From Jonathan Wells‘ The 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.
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
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.
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.
That is, obviously, assuming one human generation is 25 years.
Very interesting statement.
“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.
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??
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’:,,
These following studies, by Dr. Cano on ancient bacteria, preceded Dr. Vreeland’s work:
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:
In reply to a personal e-mail from myself, Dr. Cano commented on the ‘Fitness Test’ I had asked him about:
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:
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:
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:
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???
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 . . .
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?
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:
Which led to this startling conclusion:
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
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.
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.
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.
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).
“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
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.
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:
Here is Michael Behe, in his own words, telling exactly what his survey of 40 years worth of lab work reveals against neo-Darwinism
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.
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.”
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/
“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.
DrREC, so you use blind cave fish as well??? I suppose you ‘see’ no problem with that!
DrRec won’t acknowledge your argument that gains in FCT were already present in the parent strain.
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!!
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?
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.
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::
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.
“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.
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.
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.
“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.
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?
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.
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;
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:
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!!!
Great post, ba77. The constraint programming illustration with the palindrome is really nice.
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.
Casey Luskin has responded to Nick Matzke, on Lenski’s LTEE here;
and has responded to DrREC here: