A few weeks ago, I published the fourth part of my series on Wikipedia and common descent, in which I discussed the purported evidence for common ancestry based on biogeographical distribution. Previously, I had cross-examined the evidence from comparative physiology and biochemistry, comparative anatomy, and paleontology. In this second-to-last installment, I will address Wikipedia’s evidence from observed natural selection and speciation.
According to Wikipedia,
Examples for the evidence for evolution often stems [sic] from direct observation of natural selection in the field and the laboratory. Scientists have observed and documented a multitude of events where natural selection is in action. The most well known examples are antibiotic resistance in the medical field along with better-known laboratory experiments documenting evolution’s occurrence. Natural selection is tantamount to common descent in the fact that long-term occurrence and selection pressures can lead to the diversity of life on earth as found today. All adaptations — documented and undocumented changes concerned — are caused by natural selection (and a few other minor processes). The examples below are only a small fraction of the actual experiments and observations.
“Natural selection is tantamount to common descent”? Excuse me if I don’t follow the logical progression. Common descent does not logically entail natural selection as the evolutionary mechanism, nor does the occurrence of natural selection entail the validity of common descent. I would have thought this to be fairly basic. Evidently not.
So, how exactly is natural selection “tantamount” to common descent? According to Wikipedia, it’s because “long-term occurrence and selection pressures can lead to the diversity of life on earth as found today.” In this, Wikipedia assumes — but does not demonstrate — that the incontrovertible evidence for microevolutionary changes within and between species can be justifiably extrapolated to account for all of the complexity and diversity of life on the planet. No attempt is made to even present scientific evidence for this position. This is striking in light of the mountain of negative evidence suggesting that such an extrapolation is not justified.
Antibiotic and Pesticide Resistance
Wikipedia begins this section with a discussion of antibiotic and pesticide resistance. The article states,
The development and spread of antibiotic resistant bacteria, like the spread of pesticide resistant forms of plants and insects is evidence for evolution of species, and of change within species. Thus the appearance of vancomycin resistant Staphylococcus aureus, and the danger it poses to hospital patients is a direct result of evolution through natural selection. The rise of Shigella strains resistant to the synthetic antibiotic class of sulfonamides also demonstrates the generation of new information as an evolutionary process. Similarly, the appearance of DDT resistance in various forms of Anopheles mosquitoes, and the appearance of myxomatosis resistance in breeding rabbit populations in Australia, are all evidence of the existence of evolution in situations of evolutionary selection pressure in species in which generations occur rapidly.
Let’s briefly take a look at each cited example in turn.
Vancomycin-resistant Staphylococcus aureus
Actually, with regard to vancomycin resistance in Staphylococcus aureus, the mechanism by which this occurs is less than impressive. Vancomycin is a glycopeptide that interferes with the production of peptidoglycans. It does this by virtue of binding to the carboxyl terminus of peptidoglycan stem peptides, thus blocking the cross-linking of peptidoglycans.
In order to attain vancomycin resistance, depsipeptide D-Ala-D-lactate is synthesized, and this is made to replace D-Ala-D-Ala in the peptidoglycan cell wall. Thus, the critical mechanism of resistance is the synthesis of D-Ala-D-lactate, which has the capacity for ester formation. The replacement of the amide bond with an ester bond obviously carries consequences for the ability of the vancomycin to bind to the c-terminus of the stem peptide. This significantly reduces the potency of the antibiotic.
This type of trivial change is well within the bounds of what Michael Behe calls the edge of evolution.
Shigella strains resistant to the synthetic antibiotic class of sulfonamides
Sulfonamides work by inhibiting the synthesis of folate by targeting and competitively inhibiting the enzyme dihydropteroate synthetase (Sk�ld, 2000). The mechanism of resistance is mutations affecting this enzyme. And there are many different modifications that can be made, which result in the acquisition of resistance to sulfonamides. This suggests that merely a modification of a target site is involved in conferring resistance.
Nor does resistance come without a cost. Indeed, there is a tradeoff between resistance to sulfonamides and the performance of the dihydropteroate synthetase enzyme. The mutant bacteria thus incur a fitness cost as compared to the wild type. In order to overcome this decrease in fitness, compensating mutations are acquired in some instances.
The appearance of DDT resistance in various forms of Anopheles mosquitoes
The evolution of resistance to DDT is actually fairly trivial. Indeed, the most common way this has happened is by the simple modification of the relevant sodium channel by alteration of its amino acid sequence such that it interferes with the action of the insecticide. Actually, so far as I am aware, in every single known case this is accomplished by replacing the amino acid leucine (position 1014) with phenylalanine (Williamson et al., 1996). Granted, there are some insects that occasionally enhance this resistance by means of an additional mutation in the same protein. But it does not appear to occur independently of the first. It thus seems that the very same alterations have occurred independently in many different cases. This is to be expected, however. If we assume that the probability of mutating a particular nucleotide is something like 10^-9, there are easily adequate probabilistic resources to account for this — there is a very high probability that most of the possible single-nucleotide substitutions will occur in a large enough insect population. The more coordinated/non-adaptive mutations you require to facilitate a novel innovation in function, however, the less likely it is that mutation will stumble upon such an adaptation.
