Darwinism Intelligent Design speciation

Speciation: The triumph of hope over evidence

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From Jonathan WellsThe Myth of Junk DNA:

British bacteriologist looked for evidence of speciation and concluded in 2001: “None exists in the literature claiming that one species has been shown to evolve into another. Bacteria, the simplest form of independent life, are ideal for this kind of study, with generation times of twenty to thirty minutes, and populations achieved after eighteen hours. But throughout 150 years of the science of bacteriology, there is no evidence that one species of bacteria has changed into another … Since there is no evidence for species changes between the simplest forms of unicellular life, it is not surprising that there is no evidence for evolution from prokaryotic [e.g., bacterial] to eukaryotic [e.g., plant and animal] cells, let alone throughout the whole array of higher multicellular organisms.” (p. 12) (Original here.)

File under: More stuff you still can’t say in school.

38 Replies to “Speciation: The triumph of hope over evidence

  1. 1
    DrREC says:

    Strange quote, given the difficulty in even defining a bacterial species due to recombination between distant species. Total reproductive isolation is a tall order. This difficulty means there are more clear cut cases of eukaryotic speciation known.

    Nevertheless, some scientists have studied prokaryotic speciation:

    The effect of DNA sequence divergence on sexual isolation in Bacillus
    http://www.ncbi.nlm.nih.gov/pubmed/8325477

    Temporal Fragmentation of Speciation in Bacteria
    DOI: 10.1126/science.1144876

    Recombination and the Nature of Bacterial Speciation
    DOI: 10.1126/science.112757

    Also in simple eukaryotes:
    Starvation-Induced Reproductive Isolation in Yeast
    DOI: 10.1007/978-3-642-12340-5_3

  2. 2

    I think Wells is pretty good with his research and pretty careful with his ideas, but I’d like to clarify one definitional point, particularly because this is a point we’ve been discussing the last few days on another thread.

    Specifically, when Wells says there is “no evidence” for species changes, what he means is that either: (i) the overall evidence, taken as a whole, does not support species changes, or (ii) there is no direct observational evidence of species changes. In the context of his discussion in the quote above, he seems to be talking about the latter.

    I think we need to be clear on this definition, because there is evidence for species change, at the very least in the sense that there is some evidence that is *consistent with* the idea of species change. Whether or not the evidence, as a whole, supports the idea is another question.

    In making this technical clarification/correction, I don’t detract from Wells’ larger point, which is that after decades of research with the most likely candidate(s) for speciation, we still have no direct observational evidence that it does, or even can, occur. This is a very important point that should give pause to anyone proclaiming the powers of change by evolutionary mechanisms.

  3. 3
    Eugene S says:

    It would be nice to know for certain how many successive generations of bacteria were supervised over those 150 years in the single longest experiment. I’ve been told of an estimate of 10^4 generations per year for one particular species. But I don’t know the duration of the longest continuous period of supervision, which would be good to have. Assuming a one year long continuous experiment, we have 10,000 generations, which is equivalent to 250,000 years for the human race.

  4. 4
    Eugene S says:

    That is, obviously, assuming one human generation is 25 years.

  5. 5
    Collin says:

    Very interesting statement.

  6. 6
    DrREC says:

    “with the most likely candidate(s) for speciation”

    I think the cleverness of the quote is that it looks at those LEAST likely for speciation (in the sense of reproductive isolation).

    Evidence for Eukaryotic speciation is clearer to interpret, and as far as I know, much more abundant.

  7. 7
    bornagain77 says:

    DrREC, Perhaps you need to look closer at the Lenski Long Term Evolution Experiment of e-coli, at 50,000 generations, (equivalent to about a million years of human evolution) to see just how detached from reality your paltry evidential base truly is for establishing anything that would merit note??

    Michael Behe’s Quarterly Review of Biology Paper Critiques Richard Lenski’s E. Coli Evolution Experiments – December 2010
    Excerpt: After reviewing the results of Lenski’s research, Behe concludes that the observed adaptive mutations all entail either loss or modification–but not gain–of Functional Coding ElemenTs (FCTs)
    http://www.evolutionnews.org/2.....41221.html

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Shoot DrREC, let’s just go full bore on the bacterial evidence here and try to see what the almighty power of evolution can do over for as far back in time as we can get evidence on bacterial ‘evolution’:,,

    The Paradox of the “Ancient” (250 Million Year Old) Bacterium Which Contains “Modern” Protein-Coding Genes:
    “Almost without exception, bacteria isolated from ancient material have proven to closely resemble modern bacteria at both morphological and molecular levels.” Heather Maughan*, C. William Birky Jr., Wayne L. Nicholson, William D. Rosenzweig§ and Russell H. Vreeland ;
    http://mbe.oxfordjournals.org/...../19/9/1637

