.”

    Thus, as you can see idnet.com.au, gene transference, on such a large scale as you seem to be indicating, is severely problematic with the current state of what is known.

  38. 38
    lars says:

    It’s not totally clear to me that if your prediction were fulfilled, it would unqualifiedly support ID; rather, it would seem to disconfirm NDE. Which is fine, and useful, but I think the distinction should be made explicit, so that Darwinists don’t have a basis for saying you’re making false claims of testing ID.
    Basically it would be one more data point along the lines of Behe’s research in EoE, showing the poverty of what RM+NS is able to achieve in X number of generations, right? And he already has some data about E. coli, so this would be a nice complement to it.

    I would like to hear a Darwinist comment on this research proposal: if your prediction were shown correct, would that confirm ID and disconfirm NDE? if your prediction were shown incorrect, would it falsify ID and verify NDE? It would be great to have these reactions in advance, so that we don’t have to solicit them in a context of “My prediction was right, so now will you convert to ID?” 🙂 And as you note, it would also advance the discussion of whether ID, and NDE, are falsifiable or verifiable.

  39. 39
    SeekAndFind says:

    RE:
    ——————————
    What do you think of my predictions? Can ID make predictions? Is ID testable? Will anyone do this experiment?
    —————————-
    In respect to the E-coli, I think your proposal needs to be taken seriously.

    One of the biggest hurdles ID faces is the perception that it isn’t falsifiable.

    By extension to that, the other hurdle is this — because it isn’t falsifiable and testable, ID believers teach us nothing
    about the causes and cure for contagious diseases.

    Take this editorial from the Wall Street Journal for instance ( written yesterday by Lawrence Krauss, Professor of
    physics and astronomy at Case Western Reserve University )…

    First, he decries the fact that on average, our students are being beaten by kids from Asia and other countries in standardized science tests. Then his entire piece is essentially to present the case that we need to encourage our
    young ones to master the tools that lead to expertise in science. Fair enough.

    But here’s the key sentence that shows his anti-ID bias ( the Wall Street Journal requires registration so I’ll have to
    type the sentence for you ) :

    “… science and technology will be essential to meet the challenges to face as a society. When reports began to surface warning that the avian flu might become a threat to humans, for example, everyone from the president down called for studies to determine how quickly the virus would mutate from birds to human beings. No one suggested that ‘intelligent design’ for example, could provide the answer.”

    The unstated assumptions in the above small paragraph are :

    1) Belief in ID does nothing to help us find the cause and possible cure for the spread of diseases like avian flu.

    2) Understanding Darwinian evolution CAN help us find the cause and possible cure for the spread of diseases like avian flu.

    3) Those who believe in ID are backward and a hindrance to scientific progress.

    That’s the popular perception about ID from the elite. There really is a need to overcome this hurdle.

  40. 40
    congregate says:

    idnet.com.au at 31:

    If E Coli over 3 billion generations can engineer new systems from RM and NS then ID is unlikely to stand. Until we do the research, how will we know?

    But after the research is done, we still won’t know. If new systems arise, how do we distinguish between those that arose through RM and NS and those that arose through an intervening designer?

  41. 41
    DaveScot says:

    congregate

    If new systems arise, how do we distinguish between those that arose through RM and NS and those that arose through an intervening designer?

    To me this is equivalent to asking “if a pink elephant with wings were observed how could we distinguish between chance and design?”. Since I never expect to see such a thing it seems like nothing more than wool gathering to discuss it.

    However, the short answer is we would make the distinction the same way we do for any other case where design is suspected (murder, arson, sabotage, archeological finds, etcetera) – through statistical analysis.

    Since we haven’t made the observation you speculate about why don’t we talk about an actual observation.

    In billions of trillions of replications of P.falciparum where each replication gave RM+NS a chance to make a heritable genetic change we observed exactly what statistical analysis predicted given the number of replications and a background mutation rate of one nucleotide change per billion nucleotides copied – no phenotype change resulted that wasn’t limited to at most a few chained interdependent nucleoties.

    With this real world data regarding the performance of RM+NS in hand we’re still expected to take it on faith that with orders of magnitude fewer replications RM+NS somehow generated a plethora extremely complex novel proteins and attendant regulatory mechanisms that morphed reptiles into mammals. Non sequitur.

  42. 42
    jerry says:

    Seekandfind,

    You said

    “That’s the popular perception about ID from the elite. There really is a need to overcome this hurdle.” and also

    “2) Understanding Darwinian evolution CAN help us find the cause and possible cure for the spread of diseases like avian flu.”

    The problem would disappear if people stopped harping here on how neo Darwinism has been falsified or is bogus. It gives the impression that it has no value but in reality it is the basis for much of modern medicine and is no threat to ID and evolution. People here should embrace neo Darwinism but separate its value for medicine from evolutionary biology.

  43. 43
    lars says:

    congregate:

    But after the research is done, we still won’t know. If new systems arise, how do we distinguish between those that arose through RM and NS and those that arose through an intervening designer?

    Yeah, that’s bugged me too. It seems like an underlying assumption in Behe’s research, and this proposal too, is that whatever we see happening in known history (as opposed to prehistory) can safely be attributed to natural causes, not a designer. But if we accept a designer that worked in prehistory, why should we assume that he/it must have stopped working in observable history? There’s no reason to.

    However, if you look at it conversely, I think the research makes more sense: if undirected causes (RM+NS) are responsible for producing complex new systems, then they should continue to produce new functions the same way in observable history as they supposedly did in producing all these amazing systems. If new function does not arise in the time NDE predicts it should, or if such new function arises solely due to other causes (like lateral gene transfer), then that disconfirms the ability of RM+NS to produce new function as laid out by NDE.

    The latter effect then supports ID as the only viable alternative, whether in history or prehistory or both.

  44. 44
    bornagain77 says:

    Jerry,
    I find your comment interesting in that Dr. Behe sought to clarify what evolution could and could not do and was slandered for sticking true to empirical science. No Sir Neo-Darwinism doesn’t lead to better practice of modern medicine for it must continually battle what is becoming increasingly obvious to ID proponents. In fact a neo-Darwinists is more likely to investigate bogus areas of research as far as medicine is concerned for his foundational belief, in large scale complexity being generated naturally, is bogus to begin with.

  45. 45
    bornagain77 says:

    lars,
    Intelligent Design (CSI) was implemented at the level of parent species with loss of information from parent species upon all favorable sub-speciation events to different environments i.e. You don’t have to worry about some unknown complexity being generated in the lab. Adaptations will always conform to Genetic Entropy.

  46. 46
    lars says:

    idnet, 35:

    “The sheer magnitude of the differences was totally shocking to us,” says Perna. Though the 0157 strain was recognized only in the last 20 years, it is thought to have diverged from the harmless version some 4.5 million years ago.

    Sounds like the 4.5mya was estimated prior to this study, not as a result of finding the ‘magnitude of the differences’. So what is the impact of this discovery – that the amount of change was (as they seem to imply) much greater than predicted by the standard evolutionary model? To push back the divergence estimate? To attribute the change to other mechanisms than RM+NS, like gene transfer?

    Many of the genes in the 0157-specific islands are thought to have arisen through cross-species transfer from other bacteria.

    I wonder if that’s an inference from the new data (“RM+NS couldn’t have done it so it must have been LGT”), or an independently supported result?

  47. 47
    lars says:

    BA77 @46, I’m confused by the phrase “ID was implemented”, but I think you’re telling me this: yes, ID assumes that any that occur in the lab are due to undirected natural causes. (Am I understanding you right?)

    If so, why should that assumption be made? It doesn’t seem to be implied by the premise that design is detectable. Is it just a pragmatic assumption that’s deemed necessary for conducting research?

    Then, where does “the lab” end? Is our recorded medical history of HIV and the malaria parasite in “the lab”, even though it occurred out in the real world? Behe apparently considers it so. What about the “3X10^9 generations of separate development” of E. coli over 20-25 million years, that idnet is talking about? He seems to be making the same assumption (I think). And if these are in “the lab”, what does the lab not include?

