Speciation: The triumph of hope over evidence

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/2011/09/richard_lenskis_long_term_evol051051.html#comment-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/2011/09/richard_lenskis_long_term_evol051051.html#comment-11287481

bornagain77

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. NickMatzke_UD

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

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!!! bornagain77

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/releases/2010/08/100809142044.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/content/pdf/1742-4682-2-29.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/crev200912.htm#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/releases/2009/11/091126173027.htm

bornagain77

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

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 Anderson

"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

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. DrREC

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. DrREC

"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. DrREC

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. DrREC

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/2011/09/richard_lenskis_long_term_evol051051.html

bornagain77

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. rhampton7

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

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!! bornagain77

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

DrREC, so you use blind cave fish as well??? I suppose you 'see' no problem with that! bornagain77

"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

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/2009/10/richard_dawkins_the_greatest_s026651.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/2009/10/nature_paper_finally_reaches_t026281.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/2011/04/16/when-theory-and-experiment-collide/ bornagain77

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." DrREC

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. Eric Anderson

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.podomatic.com/entry/2010-05-10T15_24_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.podomatic.com/player/web/2010-12-23T11_53_46-08_00

bornagain77

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. Eric Anderson

"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/pubmed?term=speciation%20evolution DrREC

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). DrREC

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. rhampton7

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. Collin

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. DrREC

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 rhampton7