    These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland’s work:

    “Raul J. Cano and Monica K. Borucki discovered the bacteria preserved within the abdomens of insects encased in pieces of amber. In the last 4 years, they have revived more than 1,000 types of bacteria and microorganisms — some dating back as far as 135 million years ago, during the age of the dinosaurs.,,, In October 2000, another research group used many of the techniques developed by Cano’s lab to revive 250-million-year-old bacteria from spores trapped in salt crystals. With this additional evidence, it now seems that the “impossible” is true.”
    http://www.physicsforums.com/s.....p?t=281961

    Dr. Cano’s work on ancient bacteria came in for intense scrutiny since it did not conform to Darwinian predictions, and since people found it hard to believe you could revive something that was millions of years old. Yet Dr. Cano has been vindicated:

    “After the onslaught of publicity and worldwide attention (and scrutiny) after the publication of our discovery in Science, there have been, as expected, a considerable number of challenges to our claims, but in this case, the scientific method has smiled on us. There have been at least three independent verifications of the isolation of a living microorganism from amber.”
    http://www.uncommondescent.com.....ent-357693

    In reply to a personal e-mail from myself, Dr. Cano commented on the ‘Fitness Test’ I had asked him about:

    Dr. Cano stated: “We performed such a test, a long time ago, using a panel of substrates (the old gram positive biolog panel) on B. sphaericus. From the results we surmised that the putative “ancient” B. sphaericus isolate was capable of utilizing a broader scope of substrates. Additionally, we looked at the fatty acid profile and here, again, the profiles were similar but more diverse in the amber isolate.”:
    Fitness test which compared ancient bacteria to its modern day descendants, RJ Cano and MK Borucki

    Thus, the most solid evidence available for the most ancient DNA scientists are able to find does not support evolution happening on the molecular level of bacteria. In fact, according to the fitness test of Dr. Cano, the change witnessed in bacteria conforms to the exact opposite, Genetic Entropy; a loss of functional information/complexity, since fewer substrates and fatty acids are utilized by the modern strains. Considering the intricate level of protein machinery it takes to utilize individual molecules within a substrate, we are talking an impressive loss of protein complexity, and thus loss of functional information, from the ancient amber sealed bacteria. Here is a revisit to the video of the ‘Fitness Test’ that evolutionary processes have NEVER passed as for a demonstration of the generation of functional complexity/information above and beyond that which was already present in a parent species bacteria:

    Is Antibiotic Resistance evidence for evolution? – ‘Fitness Test’ – video
    http://www.metacafe.com/watch/3995248

    According to prevailing evolutionary dogma, there ‘HAS’ to be ‘major genetic drift’ to the DNA of modern bacteria from 250 million years ago, even though the morphology (shape) of the bacteria can be expected to remain exactly the same. In spite of their preconceived materialistic bias, scientists find there is no significant genetic drift from the ancient DNA. In fact recent research, with bacteria which are alive right now, has also severely weakened the ‘genetic drift’ argument that evolutionists use from time to time:

    The consequences of genetic drift for bacterial genome complexity – Howard Ochman – 2009
    Excerpt: The increased availability of sequenced bacterial genomes allows application of an alternative estimator of drift, the genome-wide ratio of replacement to silent substitutions in protein-coding sequences. This ratio, which reflects the action of purifying selection across the entire genome, shows a strong inverse relationship with genome size, indicating that drift promotes genome reduction in bacteria.
    http://genome.cshlp.org/conten.....091785.109

    I find it interesting that the materialistic theory of evolution expects there to be a significant amount of genetic drift from the DNA of ancient bacteria to its modern descendants, while the morphology can be allowed to remain exactly the same with its descendants. Alas for the materialist once again, the hard evidence of ancient DNA has completely betrayed their expectations.