    Finally, if there is a designer and he decides to introduce some new systems in the middle of your lab experiment, should ID be falsified by that event? Such a falsification condition doesn’t seem to me to fit the point of ID very well.

    This point may seem unimportant to the disagreement between ID and NDE, but I think we should be careful what is predicted in the name of ID, lest ID fail due to excessive modesty! If we really want to follow the evidence wherever it leads, on what basis can we exclude ongoing Designer intervention? Please correct me if I’m misunderstanding the (proposed) direction of ID research.

  48. 48
    lars says:

    Don’t get me wrong — I’m not saying (#48) that the proposed research is not useful for refuting NDE and advancing ID.

    As I write and think about it, I’m coming around to the idea that this assumption (that no designer ever, or hardly ever, intervenes in producing new biological systems in recorded history) is necessary for making predictions, even though it doesn’t seem to be really a claim of ID.

    Good to make it explicit though, so that we don’t unwittingly promote deism.

  49. 49
    jerry says:

    bornagain77,

    Your are certainly entitled to your beliefs but I believe that neo Darwinism explains a lot of things and I also believe trying to dispute it makes one look uninformed and contentious. Instead point out its limitations but I believe trying to debunk it entirely is a fools errand and very counter productive.

    Dembski has no problem wtih neo Darwinism, just the Blind Watchmaker Thesis.

  50. 50
    gpuccio says:

    lars:

    I agree with you that, in principle, an ongoing intervention of the designer is a real possibility, and that could include anything whicho happens both in the lab and in the wild. Obviously, the modalities of the implementation of design are fundamental here, and that’s exactly what we don’t know, and scientific research could help understand, once the design assumption is more widely accepted. It seems evident that some modalities of design implementation (accasional and sudden, or frontloaded) are less likely to be detected in historical time, while a low-level continuous implementation could be detected more easily.
    What we certainly know, and I think that is what Behe comments about, is that usually we “don’t” detect design implementation in what we observe, both in the lab and in the wild. We just observe random variation in the limits of what can be expected from a random phenomenon, and occasional natural selection of such a trivial variation. That’s what Behe’s book is about, and that’s perfectly consistent with Dembski’s theoretical assumptions.

    Obviously, if we were to witness a clear design implementation, that would be a very good observation to understand how design is introduced in reality. But, if the design implementation happens continuosly, it could be a very low-level phenomenon, and probably we will have to improve greatly our understanding of physical laws before we can really detect it.

    Anyway, I stay convinced that the problem of design implementation in biological beings is very similar to the problem of the interacion between our consciousness and our body: both are examples of mental properties beong superimposed to matter by conscious beings.

    Perhaps it’s not by chance that Denyse keeps two parallel blogs on those two subjects…

  51. 51
    bornagain77 says:

    Jerry, let’s see where the evidence lines up and see if what I assert has any merit.

    Behe found no evidence of complexity being generated in living organisms by RV/NS in far greater replication/mutation events than have occurred since mammals are supposed to have split from reptiles.

    As DaveScot pointed out, when this evidence is extrapolated to more complex organisms, we have no reason to believe that random processes are generating complexity for higher life-forms without intelligence. Or as he says:

    “With this real world data regarding the performance of RM+NS in hand we’re still expected to take it on faith that with orders of magnitude fewer replications RM+NS somehow generated a plethora extremely complex novel proteins and attendant regulatory mechanisms that morphed reptiles into mammals. Non sequitur.”

    As well the fossil record and all other evidence I can find supports the ID implementation at level of parent species with loss of information (Genetic Entropy) being the rule for all successful adaptations/radiations of sub-species.

    “As Niles Eldredge and Stephen Jay Gould pointed out almost three decades ago, the general pattern for the evolution of diversity (as shown by the fossil record) follows precisely this pattern: a burst of rapid diversity following a major ecological change, and then a gradual decline in diversity over relatively long periods of time.”
    Allen MacNeill PhD (teaches evolution)

    But, lo and behold, Jerry that pattern fits the front-loaded ID followed by Genetic entropy mo^del to a tee.

    Allan MacNeill used cichlids to say evolution is currently happening but let’s take real a close look at what is happening with cichlids.

    African cichlid fish: a system in adaptive radiation research

    http://www.pubmedcentral.nih.g.....id=1635482

    of special note:

    Interestingly, ecological opportunity (the availability of an unoccupied adaptive zone), though explaining rates of diversification in radiating lineages, is alone not sufficient to predict whether a radiation occurs. The available data suggest that the propensity to undergo adaptive radiation in lakes evolved sequentially along one branch in the phylogenetic tree of African cichlids, but is completely absent in other lineages. Instead of attributing the propensity for intralacustrine speciation to morphological or behavioural innovations, it is tempting to speculate that the propensity is explained by genomic properties that reflect a history of repeated episodes of lacustrine radiation: the propensity to radiate was significantly higher in lineages whose precursors emerged from more ancient adaptive radiations than in other lineages.

    Jerry, all that means that the closer to the parent species that the sub-species is, the better chance it has for a successful radiation into a new ecological niche, Thus conforming to ID/Genetic Entropy as well as having no explanation from the evolutionary theory. (another evolutionary OOPS you could say)

    This following study shines a very powerful light on what I’m saying about the ID/Genetic Entropy :

    A Cambrian Peak in Morphological Variation Within Trilobite Species
    Mark Webster

    http://www.sciencemag.org/cgi/.....7/5837/499

    http://www.geotimes.org/july07.....72707.html

    Jerry in this study Webster studies Trilobites over their 270 million year history in the fossil record!

    What Did he find?

    Webster compiled morphological data for nearly 1,000 of the 17,000 different species of trilobites, a class of marine arthropods that died out by 250 million years ago, from 49 previously published sources. By tracking different morphological features — the number of body segments, for example — Webster found that trilobite species exhibited more variation during the Cambrian than in later periods, he reported in Science July 27. “Once you go beyond the Cambrian, the diversity of forms within any one species drops off,” he says.

    That’s ID/Genetic Entropy to a tee Jerry. Why did evolution peter out Jerry. 270 million years is a long time for evolution to strut its almighty stuff Jerry! I guess it just got bashful. AGAIN.

    Tishkoff; Andrew Clark, Penn State; Kenneth Kidd, Yale University; Giovanni Destro-Bisol, University “La Sapienza,” Rome, and Himla Soodyall and Trefor Jenkins, WITS University, South Africa, looked at three locations on DNA samples from 13 to 18 populations in Africa and 30 to 45 populations in the remainder of the world.

    “We found an enormous amount of diversity within and between the African populations, and we found much less diversity in non-African populations,” Tishkoff told attendees today (Jan. 22) at the annual meeting of the American Association for the Advancement of Science in Anaheim. “Only a small subset of the diversity in Africa is found in Europe and the Middle East, and an even narrower set is found in American Indian.

    That is Genetic Entropy Jerry.

    SHHHH, don’t tell that more evolved scientist (Watson) that he actually has less genetic information than Africans!

    In this following study, for ancient human DNA, we have clear evidence of Genetic Entropy being obeyed!:

    http://www.pubmedcentral.nih.g.....rtid=33358

    Of special note:
    Adcock et al. (7) clearly demonstrate the actual extinction of an ancient mtDNA lineage belonging to an anatomically modern human, because this lineage is not found in living Australians. Although the fossil evidence provides evidence of the continuity of modern humans over the past 60,000 years, the ancient mtDNA clearly does not, providing an excellent example of why the history of any particular locus or DNA sequence does not necessarily represent the history of a population. Adcock et al.’s

    They could not believe the loss of information happened thus they said the “continuous” fossil record was wrong. OOPS on evolution again.

    That’s ID/Genetic Entropy to a tee Jerry.