Moreover, a second point that is worthy of note is that the resistant mutants are rendered less fit overall than the “wild type.” That is to say, the mutation incurs a fitness cost. The mutant insects, though resistant to DDT, are also more prone to paralysis at mildly raised temperatures.
The appearance of myxomatosis resistance in breeding rabbit populations in Australia
The basis of myxomatosis resistance in rabbits is poorly understood and various hypotheses have been advanced. In light of the evidence that we do understand, however (in which resistance is often seen to be acquired by a degradation of genetic information), it would seem unwise to triumphantly hail this example as illustrating the power of the Darwinian mechanism. What are the potential mechanisms of resistance? Kerr and Best (1998) suggest,
[R]esistance to myxoma virus could be mediated at the level of replication in the initial inoculation site or replication in distal tissues. Replication could be controlled at the level of cell permissivity, as occurs in flavivirus-resistant mice (6), i.e., the ability of the virus to attach to, enter, replicate in and spread from a cell. Alternatively, effectors of the innate or acquired immune systems could intervene to destroy infected cells by using, for example, natural killer cells (NK cells) and cytotoxic T lymphocytes or to make cells non-permissive for replication by the action of interferon. Myxoma virus actively suppresses apoptosis in infected lymphocytes and the early inflammatory response to infection (Fig. 6). In particular, critical antiviral cytokines, such as TNF and IFN-y, are targeted by specific viral proteins. Resistant rabbits may produce higher levels of antiviral effector cells and molecules, perhaps through an NK cell response such as that controlled by the rmp (resistance to mousepox) 1 gene in mousepox-virus-resistant mice (10). Ultimately, as in any acute virus infection, the outcome will depend on whether the host can slow replication and dissemination of the virus enough to enable the immune response to control and clear the infection.
None of the aforementioned proposed hypotheses would be particularly impressive from the standpoint of the delineated edge of evolution.
E. coli Long-Term Evolution Experiment
The E. coli long-term evolution experiment that began in 1988 under the leadership of Richard Lenski is still in progress, and has shown adaptations including the evolution of a strain of E. coli that was able to grow on citric acid in the growth media.
Richard Lenski’s famous experimental work on E. coli has been thoroughly addressed by ID proponents such as Michael Behe. Behe discusses Lenski’s work on pp. 140-142 of The Edge of Evolution, and — more recently — in a peer-reviewed article in the Quarterly Review of Biology. Behe has been keeping tabs on Lenski’s work on his Uncommon Descent blog. In addition, ENV’s Casey Luskin has an excellent blog post on this subject here.
As to the specific example of adaptive evolution cited by Wikipedia, the case of the citrate transporter seems, to me, to be a weak one because it has been documented that wild-type E. coli can already use citrate under low-oxygen conditions. Under these conditions, citrate is transported into the cell (Pos et al. 1998). The gene in E. coli specifies a citrate transporter. In the presence of high levels of oxygen, it is thought that the citrate transporter doesn’t function or is not produced. Thus, wild-type E. coli already possess the genes necessary for the transportation of citrate into the cell and its subsequent utilization. Indeed, Lenski et al. (2008) note: “A more likely possibility, in our view, is that an existing transporter has been co-opted for citrate transport under oxic [high oxygen level] conditions.” Such a scenario could take place by a loss of gene regulation (meaning that the gene is no longer expressed exclusively under low oxygen conditions) or a loss of transporter specificity.
Lactose Intolerance in Humans
Lactose intolerance is the inability to metabolize lactose, because of a lack of the required enzyme lactase in the digestive system. The normal mammalian condition is for the young of a species to experience reduced lactase production at the end of the weaning period (a species-specific length of time). In humans, in non-dairy consuming societies, lactase production usually drops about 90% during the first four years of life, although the exact drop over time varies widely. However, certain human populations have a mutation on chromosome 2 which eliminates the shutdown in lactase production, making it possible for members of these populations to continue consumption of raw milk and other fresh and fermented dairy products throughout their lives without difficulty. This appears to be an evolutionarily recent adaptation to dairy consumption, and has occurred independently in both northern Europe and east Africa in populations with a historically pastoral lifestyle.
This is perfectly true. But this phenomenon can hardly be construed as genetic novelty. Indeed, this adaptation is accomplished by a loss of genetic information. The “novel” ability is acquired by a mutation that shuts off the capacity for production of the enzyme lactase.
In the case of nylon-digesting bacteria, as with the other examples, there is no reason to think that the nylon-eating capacity requires any novel information. As William Dembski explains:
Nylonase appears to have arisen from a frame-shift in another protein. Even so, it seems to be special in certain ways. For example, the DNA sequence that got frame-shifted is a very repetitive sequence. Yet the number of bases repeated is not a multiple of 3 (in this case, 10 bases are probably the repeating unit).