    And when we look at the morphology of bacteria, over long periods of time, once again the evidence betrayed the prior expectations that the neo-Darwinists had:

    Static evolution: is pond scum the same now as billions of years ago?
    Excerpt: But what intrigues (paleo-biologist) J. William Schopf most is lack of change. Schopf was struck 30 years ago by the apparent similarities between some 1-billion-year-old fossils of blue-green bacteria and their modern microbial microbial. “They surprisingly looked exactly like modern species,” Schopf recalls. Now, after comparing data from throughout the world, Schopf and others have concluded that modern pond scum differs little from the ancient blue-greens. “This similarity in morphology is widespread among fossils of [varying] times,” says Schopf. As evidence, he cites the 3,000 such fossils found;
    http://www.thefreelibrary.com/.....a014909330

    AMBER: THE LOOKING GLASS INTO THE PAST:
    Excerpt: These (fossilized bacteria) cells are actually very similar to present day cyanobacteria. This is not only true for an isolated case but many living genera of cyanobacteria can be linked to fossil cyanobacteria. The detail noted in the fossils of this group gives indication of extreme conservation of morphology, more extreme than in other organisms.
    http://bcb705.blogspot.com/200.....st_23.html

    DrREC, this consistent evidence is not good for you guys. You claim you got proof, but alas, when I dig deeper into the evidence your claims always turn out to be mere bluster with no real substance. Why is this DrREC??? Why do you so dogmatically defend such a bankrupt theory? Not to mention the completely pointless, nihilistic, materialistic philosophy behind it???

  8. 8

    Just want to make sure I understand your comments.

    Are you saying that we shouldn’t expect to see speciation in the bacteriology experiments because the bacteria are reproductively isolated? If so, why would that be?

    Second, are you saying that eukaryote speciation has been clearly observed and is abundant?

    Of course we always have the challenge of defining species. This is one of the big points Darwin focused on in The Origin, and he argued that the difficulty in defining species pointed to the fact that there is no real boundary.

    Incidentally, I don’t think most folks dispute that things like geographical isolation can result in slightly different phenotypes over time. The question is, how far does that go. What has actually been observed, as opposed to hypothesized after the fact . . .

  9. 9
    rhampton7 says:

    Speciation within prokaryotes is a different beast (pun intended) then within multicellular organisms that reproduce by sex. For example, dogs and wolves are considered to belong to the same species primarily because the have the same karyotype and can interbreed. This is not the case for foxes, who themselves are members of several different species. But prokaryotes reproduce by binary fission, so the ability to interbreed is moot. How then do you define a species?

    The two most commonly used criteria today {note: circa 2002} depend on (i) DNA–DNA association (i.e., the degree of hybridization possible between the total genomic DNA of two species) and (ii) the percent identity in the sequence of that ubiquitous molecule, 16S rRNA. Curtis et al. simply accept that a meaningful distinction between kinds of organisms can be defined on the basis of 16S rRNA sequence, and most of their fellow researchers would agree in principle. Many might even agree on the conventional cutoffs of greater than 70% DNA–DNA reassociation or greater than 97% 16S rRNA identity as species definitions.

    So there is a subjective and somewhat arbitrary threshold to the number of mutations/changes that determine membership to a species — above the threshold and membership changes. But then a complication to this definition arose:

    The discovery of ecologically important differences in temperature optima attributed to hot spring microbes with less than 1% 16S rRNA sequence divergence led Ward to advocate a more “natural” or ecological species concept (ESC) of Simpson. The ESC includes information not just on genetics but on the role of the organism in its environment, some acknowledgment of its function.

    Which led to this startling conclusion:

    A species is not defined by the sequence of one functional gene even if, like amo, it is the quintessential gene that defines the organism’s metabolism. However, the organism’s interaction with the environment—its regulation by environmental variables such as temperature, oxygen, and substrate concentrations—is defined at the level of functional genes and the enzymes they encode, not 16S rRNA. These are the genes that determine the role of the species, that comprise the essence of an ecological species concept. The number of functional genes for which sizeable databases are available is very small, but from these data it is obvious that the diversity of functional genes far exceeds that of the ribosome. If the diversity of functional genes reflects potential diversity in actual ecological function, then this diversity has implications for ecosystem function, resilience, and stability. In assessing the diversity of prokaryotic communities, some recognition of this additional layer of complexity must be included.

    In other words, there may be many, many more species of prokaryotes then previously thought. So I have to wonder by what definition did Jonathan Wells use to make the “150 year” claim, and would it be true using the ESC definition of speciation?

    source: How many species of prokaryotes are there?
    PNAS August 6, 2002 vol. 99 no. 16 10234-10236

  10. 10
    DrREC says:

    Luskin has a little lie in there, does’t he? See, the mutations in the Lenski experiment weren’t mapped at the time of Behe’s review. Behe says: “If the phenotype of the Lenski Cit strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will,
    of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.”
    http://www.lehigh.edu/bio/pdf/Behe/QRB_paper.pdf

    See the word “IF”? Behe doesn’t know what class it falls in. He’s listing the possibilities. ALL THE POSSIBILITES, including “a noteworthy gain-of-FCT mutation.” Considering the review gives many examples of gain-of-FCT mutations, it is wholly disingenuous to conclude Lenski’s must be loss of function/information, and that gain of function/information are impossible.