    As well fossilized plants follow the pattern for ID?Genetic Entropy:

    At one of the few petrified forests that sports ginkgo wood, I was told by the naturalist that ginkgos are old in the fossil record—they date from the Permian back when trees were first “invented”. She said that there are a number of species of fossilized Ginkgoaceae, with Ginkgo biloba, the only living (surviving) species, being one of them.

    That is Genetic Entropy to a tee Jerry.

    Here is a Paper that has confirmation of dogs and grey wolves staying within principle of Genetic Entropy.

    http://jhered.oxfordjournals.o.....0/1/71.pdf

    of special note:
    Some sequences found in dogs were identical to those in wolves…
    The sequence divergence within dogs was surprisingly large: the mean sequence divergence in dogs 2.06 + or – 0.07% was almost identical to the 2.10 + or – 0.04% (sequence divergence) found within wolves. (notice that sequence divergence is slightly smaller for the population of dogs than for the population of wolves)
    Coupled with the diverse morphology of domesticated dogs and known hazards of dog breeding, this evidence strongly indicates “front loaded adaptations” at a loss of information from parent species. Thus, this is genetic confirmation of the principle of Genetic Entropy for dogs from wolves!

    Of special note for the Mexican hairless dog (chihuahas);

    many founder halotypes were likely lost because of “genetic drift”

    The gene that determines hairlessness is nt but let^hal when homozygous.

    Thus clearly the “mutation” that causes hairlessness is not a gain in information.

    This following paper is more recent and more concrete in establishing the principle of Genetic Entropy for dogs/wolves:

    Origin of dogs traced

    http://news.bbc.co.uk/2/hi/sci.....498669.stm

    of special note:

    Their findings, reported in the journal Science, point to the existence of probably three founding females – the so-called “Eves” of the dog world.

    They conclude that intensive breeding by humans over the last 500 years – not different genetic origins – is responsible for the dramatic differences in appearance among modern dogs.

    and the paper itself:

    http://www.sciencemag.org/cgi/.....type=HWCIT

    Genetic Evidence for an East Asian Origin of Domestic Dogs

    Peter Savolainen,1* Ya-ping Zhang,2 Jing Luo,2dagger Joakim Lundeberg,1 Thomas Leitner3

    The origin of the domestic dog from wolves has been established, but the number of founding events, as well as where and when these occurred, is not known. To address these questions, we examined the mitochondrial DNA (mtDNA) sequence variation among 654 domestic dogs representing all major dog populations worldwide. Although our data indicate several maternal origins from wolf, >95% of all sequences belonged to three phylogenetic groups universally represented at similar frequencies, suggesting a common origin from a single gene pool for all dog populations. A larger genetic variation in East Asia than in other regions and the pattern of phylogeographic variation suggest an East Asian origin for the domestic dog, ~15,000 years ago.

    How did they trace the lineages?

    They traced it by the loss of genetic variation (the loss of “front-loaded” information from original parent species) Jerry.

    That is ID/Gentic Entropy to a tee Jerry.

    So you can call me uninformed and contentious and say that I’m running a fools errand, but I will stay true to evidence no matter what you think about me, because if you want to believe a lie that is your, God given, American right, just don’t drag me along and tell me I have to believe in the fairy tales as you do.

  52. 52
    idnet.com.au says:

    Jerry

    “NDE is the basis for much of modern medicine and is no threat to ID and evolution. People here should embrace neo Darwinism but separate its value for medicine from evolutionary biology.”

    I differ with you on the value of NDE to medicine. Antibiotic resistance was attributed to NDE. It kept research at bay for a long time because most resistance is actually due to plasmid gene transfer not NDE. Antibiotic resistance is still the champion of many texts when they look for “evidence” of NDE.

    To embrace neo Darwinism is a mistake. NDE is a way of explaining what we see in the biosphere. It does not explain the vast majority of what we see. Natural Selection is not in dispute. The power of Natural Selection to create complex specified information is in dispute. Everything non trivial in biology depends on CSI. NDE has no mechanism for generating CSI.

  53. 53
    pk4_paul says:

    “NDE is the basis for much of modern medicine and is no threat to ID and evolution. People here should embrace neo Darwinism but separate its value for medicine from evolutionary biology.”

    What nonsense.

  54. 54
    jdd says:

    idnet,

    again I am a little confused. Are you saying that all LGT is the result of ID?? I am not sure how LG is in conflict with NDE.

    thanks,

    j

  55. 55
    idnet.com.au says:

    jdd

    I am saying nothing of the sort. I am saying much as Prof Behe says, that NDE does not achieve much of substance.

    The experiment (which I hope might be done) extends the time and opportunities for NDE to produce the goods to 3 billion generations of E. coli.

    NDE must be able to perform something impressive in that amount of generations.

  56. 56
    hrun0815 says:

    NDE must be able to perform something impressive in that amount of generations.

    Wouldn’t we only expect ‘NDE’ to perform something impressive in that amount of generations if the environment those E. coli find themselves in were to change? You know, things like available sugars would be one such change in the environment, so we’d expect changes in genes that metabolize these sugars.

    But this expectation is true whether you look at it with ID eyes or with NDE eyes, is it not? Yet, I really don’t understand why you would expect changes in flagellar genes (again ID or NDE is irrelevant). Do you think the environment inside a baboon is significantly different from a human such that a different flagellum would be advantageous?

    Finally, I have to admit that I also do not understand why lateral gene transfer is submitted as an ‘ID mechanism’ and not part of NDE. Does NDE have some problem with LGT? Has it been shown that a potential designer uses LGT to design?

    So I really don’t understand why you would look at changes in

  57. 57
    congregate says:

    42 DaveScot- Your response is, well, nonresponsive.

    Since we haven’t made the observation you speculate about why don’t we talk about an actual observation.

    I was asking about the observation idnet.com.au speculated about. idnet.com.au claimed that evolution of some complexity within three million generations would significantly undercut ID. I don’t see how it would do so if ID has the same capabilities as RM+NS, plus more.

    With regard to the observations you discuss, I don’t understand why one set of real world data, the genetic history of one organism over a period of a few score years, is so convincing to you. Why is that?

    Is there good reason to believe that the current genetic state of P. falciparum and the environment in which that genetic history occurred are so representative of all of the history of life that the results should be taken as conclusively settling the capability of unguided evolution?

    For that matter, how can any observation provide evidence for the limits of evolution if a designer might have intervened at any point? Perhaps RM + NS was on the verge of making a significant change at some point, but a designer stepped in and redirected the process.

    If we allow for an omnipotent or “nonmaterial” designer, there can be no conclusive determination of what RM + NS is capable of, can there?

  58. 58
    jerry says:

    Any one who criticized what I said about neo Darwinism should learn about neo Darwinism and what I have actually said about it.

    ID is completely consistent with neo Darwinism as a science. Mutations do happen and are a major concern for modern medicine, natural selection and genetic drift do happen, allele frequencies in population change and medical health is affected by these processes. All are easily demonstrated. All are very relevant for modern medicine. I never said it had much to do with evolutionary biology. I believe people here need to upgrade their reading comprehension skills. Everybody is too quick to criticize as oppose to think.

    bornagain77 wrote a long comment completely unrelated to anything I said on this thread or have ever said at any time in the past on this blog. I read his comments though apparently doesn’t read mine. My guess is that genetic entropy is entirely consistent with neo Darwinism. I see no reason why it isn’t.

    As I continually say, neo Darwinism has a lot relevance for medical science but only explains trivial things in terms of evolutionary biology. This statement is unchallengeable because it fits the evidence closely. But if anyone wishes to respond, read what has actually been said.

    What is the basis for my statement? Behe’s Edge of Evolution for starters. It is an extensive discussion of the relevance of neo Darwinism.

  59. 59
    DaveScot says:

    congregate

    I was not non-responsive. I clearly stated the distinction between chance and design is made by statistical analysis. That’s as much as can be said until an actual case is observed so we have something to analyze. I doubt we will ever make such an observation because I don’t think the designer(s) of life are active in the process anymore and the best explanation is that life was front-loaded billions of years ago with all the complexity extant today and all the time since then has been an unfolding of a pre-planned phylogenesis with no subsequent intervention or design input.