What this means is that the original protein consisted of repeats of these 10 bases, and since it is not a multiple of 3, it means that these 10 bases were translated in all three possible reading frames (the second repeat was one base offset for translation relative to the first repeat, and the next was offset one more base, et.c). Moreover, none of those reading frames gave rise to stop codons. Since the 10-base repeat was translatable in any reading frame without causing any stop codons, the sequence was able to undergo an insertion which could alter the reading frame without prematurely terminating the protein.
Actually, the mutation did cause a stop codon; but the stop codon was due not to frame shift but to the sequence introduced by the inserted nucleotide. Simultaneously, the mutation introduced a start codon in a different reading frame, which now encoded an entirely new sequence of amino acids. This is the key aspect of the sequence. It had this special property that it could tolerate any frame shift due to the repetitive nature of the original DNA sequence. Normally in biology, a frame shift causes a stop codon and either truncation of the protein (due to the premature stop codon) or destruction of the aberrant mRNA by the nonsense-mediated decay pathway. Nonetheless, the nylonase enzyme, once it arose, had no stop codons so it was able to make a novel, functional protein.
Most proteins cannot do this. For instance, most genes in the nematode have stop codons if they are frame-shifted. This special repetitive nature of protein-coding DNA sequences seems really rare; one biologist with whom I’ve discussed the matter has never seen another example like it. Maybe it’s more common in bacteria. Thus, contrary to Miller, the nylonase enzyme seems “pre-designed” in the sense that the original DNA sequence was preadapted for frame-shift mutations to occur without destroying the protein-coding potential of the original gene. Indeed, this protein sequence seems designed to be specifically adaptable to novel functions.
Even aside from these points raised by Dembski, it is not clear that the basis of this type of evolution is sufficiently well understood to allow for any triumphal assertions. Perhaps the answer is that the mutated enzyme had very low activity. And nylon is also similar to other substances that the bacterium could already metabolize — so we may be looking at small-scale evolutionary change, perhaps involving a loss of enzyme specificity. This hypothesis gains traction from Ohki et al. (2006), which shows strong structural similarity to the enzyme carboxylesterase. And it has been suggested that mutations affecting this enzyme’s catalytic cleft altered the substrate specificity of this enzyme such that it could hydrolyze nylon.
The mechanistic basis of resistance of vertebrate populations to contaminants, including Atlantic tomcod from the Hudson River (HR) to polychlorinated biphenyls (PCBs), is unknown. HR tomcod exhibited variants in the aryl hydrocarbon receptor2 (AHR2) that were nearly absent elsewhere. In ligand binding assays, AHR2-1 protein (common in HR) was impaired compared to widespread AHR2-2 in binding TCDD (2,3,7,8-tetrachlorodibenzo-p-dioxin) and in driving expression in reporter gene assays in AHR-deficient cells treated with TCDD or PCB126. We identified a six-base deletion in AHR2 as the basis of resistance and suggest that the HR population has undergone rapid evolution probably due to contaminant exposure. The mechanistic basis of resistance in a vertebrate population provides evidence of evolutionary change due to selective pressure at a single locus. [Emphasis added]
As it turns out, then, the mechanistic basis for fish resistance to PCB is a loss-of-function adaptive mutation at a single locus, resulting from a six-base deletion in a particular gene, AHR2. The receptor gene, AHR2, is ordinarily involved in mediating toxicity. In the study, the researchers find that the protein specified by the AHR2 gene is missing two of the 1,104 amino acids that are ordinarily found in the protein. This means that the receptor binds with weaker affinity to the PCB, conferring a measure of resistance to the fish. But such resistance does not come without a cost, as the associated genetic changes result in the tomcod becoming sensitive to other toxic compounds, and their ability to degrade such toxic compounds is reduced.
Other Weak Examples
Other weak examples given by Wikipedia include the peppered moth, radiotrophic fungus, and adaptation of urban wildlife. The page also lists several arguable cases of speciation (depending on how one chooses to construe the term). Like those noted above, however, these examples are trivial and unimpressive. Not even the most rock-ribbed young earth fundamentalist creationists reject these examples of natural selection in action.
Summary & Conclusion
In summary, as before, Wikipedia has failed to deliver what it has promised. We are given multiple concrete examples of what evolution can do. What we are not given, however, is concrete evidence that the extrapolation from these small-scale changes to evolution on a grander scale is justified. In fact, in all of the cases given, the adaptation falls well within the bounds of the edge of evolution. And most of these cases involve a loss, and not a gain, of genetic information. If these examples are really the best cases the Darwinists have to offer, the paradigm is in deep trouble.
Furthermore, it bears mentioning that Wikipedia is not supposed to be promoting a “point of view.” But Wikipedia has not only produced pages that promote a particular point of view, the online encyclopedia has also attempted to construct arguments and original research. When Wikipedia asserts that “Natural selection is tantamount to common descent in the fact that long-term occurrences and selection pressures can lead to the diversity of life on earth as found today,” it is adopting a particular stance. Wikipedia’s own rules concerning neutrality are apparently suspended when it helps with the advocacy of evolution to the public.