    I’ve already provided you references of antibiotic resistant bacteria with greater fitness than the parental strain. Not that it stops you from regurgitating the same quotes again and again.

  11. 11
    Collin says:

    We’re not talking about greater fitness. Greater fitness is dependent on the environment. We’re talking about increase of complexity or information. Sometimes a loss of complexity or information results in better fitness. But is there ever an increase in complexity or information?

    By the way, the ancient bacteria “was capable of utilizing a broader scope of substrates” than the modern bacteria. This fits in well with Genetic Entropy theory. It does not fit in well with Darwinism. Newer bacteria should be more fit for more environments, but instead we see them impoverished, being able to thrive in fewer environments.

  12. 12
    rhampton7 says:

    Are you saying that we shouldn’t expect to see speciation in the bacteriology experiments because the bacteria are reproductively isolated?

    Well speciation would occur much, much more slowly if the bacteria were reproductively isolated. This is because horizontal gene transfer (HGT) is a significant factor in the recombination of bacterial DNA. For example, many plasmids can cross species by way of conjugation. Plasmids vary is size from 1,000 to 1,000,000 base pairs in length, so one conjugation event can induce massive changes compared to a single point mutation that changes only 1 base or 1 base pair.

  13. 13
    DrREC says:

    In Behe’s review, he lists several gain-of-fct mutations, where “A “gain-of-FCT” adaptive mutation is a mutation that produces a speci?c, new, functional coded element while adapting an organism to its environment”

    So, yes.

    “By the way, the ancient bacteria “was capable of utilizing a broader scope of substrates” than the modern bacteria. This fits in well with Genetic Entropy theory. It does not fit in well with Darwinism.”

    Why would specialization not fit in well with Darwinism? (Also note the DNA sequences from these fossil bacteria are extremely controversial, and there is a pretty good chance they represent more modern contamination).

  14. 14
    DrREC says:

    “Are you saying that we shouldn’t expect to see speciation in the bacteriology experiments because the bacteria are reproductively isolated? If so, why would that be?”

    I’m saying if we define speciation as reproductive isolation, and reproductive isolation in bacteria is extremely rare, perhaps we shouldn’t expect it.

    If we define speciation by metabolism, percent genome difference, or differential/reduced recombination, then we’ve seen plenty of it.

    “Second, are you saying that eukaryote speciation has been clearly observed and is abundant?”

    Yes.

    http://www.ncbi.nlm.nih.gov/pu.....0evolution

  15. 15

    DrRec:

    Would you please stop linking to this paper and misrepresenting Behe’s results? I’ve responded to this red herring before, but I don’t know what happened to the thread.

    In short, even in those cases where there is arguably a gain-of-function mutuation, the primary lesson coming from all this is that it was a break or dulling of an existing part, *not* creation of some new part or creation of CSI.

    Stop referring to Behe’s paper and saying that Behe cites “many examples of gain-of-function” mutations, without acknowledging the takeaway lesson.

  16. 16
    bornagain77 says:

    DrREC, you really are willingly misleading!!! You’ve been corrected a few times on your severe misuse of the Behe paper for he certainly wasn’t arguing that ANYTHING he could find, over the past 40 years of lab work, supported neo-Darwinism in any way shape or form. In fact his paper is entitled, “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain – Michael Behe – December 2010, yet you act as if he has provided you support for your position. That is just plain sad DrREC!! Moreover, it is only by your severe misapplication of ‘compensatory mutations’, which is a inherent design mechanism, in which genes were experimentally deleted and then ‘compensated’ for fairly quickly by the internal programming of the cell, that you have any ‘gain’ of functional coded element. But yet you never mention that no gain is ever observed above what was already present in the parent strain before the deletion. This is simply intellectually dishonest on your part as well as extremely bad propaganda and is certainly not maintaining integrity in science when you do as such.

    And yet when we get past all the neo-Darwinian rhetoric, and look for ‘vertical’ evolution i.e. a gain in functional information above and beyond what is already present in a parent strain of bacteria we consistently find these kinds of following results:

    Testing Evolution in the Lab With Biologic Institute’s Ann Gauger – podcast with link to peer-reviewed paper
    Excerpt: Dr. Gauger experimentally tested two-step adaptive paths that should have been within easy reach for bacterial populations. Listen in and learn what Dr. Gauger was surprised to find as she discusses the implications of these experiments for Darwinian evolution. Dr. Gauger’s paper, “Reductive Evolution Can Prevent Populations from Taking Simple Adaptive Paths to High Fitness,”.
    http://intelligentdesign.podom.....4_13-07_00

    Here is Michael Behe, in his own words, telling exactly what his survey of 40 years worth of lab work reveals against neo-Darwinism

    Michael Behe: Challenging Darwin, One Peer-Reviewed Paper at a Time – December 2010
    http://intelligentdesign.podom.....3_46-08_00

  17. 17

    DrRec:

    Wow, that is quite a literature bomb there, just searching for evolution and speciation. Remember, we were talking about actual observed speciation events, not after-the-fact attempts to explain certain features.