    The case of P.falciparum is important because it is the largest test of evolutionary mechanisms in progress that we have available to study. No other eukaryote anywhere near as well studied as P.falciparum and that has replicated as many times while under observation exists. Even better the organism has been subjected to intense selection pressures by both man-made and natural obstacles to its survival. It is revealing to see which obstacles were overcome, which were not, and exactly how it was able to overcome some of those obstacles.

  60. 60
    bornagain77 says:

    Jerry,
    neo-Darwinism is completely inconsistent with the molecular evidence we now have. Genetic Entropy is completely incompatable with neo-Darwinism. For you to try to make some kind of peace, with the fallacy that blind purposeless processes (neo-Darwinist scenarios) are producing outstanding and stunning complexity on the molecular level, is far beyond me. If anything I will staunchly argue that neo-Darwinism severely pollutes a pure view for what is truly happening on the molecular level, for that is, IN FACT, what neo-Darwinism is actually doing. Shoot Jerry, neo-Darwinism isn’t even consistent with the fossil record (that is why punctuated equilibrium was postulated) I ask you, “How in the world is a known fallacy going to help medical research?” The last time I checked lies were a bad thing!
    I have no problem with natural selection (in fact I suspect an environmental feedback loop to the genome in the natural selection process of favorable adaptations to explain the speed of favorable adaptations), but the fact is that CSI IS in fact being degraded with each and every observed favorable adaptation we are seeing…I repeat and I stress this principle of Genetic Entropy (degradation of the genome) is completely inconsistent with what neo-Darwinism predicts and expects for complexity being generated. In fact in my long response to you, which you claim you read but clearly did not understand, you stated;

    “My guess is that genetic entropy is entirely consistent with neo Darwinism. I see no reason why it isn’t.”

    This statement of yours is so blatantly wrong I really don’t know where to start to try to correct you in this matter.

    How in the world is a theory that predicts no complexity will ever be generated without intelligence, and that all favorable adaptations to new environments will result in loss of CSI, comparable with a theory that says fantastic complexity can be generated by natural processes with no problem.

    Shoot man, you even said this:

    “ID is completely consistent with neo Darwinism as a science.”

    What amazes me is that you actually believe that.

    Man I can’t even write any more you got me so upset.

  61. 61
    Frost122585 says:

    Davescot, you need to recognize dog- there could be all kinds of stuff going on in other dimentions that we dont even know about. It is matter that is suspended inspace that makes the whole thing work- I mean look I dont think that this whole universe just went “poof” and unrolled a bunch of super SC- I think it is far more likly that there were processes inside of the universe relative in time and space to one another that interected to form the SC. Im not a big “Poof” its a tiger guy- that is either by DE or ID- i think you probably had matter that was transformed and built via inter-universal injections of information through a different dimention. It was somthing that Michio Kaku one said that brought this idea to my attention- Dembski said in NFL that information can in theory be introduced into matter wihtout adding any energy. Kaku pointed out once in a documentry about UFO’s that the shortest path between two points is not a straight line or any string at all but a hole. A worm hole can in effect introduce information into the universe from somewhere else without having to be part of the physical universe- this way information could be downloaded “directly” requiring no wave length.

    Just an Idea but I like it better than front loaded design becasue this way we can look for more design along the way and the possiblity of an active ID working from time to time in our universe.

  62. 62
    Frost122585 says:

    To visually support my idea of how it might have happened – think about a computer- now say you we inside of the computer- one of those programs for instance – what if you knew that there was a history of the program – a computation history- you might suppose that everything was front loaded but you know that we can go into a program at any pint and alter or add information- The person inside the computer would not understand this though because to him it was all part of the unfolding process. Perhaps the computer mind in this case is a program that moves across the spectrum and while considers historicity cant differentiate between what was and what is. There is no way this computer mind short of programming it could understand that there is another world where biological entitles are controlling its fate- when the new information appears it seems to be normal but not new-

    I think that we maybe living in a matrix like world more complex and real though. Where injections of information can govern the way we exist and experience life- but all of this appears to be in a historical linear patter- “possibly to both the program and the designer” but only the program (us) actually exists in a relativistic universe.

    As far as practical application it has the philosophical advantage of oppening up doors. As far as scientific explanation it opens up the feild of statistical analysis to a relativistic corralative process- lest we forget it is quantum physics and relativity that the “establishment” has failed to reconicle- In other words things might be happening that are not statistically related but part of the greater picture which we see linearly.

    This view might encourage us to take the history of what we do know and predict the next unexpected change not by linear statistical analysis but by “obejective coheisive arrangemnent”-

    Marying the ralative to the statisitical or the specificity to to the complexity finding trends that are “objectively likely” but not mathematically supported.

    Kant called this intuitive transcendentalism-

    IMO Kant was the greatest philosophical-“scinetific” mind of all time. Even though he said euclidian geomatry was the end all be all and non-euclidian geomatry through einstein proved him worng- I am one who thinks that he expected this but merely reduced the non-euclidian to regular geomatry as a whole because he expected einstein and that it would eventually revert back as mathematics cleared up and reconciled the templet of euclid with einstein.

    Anyways, “my fasination with realities origins” maybe somthing to think about though-

  63. 63
    Frost122585 says:

    My argument against statistical analysis is from the perspective of Johannes Keplar who said it was like living in Plato’s cave- taking everything and putting it into math and worse incomplete mathematical analsys as Kurt Godel pointed out- does not describe actual reality because it is incomplete and therefore not suficient to describe “the world as we know it” -this is why those stupid computer programs where DE works are incorrect. They are essentially a human logical mind that takes subjective information and makes it horribly communicable-

    The real universe is out of our reach- but in our reach to investigate- this objective idealism opens up the possibility for differing modes of investigation – ways of guessing based on intuitive apriori knowledge instead of being forced to live in a cave where all we can know and think about is merely a “shadow” of the actual world.

    We should expect design- and prepare for it even if we cant yet predict its nature- this is the true mode of inquiry (what is possible)- not one where you know what’s going to happen and you test it but where you prepare for things the best you can and shape your view point based on its intuitive impact on you – open-minded with expectations.

    The shape of things to come is more important than the rules by which you must fallow to know what comes next- any rule that exists must be ignored as it only confines one’s intuitive sense which is the true guider of a man’s compass-

    Or as Einstein put it when he was talking to J D Rockefeller

    Rockefeller: You know Einstein to me its all about organization- I put my faith in organization…

    Einstein: I put mine in intuition.

    There was a book recently written called the deviant advantage. As the other quickly pointed out his definition of deviation was statistical not moral- but as one can see statistical deviation is almost an oxymoron- if it doesn’t fit stats how can we account for it? The book was about how all of the great ideas have come from minds which chose to deviate from the norm. But why did they do it? It was given their intuitive insights and adventurous unbridled spirit that moved those accomplishments and theories to th forefront- This is the way we should do science- this is the true way to do experimentation – this is where the real break troughs reside. This explains why we havent had the success treating degenerative diseases and th elike that we once expected would be eradicated so quickly- people’s ignorance and demand for control of other people’s minds have constrained expierementation in recent years- you cant get a grant unless you idea is liked- you cant get into a pristine college unless you have a 4.0 –

    Albert Einstein failed the liberl arts section of his college enterance exam.

    A statistical society is a stupid society- statistically speaking that is.

  64. 64
    jerry says:

    bornagain77,

    said

    “For you to try to make some kind of peace, with the fallacy that blind purposeless processes (neo-Darwinist scenarios) are producing outstanding and stunning complexity on the molecular level, is far beyond me.”

    I am not making any peace at all. In fact I am being a little belligerent and trying to rid a nonsense mentality exhibited by many on this blog. Probably an impossible task since many come here with with moral certainty and blinders on about things they do not understand. As I said the reading comprehension skills are not the best on this blog of which your comment above is an exemplar. Blind knee jerk reactions describe a lot of the posts. I am merely stating the facts as I see them. By the way when did I bring up anything about the fossil record that you disagree with?

    I suggest you try and understand just what neo Darwinism is and can do. After all both Behe and Dembski accept it so try to understand why. The thing they say about it is that it is limited. Which is completely consistent with what I have said. There do I have to spell it out any clearer. Neo Darwinism works but it is limited and is very appropriate as a model for much of genetic diseases and because of this is very valuable in modern medicine.

    An aside; explain to me what novelty genetic entropy has created. I never said neo Darwinism created any novelty. If you can show me where I said that it would be appreciated so I can correct it.

  65. 65
    bornagain77 says:

    Jerry,
    I respectfully disagree with you,

    Here is a interesting article by Philip Skell refuting your assertion that neo-Darwinism is important to biology and medicine;

    Your assertion:

    “It gives the impression that it (neo-Daewinism) has no value but in reality it is the basis for much of modern medicine and is no threat to ID and evolution.”
    Jerry post #43

    The article;

    http://www.discovery.org/scrip.....38;id=2816

    of special note from the article:

    ” the modern form of Darwin’s theory has been raised to its present high status because it’s said to be the cornerstone of modern experimental biology. But is that correct? “While the great majority of biologists would probably agree with Theodosius Dobzhansky’s dictum that ‘nothing in biology makes sense except in the light of evolution,’ most can conduct their work quite happily without particular reference to evolutionary ideas,” A.S. Wilkins, editor of the journal BioEssays, wrote in 2000 “Evolution would appear to be the indispensable unifying idea and, at the same time, a highly superfluous one.”

    I would tend to agree. Certainly, my own research with antibiotics during World War II received no guidance from insights provided by Darwinian evolution. Nor did Alexander Fleming’s discovery of bacterial inhibition by penicillin. I recently asked more than 70 eminent researchers if they would have done their work differently if they had thought Darwin’s theory was wrong. The responses were all the same: No.

    I also examined the outstanding biodiscoveries of the past century: the discovery of the double helix; the characterization of the ribosome; the mapping of genomes; research on medications and reactions; improvements in food production and sanitation; the development of new surgeries; and others. I even queried biologists working in areas where one would expect the Darwinian paradigm to have most benefited research, such as the emergence of resistance to antibiotics and pesticides. Here, as elsewhere, I found that Darwin’s theory had provided no discernible guidance, but was brought in, after the breakthroughs, as an interesting narrative gloss.

    In the peer-reviewed literature, the word “evolution” often occurs as a sort of coda to academic papers in experimental biology. Is the term integral or superfluous to the substance of these papers? To find out, I substituted for “evolution” some other word – “Buddhism,” “Aztec cosmology,” or even “creationism.” I found that the substitution never touched the paper’s core. This did not surprise me. From my conversations with leading researchers it had became clear that modern experimental biology gains its strength from the availability of new instruments and methodologies, not from an immersion in historical biology.”

    Jerry you stated:

    “ID is completely consistent with neo Darwinism as a science.”

    This is blatantly false! Please tell me how you reached this fallacious conclusion. (please use small words, as my reading comprehension is not as advanced as yours, as you have pointed out)

    You stated:

    An aside; explain to me what novelty genetic entropy has created.

    ID (Intelligent Design) creates all novel complex information (CSI). Genetic Entropy states that no new information will ever arise by natural processes and will decrease upon sub-speciation events. (I can go get a dictionary, if you want, and try to put Genetic Entropy into bigger words so you will finally be able to understand it.)

    Since I am having such a hard time reaching your superior intellect, and you think I’m retarded and will not listen to me, may I refer you to Dr. Sanford’s book; “Genetic Entropy” (It has plenty of big words for you to chew on.)

    http://www.amazon.com/Genetic-.....1599190028

    Book Description:

    “Dr. John Sanford, a retired Cornell Professor, shows in Genetic Entropy and the Mystery of the Genome that the “Primary Axiom” is false. The Primary Axiom is the foundational evolutionary premise – that life is merely the result of mutations and natural selection. In addition to showing compelling theoretical evidence that whole genomes can not evolve upward, Dr. Sanford presents strong evidence that higher genomes must in fact degenerate over time. This book strongly refutes the Darwinian concept that man is just the result of a random and pointless natural process.”

  66. 66
    jerry says:

    bornagain77,

    You should read what I say. At the end of my post, I said

    “I never said neo Darwinism created any novelty. If you can show me where I said that it would be appreciated so I can correct it.”

    So that should give anyone reading it a hint that I do not think neo Darwinism is the source of much of the change in biological organisms for the last 3.5 billion years. In fact on numerous occasions in the last couple years I have argued just the opposite. So there we have a starting point and any discussion should not be about evolution unless you want to argue that neo Darwinism explains a lot of evolution and then I will argue against it.

    Does the fact that I hold this belief mean that the theory is totally useless. The answer is no. Numerous theories are very good at certain things but not good at others. Is this hard to understand. A good example is Newton’s theories of motion. A great theory for most motion we observe but breaks down when the relative motion gets very high.

    So where are we. I maintain that ID is completely consistent with neo Darwinism as a science and I see no problem with this if you look at just the mechanisms of neo Darwinism. Mutations do happen. ID does not deny this. These are a major concern for modern medicine. ID does not deny this. Natural selection and genetic drift do happen. ID does not deny this. Allele frequencies in population change and medical health is affected by these processes. ID does not deny this. All are easily demonstrated. All are very relevant for modern medicine. I never said it had much to do with evolutionary biology. So leave it out of the discussion.

    And I bet if you asked John Sanford, he would agree with each of the previous statements. I bet Behe, Dembski, Meyers and anyone else you get from the ID proponents would agree. What they disagree with is the claims many make for neo Darwinism in terms of evolutionary biology not that the mechanisms of neo Darwinism don’t happen.

    Please read that I am using neo Darwinism in modern medicine not evolutionary biology. Mucho, mucho modern medicine is about mutations to the genome and its effect on people and what types of drugs, procedures, operations can be used to counteract the deleterious effects of these mutations. The huge growth in medicine can mainly be explained by this phenomena. Behe’s book, The Edge of Evolution was essentially about mutations in microbes and how they have had a devastating effect on humans. He looked at mutations in both the microbes and humans and how natural selection played a role. That sounds like neo Darwinism to me. The main thrust of the book was not that neo Darwinism didn’t work but what were its limits or the edge of change that it could produce.

    From what I understand Sanford’s book is about natural selection and what it can do when presented with various types of mutations. That sounds like neo Darwinism to me. The issue with medicine is much different than that for evolutionary biology. Here we are dealing with negative mutations and what effect it can have on the person or population of a species. A lot of the mutations which are negative on the Kimura curve are in a selectable region. And neo Darwinism works in the negative region as well as the positive region and has deleterious effects.

    So neo Darwinism is not very good for the big things of evolution but it is very good for explaining a lot of the problems of modern medicine. And to deny this is foolish.

    An aside. I believe the best way to approach the argument about the relevance of neo Darwinism in evolution is to accept the theory and its mechanisms and then point out the real benefits are in medicine where mutations have a significant role but that in the evolution area it is mainly a complete bust with only trivial changes to point to. It is great at the negative end as an explanation and terrible at the positive end in explaining evolution. But to continually pan it is counter productive. Unfortunately it works but mainly in a negative direction.

  67. 67
    bornagain77 says:

    Jerry,

    A boy brings an F home for a grade in English class. The father looks at his son and says,”But son, English is the language that you speak at home.”

    Neo-Darwinism, the primary axiom of biology as Sanford calls it, is the reigning paradigm of biology.

    Its common meaning in society, and especially on this very blog, is that all life arose by common descent by purely natural causes i.e. by RV/NS.

    You are clearly obfuscating neo-Darwinism’s common meaning by saying, “Well I didn’t mean neo-Darwinism in that very large sense, I meant neo-Darwinism in only this very limited, restricted, sense.
    That limited, very restricted, sense for neo-Darwinism is commonly called micro-evolution, especially on this blog Jerry.