  18. 18
    DrREC says:

    You’re just wrong on this, Eric.

    Behe says “I show that by far the most common adaptive changes seen in those examples are due to the loss or modi?cation of a pre-existing molecular function”

    but goes on to discuss “A “gain-of-FCT” adaptive mutation is
    a mutation that produces a speci?c, new, functional coded element while adapting an organism to its environment. The construction by mutation of a new promoter, intron/exon splice site, or protein processing site are gain-of-FCT mutations. Also included in this category is the divergence by
    mutation of the activity of a previously duplicated coded element.”

    Those aren’t breakages, are they? And they are clearly distinguishing them from “loss-of-FCT” and “modi?cation-of-function”

    Behe: “It is certainly true that, over the long course of history, many critical gain-of-FCT events occurred.”

  19. 19
    bornagain77 says:

    Sequence comparisons DrREC, well let’s dig deeper and look at the real evidence instead of what you just imagine to be true:

    Dr. Behe states in The Edge of Evolution on page 135:

    “Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would actually explain the generation of the complex molecular machinery we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite.”

    That order of difficulty is put at 10^20 replications of the malarial parasite by Dr. Behe. This number comes from direct empirical observation.

    Richard Dawkins’ The Greatest Show on Earth Shies Away from Intelligent Design but Unwittingly Vindicates Michael Behe – Oct. 2009
    Excerpt: The rarity of chloroquine resistance is not in question. In fact, Behe’s statistic that it occurs only once in every 10^20 cases was derived from public health statistical data, published by an authority in the Journal of Clinical Investigation. The extreme rareness of chloroquine resistance is not a negotiable data point; it is an observed fact.
    http://www.evolutionnews.org/2.....26651.html

    “The likelihood of developing two binding sites in a protein complex would be the square of the probability of developing one: a double CCC (chloroquine complexity cluster), 10^20 times 10^20, which is 10^40. There have likely been fewer than 10^40 cells in the entire world in the past 4 billion years, so the odds are against a single event of this variety (just 2 binding sites being generated by accident) in the history of life. It is biologically unreasonable.”
    Michael J. Behe PhD. (from page 146 of his book “Edge of Evolution”)

    Nature Paper,, Finds Darwinian Processes Lacking – Michael Behe – Oct. 2009
    Excerpt: Now, thanks to the work of Bridgham et al (2009), even such apparently minor switches in structure and function (of a protein to its supposed ancestral form) are shown to be quite problematic. It seems Darwinian processes can’t manage to do even as much as I had thought. (which was 1 in 10^40 for just 2 binding sites)
    http://www.evolutionnews.org/2.....26281.html

    When Theory and Experiment Collide — April 16th, 2011 by Douglas Axe
    Excerpt: Based on our experimental observations and on calculations we made using a published population model [3], we estimated that Darwin’s mechanism would need a truly staggering amount of time—a trillion trillion years or more—to accomplish the seemingly subtle change in enzyme function that we studied.
    http://biologicinstitute.org/2.....t-collide/

  20. 20
    DrREC says:

    “The First Rule of Adaptive Evolution”: Break or blunt any functional coded element whose loss would yield a net fitness gain”

    Darwinian evolution. Blind cave fish. That evolution can and does sometimes proceed by breaking functional elements and by loss of information is not controversial.

    But it is wrong to conclude Behe’s review demonstrate evolution doesn’t produce novel functions and gains of information.

  21. 21
    bornagain77 says:

    DrREC, so you use blind cave fish as well??? I suppose you ‘see’ no problem with that!

  22. 22
    Collin says:

    DrRec won’t acknowledge your argument that gains in FCT were already present in the parent strain.

  23. 23
    bornagain77 says:

    DrREC, well even if you were right about material processes generating information in Behe’s survey,, which you are not for technical ‘non-Darwinian’ reasons,,,, but supposing you were right, then it would ‘merely’ show Genetic Entropy to be true! Which once again completely undermines your neo-Darwinian worldview:

    Evolution Vs Genetic Entropy – Andy McIntosh – video
    http://www.metacafe.com/watch/4028086

    further notes:

    Then of course DrREC, there is the little matter of the recent finding of ‘non-local’ quatum information in molecular biology which completely falsifies neo-Darwinian evolution to the basis of reality itself!!! But of course, I’m sure you don’t want to talk about that!!