    Dr. Behe and others are very clear, and take great pains of effort, to show that neo-Darwinism, as it is commonly understood in society, and commonly used on this very blog, is blatantly false. And Yes, they (Dr. Behe and others) do say that “micro-evolution”, which has a much more specific meaning than neo-Darwinism does, does indeed occur.

    I can assure you that Dr. Behe, Dr. Sanford, Dr. Dembski, as well as numerous others, will, without any hesitation whatsoever, say a resounding NO! when asked the question, “Do you believe in neo-Darwinism?”

    So why not use the term micro-evolution instead of neo-Darwinism when that is what you really mean Jerry?

  68. 68
    Joseph says:

    Why don’t you just read what Jerry writes instead of jumping to the wrong conclusion?

  69. 69
    idnet.com.au says:

    hrun0815

    Classical NDE is envoked to explain the origin of new traits by very small changes over long periods of time. The changes occur by mutation of existing DNA and the resulting changes in proteins, processes and structures. Lateral gene transfer supplies material for change but it does not come from neodarwinian processes. It is simply borrowed from another organism. Explaining the origin of the genes that are transfered in is another question.

    Flagellar proteins are interesting. We should see some mutations that are neutral in these genes.

    It will take years to assess the data gained from the sequencing I have suggested. I think it will add to our understanding of how powerful NDE is over 3 Billion generations and whether ID is threatened by NDE.

  70. 70
    pk4_paul says:

    Please read that I am using neo Darwinism in modern medicine not evolutionary biology.

    You just think you are.

    Mucho, mucho modern medicine is about mutations to the genome and its effect on people and what types of drugs, procedures, operations can be used to counteract the deleterious effects of these mutations.

    Mutations were discovered independently of the efforts of Darwin’s successors to spread his theory. They were subsequently incorportated into a pre-existing theory. Had Darwin never lived mutations would still have been discovered and their deleterious effects observed in the practice of medicine.

  71. 71
    tribune7 says:

    Frost122585–you need to recognize dog- there could be all kinds of stuff going on in other dimentions that we dont even know about.

    I think what we can know is that when someone posts something like this at 7:33 a.m. on a Saturday morning he has had one heck of a Friday night.

  72. 72
    bornagain77 says:

    Jerry and Joseph,

    Why should anyone here on this site try to make peace with the term neo-Darwinism when the term neo-Darwinism is exactly what has been fought against for so long by so many, and need I remind, with severe consequence to reputation and career?

    From the mountain of evidence I’ve seen, The whole theory (neo-Darwinism) is a blatant fallacy with no redeeming quality whatsoever, as far as foundational science is concerned, and I will not compromise by saying “Oh this one little part of neo-Darwinism is true”, When in fact micro-evolution and Genetic Entropy explain what we are seeing, in the evidence, much more clearly and with a lot more explanatory power than the term neo-Darwinism does.

    As you stated Jerry everyone is entitled to their opinion, I respect your opinion, but I will stick to my fool’s errand as you put it.

  73. 73
    getawitness says:

    tribune7,

    I think what we can know is that when someone posts something like this at 7:33 a.m. on a Saturday morning he has had one heck of a Friday night.

    Uncommon descent = hair of the dog? 🙂

  74. 74
    tribune7 says:

    Exactly!! 🙂

  75. 75
    hrun0815 says:

    Classical NDE is envoked to explain the origin of new traits by very small changes over long periods of time. The changes occur by mutation of existing DNA and the resulting changes in proteins, processes and structures. Lateral gene transfer supplies material for change but it does not come from neodarwinian processes. It is simply borrowed from another organism. Explaining the origin of the genes that are transfered in is another question.

    idnet.com.au, I think you misrepresent NDE. THere is nothing in NDE is mandates changes in organisms to either take long or to be small. Nobody looks, for example, at drug resistance in bacteria and claims this runs counter to NDE. And that certainly is a fast process. Likewise, nobody looks at horizontal gene transfer and claims it runs counter to NDE. If I’m wrong, could you point me to an actual reason why HGT runs counter to NDE. What would make it run counter would be if it could be shown that the HGT was pre-planned to achieve a certain goal and not a randomly occurring process.

    Flagellar proteins are interesting. We should see some mutations that are neutral in these genes.

    Why would neutral mutations in flagellar proteins be interesting? Or, why would they be more interesting than any other neutral mutations. What is the actual goal in looking at neutral mutations in the first place? Do you want to use a ‘molecular clock’ to determine if the split between humans and baboons occurred at a certain timepoint?

    It will take years to assess the data gained from the sequencing I have suggested. I think it will add to our understanding of how powerful NDE is over 3 Billion generations and whether ID is threatened by NDE.

    I think you overestimate the complexity of the project. You can get the two E.coli strains for a couple of hundred bucks from strain collections (or for free from other labs). The sequencing cost for the two strains would run under $20.000. And for the analysis you can rely exclusively on the NCBI databases which are available for free. All you’d need is a personal computer and internet access. All in all, the project could be done by a single person in a few months and cost less than $50.000 (including pay for that person).

    But I doubt the even the DI would offer a grant to do this, unless you can actually articulate what you would hope to achieve.

    Judging from an NDE point of view we would expect the following results: The E.coli in baboons should differ from the E.coli in humans in the key genes that allow them to be better adapted to the different environments. Probably the main difference between the two would be the available food sources. Apart from that we would expect neutral mutations in all genes.

    How does this differ from the ID predictions?

    Secondly, why would this experiment show what “evolution (or ID for that matter) can achieve”. The environment that E.coli find themselves in (be it baboon or human) to me appear to be quite constant throughout the history of the species (except for available nutritional sources). Why would we expect to see much of any change (be it from evolution or ID)? If I was an intelligent designer, I would give my baboon bacterium a few enzymes to break down the sugars baboons ingest most commonly and then sit back, relax and enjoy the show. In humans, I guess in the past 50 years or so, I would add in a few genes that confer resistance to antibiotics. Unfortunately, that is also exactly what ‘evolution would do’.

  76. 76
    Telic-meme says:

    Hi

    I’ve been a lurker for while, and enjoy the banter and useful information regarding the ID/neo-Darwin/Creation debacle. Has anyone proposed a research project that is ID friendly or is anyone busy in such a project? I am interested. Also, here a possible proposal for such a project that might turn out to be useful, not only in the ID/non-ID debate but also with practical implications.
    http://telic-meme.blogspot.com.....n-and.html
    Any thoughts?
    Thank you

  77. 77
    jerry says:

    I personally believe that ID should embrace neo Darwinism for two very important reasons

    1. It describes a process that produces a lot of change in living organisms and these changes have highly significant effects on life’s progress. Consequently, it is foolish to rail against it.

    2. I believe it is part of the design of life and as such is totally in sync with ID.

    I have often used the phrase that ID subsumes neo Darwinism and I firmly believe it because without neo Darwinism life would be very limited and stilted on this planet. People who support ID go immediately to what many neo Darwinists claim about the ability of this process to produce all the changes in biological organisms and then trash the whole theory. That is not good science. That is not logical. That is foolishness.

    I believe we should add a term to the concepts we use and that is “devolution” and point out that devolution is also part of the life change process and its main engine is neo Darwinism. While the term devolution usually carries a negative connotation, not all devolution is negative.

    We have had peripheral discussion over the last two years about where does all the variation come from in a population. It is something that neo Darwinism would not predict because the processes of neo Darwinism tend to remove variation from a population. Of course the obligatory response by those who support gradualism is that mutations are the source for this variation but what the Edge of Evolution has shown is that is highly unlikely. I remember great_ape saying that this was a problem for gradualism or naturalistic evolution. The genetic side of neo Darwinism causes population variation to decline.

    And while Sanford’s book argues that this will eventually lead to extinction of a species, new species constantly appear suddenly in life’s history and presumably the new populations appear with lots of variation because they seem to radiate out into many sub-species.