  24. 24

    rhampton7:

    Fair enough. So from the bacteriology experiments you’re saying that we shouldn’t expect point mutations to be able to result in speciation changes, even over 1000’s of generations?

  25. 25
    rhampton7 says:

    Eric Anderson, RE: 2.1.1.1.4

    Well what we can say is that we would expect speciation solely by single point mutations to be slower (less frequent) by many orders of magnitude. That, of course, assumes a definition of bacterial species based upon a threshold of accumulated change (see my comment 5).

    Now the reproduction of bacteria in cultures follows a known pattern. Initially growth is exponential but as the amount of physical space and/or nutrients decrease, and/or the amount of toxins increase, reproduction and death reach a temporary equilibrium, after which the rate growth reverses (death is exponential). It’s the artificial condition – a single bacteria colonizing a constrained, sterile environment – that causes this pattern to arise. Obviously this affects the likelihood that speciation will occur (e.g. a population crash before a sufficient number of generations.)

    In reality (in situ), bacterial growth rates are much harder to measure and have more complicated patterns. Also, bacterial growth can remain relatively stable over much, much longer periods of time because of predation and other balancing factors. And as I mentioned previously, in reality bacteria can gain new information (meet the threshold for speciation) much faster in the presence of other life.

    So I suspect that most bacterial studies just don’t provide the conditions necessary to observe speciation solely by single point mutation.

  26. 26
    bornagain77 says:

    DrREC, to completely drive the point home that Behe’s paper completely undermines your neo-Darwinian delusions and is indeed in compliance with the principle of Genetic Entropy::

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information
    Excerpt: Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.

    (Michael J. Behe, “Experimental Evolution, Loss-of-Function Mutations and ‘The First Rule of Adaptive Evolution’,” Quarterly Review of Biology, Vol. 85(4) (December, 2010).)

    The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation.

    Consider an imaginary order of insects, the Evolutionoptera. Let’s say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium. The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years. At these rates, every thousand years 1000 species of Evolutionoptera will die off, while one new species will develop–a net loss of 999 species. If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth.
    http://www.evolutionnews.org/2.....51051.html

  27. 27
    DrREC says:

    2.1.1.1.2
    Eric AndersonSeptember 21, 2011 at 2:26 pm
    DrRec:

    Wow, that is quite a literature bomb there, just searching for evolution and speciation. Remember, we were talking about actual observed speciation events,

    You have google. I don’t have time to spell them all out.

  28. 28
    DrREC says:

    “2.1.1.1.3
    bornagain77September 21, 2011 at 2:30 pm
    Sequence comparisons DrREC, well let’s dig deeper and look at the real evidence instead of what you just imagine to be true:

    Dr. Behe states in The Edge of Evolution on page 135:

    “Generating a single new cellular protein-protein binding site (in other words, generating a truly beneficial mutational event that would actually explain the generation of the complex molecular machinery we see in life) is of the same order of difficulty or worse than the development of chloroquine resistance in the malarial parasite.”

    That order of difficulty is put at 10^20 replications of the malarial parasite by Dr. Behe. This number comes from direct empirical observation.?”

    Based on sequence comparisons, and assuming methodological naturalism. Hilarious.

  29. 29
    DrREC says:

    1.1.1.3.3
    CollinSeptember 21, 2011 at 2:41 pm
    DrRec won’t acknowledge your argument that gains in FCT were already present in the parent strain.

    I saw no such argument. Please elaborate. This comment seems totally at odds with the observation, so I;m a bit perplexed.

  30. 30
    DrREC says:

    1.1.1.3.4
    bornagain77September 21, 2011 at 2:48 pm\

    “DrREC, well even if you were right about material processes generating information in Behe’s survey,, which you are not for technical ‘non-Darwinian’ reasons,,,, but supposing you were right, then it would ‘merely’ show Genetic Entropy to be true! Which once again completely undermines your neo-Darwinian worldview”

    “even if you were right about material processes generating information in Behe’s survey,,”

    Behe’s survey clearly lists gain-of-fct mutations through material processes.

    ” which you are not for technical ‘non-Darwinian’ reasons,,,, ”
    Four commas! But do share, what technical non-Darwinian reasons am I wrong for? Seriously, I have no clue what you mean here.

    “but supposing you were right, then it would ‘merely’ show Genetic Entropy to be true!”

    Behe’s Gain-of-fct mutations appear to emerge through random means. If entropy (always favored) increases fCSI, then ID is screwed. Some logic there, my friend.

  31. 31
    DrREC says:

    “the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene.”

    How did Behe arrive at those numbers? His article lists less than 100 total mutations, many of which are modification of function, and several are gain-of-function. Not 100 to 1 loss-of-fct by any means.

    Oddly loose with numbers.

  32. 32

    DrRec:

    Please stop bluffing (or purposely misrepresenting Behe’s paper). The takeaway lesson is that it is possible to have a fitness gain by breaking a functional element. Indeed, he formulates what he calls the First Rule of Adaptive Evolution to summarize the results of his survey: “Break or blunt any functional coded element whose loss would yield a net fitness gain.” Indeed in the few cases in which we find a fitness gain, it is typically accompanied by a breakage in a pre-existing element, not creation of some new function de novo.

    Simple logic test: Do you understand that breaking an existing functional element is *not* the same a generating complex specified information de novo?

  33. 33
    DrREC says:

    Eric….some simple logic tests in return:

    What is the difference between generally and always (as in of the cases Behe selects, he generally sees loss of function, but not always)? How does one proceed to concluding that it is ONLY possible to have a fitness gain by breaking a functional element in light of the exceptions to the rule?

    Breaking on element in formation of another falls under modification-of-fct. Why is there a gain-of-fct category?

    Maybe I shouldn’t be so harsh. I’m sure you read Luskin’s summary of Behe’s paper, which, as I’ve pointed out above, is deeply misleading.

  34. 34
    bornagain77 says:

    DrREC, let’s look, once again, at Lenski’s e-coli after 50,000 generations, since you seem so driven to mislead from what is the obvious implication;

    Mutations : when benefits level off – June 2011 – (Lenski’s e-coli after 50,000 generations)
    Excerpt: After having identified the first five beneficial mutations combined successively and spontaneously in the bacterial population, the scientists generated, from the ancestral bacterial strain, 32 mutant strains exhibiting all of the possible combinations of each of these five mutations. They then noted that the benefit linked to the simultaneous presence of five mutations was less than the sum of the individual benefits conferred by each mutation individually.
    http://www2.cnrs.fr/en/1867.htm?theme1=7

    Now DrREC, how in blue blazes can you be so deprived of common sense that you cannot see the problem here??? You continue to insist that generating functional information/complexity is no problem for neo-Darwinian evolution, and yet, as Lenski’s latest work shows, when even 1 ‘beneficial’ mutation is attempted to be added upon by any or all of the other 4 ‘promising’ beneficial mutations, the effect is less than the presence of just the one beneficial mutation individually alone? Have can you possibly contort this result to mean that neo-Darwinism can produce sophisticated functional information??? i.e. produce the programming in cells that vastly outclasses anything human programmers have done in computers? Do you think that the multiple parallel codes we find in DNA was encoded by such a impotent process? This severe limit for the ability of neo-Darwinian processes to ‘additively’ build functional information on top of even one beneficial mutation that had conferred a fitness advantage, which was found by Lenski and company personally, is exactly what we should expect for the extremely polyconstrained complexity that we see in the genome:

    Poly-Functional Complexity equals Poly-Constrained Complexity

    The primary problem that poly-functional complexity presents for neo-Darwinism, or even Theistic Evolutionists is this:

    To put it plainly, the finding of a severely poly-functional/polyconstrained genome by the ENCODE study has put the odds, of what was already astronomically impossible, to what can only be termed fantastically astronomically impossible. To illustrate the monumental brick wall any evolutionary scenario (no matter what “fitness landscape”) must face when I say genomes are poly-constrained to random mutations by poly-functionality, I will use a puzzle:

    If we were to actually get a proper “beneficial mutation’ in a polyfunctional genome of say 500 interdependent genes, then instead of the infamous “Methinks it is like a weasel” single element of functional information that Darwinists pretend they are facing in any evolutionary search, with their falsified genetic reductionism scenario I might add, we would actually be encountering something more akin to this illustration found on page 141 of Genetic Entropy by Dr. Sanford.

    S A T O R
    A R E P O
    T E N E T
    O P E R A
    R O T A S

    Which is translated ;
    THE SOWER NAMED AREPO HOLDS THE WORKING OF THE WHEELS.

    This ancient puzzle, which dates back to 79 AD, reads the same four different ways, Thus, If we change (mutate) any letter we may get a new meaning for a single reading read any one way, as in Dawkins weasel program, but we will consistently destroy the other 3 readings of the message with the new mutation.

    This is what is meant when it is said a poly-functional genome is poly-constrained to any random mutations.