    And this is where neo Darwinism is essential for survival because given all the new variation, natural selection allows the species to survive in many different environments. In other words it allows sub variants to blossom where if not for neo Darwinism the species might go extinct sooner in the new environment. In other words the built in variation and neo Darwinism allow life to flourish, But we have not built a taxonomy that goes up as gradualist claim but a taxonomy that goes down to finer and finer variations of the original population. And to me this fits ID to a “T.”

    So I suggest we embrace neo Darwinism, argue against gradualism especially the Blind Watchmaker Thesis but point out how neo Darwinism helps make life flourish in many cirucmstances.

    I already above have made the point that neo Darwinism is essential for modern medicine. If one wants to go over again how that discussion started, read Seekandfind’s comment at #40 where he points out that the perception is that those who believe in ID are backward and a hindrance to science and that this hurdle has to be overcome. One way to overcome this is to embrace neo Darwinism and it devolution effects, some of which are good and some of which are bad for life. In evolution some are good and some are bad; in medicine nearly 100% are bad.

  78. 78
    PaV says:

    I’m gone for the rest of the day, but let me just add the following:

    1.) Neo-Darwinism=RM+NS

    2.) Are mutations random? Well, yes and no. Do they happen in a random fashion? Yes. Are they completely random? No. Why do I say that? Because we now know that bacteria under stress “increase” their mutation rate, and the increase rate occurs in specific areas of the genome. Well, how does that happen? I suspect that bacteria simply shuts down the normal error-correction-mechanism for these specific areas of their genome. If, indeed, this is the mechanism, would it be correct to call this overall process ‘random’? I don’t think so.

    3.) Here’s what Willian B. Provine writes in the “Afterword” of the re-issue of his “The Origins of Theoretical Population Genetics.” (jerry: neo-Darwinism=population genetics + inordinate extrapolation):

    “MY VIEWS IN 1959-70
    1.

  79. 79
    PaV says:

    [Don’t know what happened. I hit something and the above just posted. Here’s the quote]

    1. Natural selection was the primary mechanism at every level of the evolutionary process. For any change in an adaptation or gene frequencies, natural selection was the null hypothesis.”

    Then, in 2001:

    “As John Endler has argued eloquently in Natural Selection in the Wild (1986), natural selection is not a mechanism. Natural selection does not act on anything, nor does it select (for, or against), force, maximize, create, modify, shape, operate, drive, favor, maintain, push, or adjust. Natural selection does nothing. Natural selection as a natural force belongs in the insubstantial category already populated by the Becker/Sthal phlogiston (Endler 1986) or Newton’s ‘ether’. . . .
    Having natural selection select is nifty because it excuses the necessity of talking about the actual cuasation of natural selection. . . .

    . . . . The chances are small that a particular DNA sequence in mammals is ‘adapted through natural selection’. The chances are great that the evolution of selectively neutral factors produced the sequence. Thus at the DNA level, explaining any random sequence invokes selectively neutral or nearly neutral factors as the null hypothesis, an amazing turnabout since the late 1960’s. I now argue that each level (phenotypic, protein, and DNA sequence) marches to different drummers.”

    Should we be going back to the 1960’s?

  80. 80
    jerry says:

    PaV,

    What do you mean by

    “Should we be going back to the 1960’s?”

  81. 81
    magnan says:

    77

    Telic-meme (#77), thanks for an interesting link. This does seem to be a research study proposal with certain very limited ID implications. It definitely is looking to find a form of Endogenous Adaptive Mutagenesis (EAM) in microorganisms. Hypothesis 1 if confirmed would show that the bacteria can increase the frequency of certain types of mutation in response to stressors. A research paper that offers some evidence for this along with important applications to antibioic research was posted on another thread. This is Cirz RT, Chin JK, Andes DR, de Crécy-Lagard V, Craig WA, et al. (2005) Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance. PLoS Biology 3(6): e176 doi:10.1371/journal.pbio.0030176.

    Hypotheses 2 and 3 if confirmed would show some sort of epigenetic control mechanism in the bacteria that “directs” certain types and locations of mutation in response to certain stressors, based on the “need” of the microorganism to change particular expressed proteins.

    It isn’t clear to me how confirmation of Hypothesis 3 would advance ID theory, however. Being a mechanism, however complex, it couldn’t act as a teleological intelligent agent in originating IC biological structures. One of the core arguments of ID is that the IC and CSI of life inherently demand such an influence.

    Secondly, Behe in TEOE shows how E. coli, HIV and Plasmodium Falciparum in recent historical time failed to create significant new complex innovative structures and mechanisms despite astronomical numbers of replications. Behe points out that this shows an inherent limit to the power of undirected Darwinist mechanisms. If the bacteria have EAM mechanisms such as suggested in the research proposal, then they must have been operating during the long term studies cited by Behe. The very limited results would seem to show the very limited power of whatever EAM mechanisms exist in creating innovation.

  82. 82
    Bad says:

    Yes. ID predicts that RM and NS will achieve only very minor feats.

    Making a claim that some other theory is wrong or insufficient is not making a positive prediction for your theory.

    The core problem with ID is that it has the potential to explain anything at all. You cannot escape this problem simply by making a bunch of random predictions and then declaring yourself proven correct if some of them happen to come true. The predictions have to flow from some specific and limited range of explanation that your theory supplies.

    It’s only if ID theorists are willing to careful specify a sort of designer and its parameters and limitations that we could pick out its actions. But instead, we are left with a cause that can do literally anything in any way at all.

    This may enable processing a substrate with a slightly different side chain at most. ID theory suggests that totally new metabolic pathways and molecular machines do not arise by RM and NS.

    Except that we’ve watched new metabolic pathways evolve in the lab, and especially in bacteria: and so commonly observed that it’s not even of particular note anymore.

    It’s also worth noting that known instances of Lateral Gene Transfer, since the mechanisms are almost always related to virii or error, works as just a different source of mutation.

    There IS a sort of lateral gene transfer however, that would make it extremely obvious that a designer was involved: if whole functional systems were transferred from one species to another completely different species in another taxa without any method of transmission via contact (the most common, and the only one reliably used by evolution being through ancestry). Human geneticists can already do this even with our primitive techniques. And yet this sort of thing is stunningly absent from nature, as are most of the ways in which the design of an intelligent designer could be made extremely conspicuous.

    magnan: Secondly, Behe in TEOE shows how E. coli, HIV and Plasmodium Falciparum in recent historical time failed to create significant new complex innovative structures and mechanisms despite astronomical numbers of replications.

    Claiming and showing are not the same things. Behe’s book is a lot less convincing than actual people who study these virii and bacteria, and say that Behe is, in fact, wrong about this.

  83. 83
    StephenB says:

    Jerry:

    What is your philosophical position seperate from science? Do you accept metphysical materialsm/naturalism or some form of it.

  84. 84
    jerry says:

    StephenB,

    I believe we are all God’s children made in his image. To me metaphysical materialism is pap for the uninformed which is what I consider atheists. Atheism is intellectual bankruptcy and the mark of one who is lazy or dishonest.

    However, for the most part I stick to science on this blog because discussing philosophy and religion gets in the way of what has to be accomplished.

  85. 85
    Joseph says:

    It’s only if ID theorists are willing to careful specify a sort of designer and its parameters and limitations that we could pick out its actions.

    The beauty of a design inference is that it can be had without knowing anything about the designer(s).

    Obviously the parameters and limitations are the physical laws that govern our universe.

    See also:

    Intelligent Design: The Design Hypothesis

  86. 86
    PaV says:

    William Provine believed that natural selection was the null hypothesis for all evolutionary change in the 60’s. In 2001, he believed that natural selection did absolutely nothing. There’s been a lot of science done since the 60’s. It changed Provine’s mind—an emminent population geneticist; why shouldn’t it change ours? Or, at least allow us to suspend judgment on what we are spoon-fed by the neo-Darwinists?