    The puzzle I listed is only poly-functional to 4 elements/25 letters of interdependent complexity, the minimum genome is poly-constrained to approximately 500 elements (genes) at minimum approximation of polyfunctionality. For Darwinist to continue to believe in random mutations to generate the staggering level of complexity we find in life is absurd in the highest order!

    As to Theistic Evolutionists, who believe God guides evolution incrementally, all I ask you to consider is do you think that it would be easier for God to incrementally change the polyfunctional genome of a organism, maintaining functionality all the time, in a bottom up manner or do you think it would be easier for Him to design each kind of organism in a top down manner? The evidence clearly indicates ‘top-down’ design.

    “Whatever we may try to do within a given species, we soon reach limits which we cannot break through. A wall exists on every side of each species. That wall is the DNA coding, which permits wide variety within it (within the gene pool, or the genotype of a species)-but no exit through that wall. Darwin’s gradualism is bounded by internal constraints, beyond which selection is useless.”
    R. Milner, Encyclopedia of Evolution (1990)

    Notes:

    Scientists Map All Mammalian Gene Interactions – August 2010
    Excerpt: Mammals, including humans, have roughly 20,000 different genes.,,, They found a network of more than 7 million interactions encompassing essentially every one of the genes in the mammalian genome.
    http://www.sciencedaily.com/re.....142044.htm

    Insight into cells could lead to new approach to medicines
    Excerpt: Scientists expected to find simple links between individual proteins but were surprised to find that proteins were inter-connected in a complex web. Dr Victor Neduva, of the University of Edinburgh, who took part in the study, said: “Our studies have revealed an intricate network of proteins within cells that is much more complex than we previously thought.
    http://www.physorg.com/news196402353.html

    Three Subsets of Sequence Complexity and Their Relevance to Biopolymeric Information – David L. Abel and Jack T. Trevors – Theoretical Biology & Medical Modelling, Vol. 2, 11 August 2005, page 8
    “No man-made program comes close to the technical brilliance of even Mycoplasmal genetic algorithms. Mycoplasmas are the simplest known organism with the smallest known genome, to date. How was its genome and other living organisms’ genomes programmed?”
    http://www.biomedcentral.com/c.....2-2-29.pdf

    Simplest Microbes More Complex than Thought – Dec. 2009
    Excerpt: PhysOrg reported that a species of Mycoplasma,, “The bacteria appeared to be assembled in a far more complex way than had been thought.” Many molecules were found to have multiple functions: for instance, some enzymes could catalyze unrelated reactions, and some proteins were involved in multiple protein complexes.”
    http://www.creationsafaris.com.....#20091229a

    First-Ever Blueprint of ‘Minimal Cell’ Is More Complex Than Expected – Nov. 2009
    Excerpt: A network of research groups,, approached the bacterium at three different levels. One team of scientists described M. pneumoniae’s transcriptome, identifying all the RNA molecules, or transcripts, produced from its DNA, under various environmental conditions. Another defined all the metabolic reactions that occurred in it, collectively known as its metabolome, under the same conditions. A third team identified every multi-protein complex the bacterium produced, thus characterising its proteome organisation.
    “At all three levels, we found M. pneumoniae was more complex than we expected,”
    http://www.sciencedaily.com/re.....173027.htm

  35. 35
    bornagain77 says:

    DrREC, do you want to go through the supposed ‘gain of function’ mutations individually??? I think it will be become clear extremely quickly exactly who is playing fast and loose with the evidence here, and it sure ain’t Dr. Behe!!!

  36. 36
    Eugene S says:

    Great post, ba77. The constraint programming illustration with the palindrome is really nice.

  37. 37
    NickMatzke_UD says:

    What the heck does “speciation” even mean in bacteria? It is literally conventional wisdom in mainstream biology that the “species” concept doesn’t work very well in bacteria, and that there IS no obvious way to rigorously define which bacteria are “one species” and which are “two species”. They aren’t sexually reproducing, thus the concepts of “gene pool”, interbreeding etc. don’t work.

    You could find hundreds of quotes in the literature to this effect — but no, the creationists keep dragging out this one weird quote mine because they and their audiences are naive enough to ignore the obvious glaring problems with using it as evidence.

  38. 38
    bornagain77 says:

    Casey Luskin has responded to Nick Matzke, on Lenski’s LTEE here;

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information
    http://www.evolutionnews.org/2.....t-11290411

    and has responded to DrREC here:

    Richard Lenski’s Long-Term Evolution Experiments with E. coli and the Origin of New Biological Information
    http://www.evolutionnews.org/2.....t-11287481

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