    I’m perfectly comfortable with Darwinism (macroevolution)—if it is proved to be correct science. I’m perfectly comfortable with neo-Darwinism (microevolution)—if it holds up as correct science. I just personally happen to believe that there are a lot of surprises ahead, and that with these surprises, natural selection will seen, in the end, to “do nothing”, just as Provine now asserts. In the meantime, I’m not ready to concede much.

  87. 87
    PaV says:

    “The core problem with ID is that it has the potential to explain anything at all.”

    This is the pan calling the kettle black. Let’s remember that ID predicted that “junk-DNA” would turn out not to be junk. The neo-Darwinist scenario was that all this non-coding DNA was just left-over stuff. Neo-Darwinism gets this prediction wrong, and, it’s as if nothing at all has happened. We hear a collective, “Oh well….” Sorry. That won’t work.

  88. 88
    idnet.com.au says:

    Bad at 83 revisited

    Neo-Darwinian Evolution predicts that RM and NS will achieve major feats.

    Making a claim that ID theory is wrong or insufficient is not making a positive prediction for Neo-Darwinian Evolution.

    The core problem with NDE is that it has the potential to explain anything at all. You cannot escape this problem simply by making a bunch of random predictions and then declaring yourself proven correct if some of them happen to come true. The predictions have to flow from some specific and limited range of explanation that your theory supplies.

    It’s only if NDE theorists are willing to careful specify the proposed mechanisms and their parameters and limitations that we could pick out its actions. But instead, we are left with a cause that can do literally anything in any way at all.

    Except that we’ve watched new metabolic pathways created by Intelligent Designers in the lab, and especially in bacteria: and so commonly observed that it’s not even of particular note anymore.

    There IS a sort of evidence however, that would make it extremely obvious that a NDE was involved: if whole functional systems arose in one species without any method of transmission via contact with plasmids or LGT from other species.

    Claiming and showing are not the same things.

  89. 89
    jerry says:

    PaV,

    Maybe this should be the subject of another thread some time in the near future. I bet that Provine and MacNeill don’t disavow natural selection as uniformly as you say they do. We can certainly ask Allen MacNeill who when he was last here talked extensively about different forms of natural selection.

    The problem with natural selection is not that it cannot do anything, it does, but that it rarely if ever presented with anything of consequence on which to operate. That I think MacNeill will agree.

    If a population that had considerable variation in it migrated from the forrest and plains to the dessert, we would probably see a new variant that adapted to the dessert. But it is likely that this species over time would have less variation than the original population. The only way to replenish the gene pool would be by gene flow with mating outside its population.

    In other words natural selection tends to narrow the gene pool of a population but in the process create species that can adopt to a new environment such as isolated islands. Occasionally a mutation comes along that helps, such a color change of fur, but rarely if never is there any major functional change that arises. In addition to this genetic drift will also reduce the gene pool so both processes narrow the variation in a population.

    If neo Darwinism is thought of in this way, without any philosophical baggage about grandiose changes in the genome, it is true and makes a good addition to the ID paradigm.

    And an ID research paradigm will argue that such process are what to be expected by evolution. And such claims of new speciation in such things as cichlids are really just neo Darwinism acting to reduce variation and not increasing it. But this reduced variation results in a species that is better adapted to its environment. But in the long run is the road to extinction because if the environment ever changes it will not be able to handle it.

  90. 90
    Frost122585 says:

    id.net,

    Thanks for using the “not a specified argument” argument.

  91. 91
    PaV says:

    jerry:

    Here’s what Provine (2001) says about the concept of “gene pool”:

    The notion of “gene pools” now strikes me as one of the most artificial concepts of population genetics. What exists in the “gene pool” is vague, but perhaps most often either “genes” or “alleles.” Other candidates for the gene pool are chromosomes, gametes, and whole organisms. Neither genes nor alleles float free, but are on chromosomes, and do not cleave every generation. Talking about the cohesion, coadaptation, and homeostasis of the gene pool means attribution of aesthetically desirable characteristics to a non-existing entity. In small populations, invocation of the gene pool as the biological source of the random sampling for genetic drift leads to serious problems.

    You write:

    “If neo Darwinism is thought of in this way, without any philosophical baggage about grandiose changes in the genome, it is true and makes a good addition to the ID paradigm.”

    First, I’m not denying the very real molecular effects we see happen in bacterial populations. It is real. Rather, I object to it being called “natural selection” for two reasons: (1) NS is an “effect”; not a “cause” (Provine’s exact point) (2) there is no “selection” taking place. In the case of artificial selection, humans, causative beings, are both cause and select outcomes for future breeding; and , so, the term “artificial selection” makes perfect sense.

    What if instead of calling the process whereby bacteria develop antibacterial resistance “natural selection”, we simply term it a “process of adaptation”? Doesn’t this truly describe what we see happen?

    In terms of ID, I simply see—as you propose—this “process of adaptation” as part of the Designer’s original design.

    When it comes to “adaptation” to a particular environment, Mendelian genetics makes sense. It provides for various combinations of factors to interplay with one another in such a way as to allow an appropriate phenotype to emerge, dependent upon the particular environment presently encountered. So, of course, we would see Mendelian genetics at work. Now this may be great for ‘eye color’; but what about the ‘eye’ itself? Would you want it to be subject a whole host of possible combinations, or would you want it to always be expressed? If it is to be always expressed, then what is the need for “alleles”?

    Provine talks about the “one-locus, two-allele models” this way:

    The persistence of the one-locus, two-allele models raises a fascinating historical issue. Why have the earliest models of the theoretical population genetics managed to survive almost unscathed into modern textbooks on evolution and genetics? Surely the misleading limitations of these models are understood by evolutionists and geneticists. Do teachers think the students must first learn what they did as students, and later correct these beliefs? I find that most evolutionists and geneticists still adhere to belief in rampant random genetic drift in small populations, which matches their firm belief that natural selection is a mechanism that creates adaptations.
    In 1970 I could see the origins of theoretical population genetics as being an unalloyed good for evolutionary biology, and thus obviously a great subject for an historian. Now I see these same theoretical models of the early 1930’s, still widely used today, as an impediment to understanding evolutionary biology, and their amazing persistence in textbooks and classrooms as a great topic for other historians.

    The “one-locus, two allele” model was developed in the early part of the 20th century, fifty years before the discovery of DNA. Knowing what we do about genetics, think through this problem:

    I have thalassemia. I got it from my mother. I have one wrong amino acid in my hemoglobin chain. The protein is defective. Some nucleotide along the string of nucleotides that code for the hemoglobin protein has an error. Here are some questions:

    (1) the DNA I have comes half from my dad and half from my mom. Since my dad’s hemoglobin is natural, that means, assuming my mom and dad’s DNA lined up correctly, that the nucleotide from my dad’s side of hemoglobin is different from my mom’s side of the DNA. So, how did they match up?

    (2)Was some “correction mechanism” involved? If so, why didn’t it correct my mom’s DNA instead of my dad’s?

    (3)If my dad’s side of the DNA was corrected to match my mom’s, then where is the second allele for thalassemia? Is it the complementary side of the hemoglobin string of nucleotides? Or is it at some entirely different portion of the genome?

    (4)If it is the complementary side, and if my dad’s side is being corrected to match my mom’s side, then why am I alive, since that would make me “homzygous” for thalassemia—which is lethal in the homozygous form after age 3-4?

    I think this is why Provine says:

    Using these [one-locus, two-allele] models to understand random drift, selection, fitness surfaces, and gene pools is an invitation to misunderstandings. I view these simple models as impediments to understanding evolution in either natural or domestic populations.

    Let’s remember that Mendelian genetics are 150 years old. We need to completely re-think genetics. That’s what evo-devo proposes; but, of course, they assume too much pre-existing information to be right on the merits. I think the answer will come from viewing the genome as a complicated software program that has enormous regulating loops. “Junk-DNA” is proving to be the province of these regulatory elements—you know, that 97% of the genome that is “non-coding” (for proteins, but does code for small, interfering RNA’s, the secret to the cell’s regulatory mechanisms).

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