Life knows all about Darwinism. That’s why it is intelligently designed to resist it.
Neo-Darwinian theory teaches that mutations are random, then a process of “selection” chooses which ones to preserve (Darwin himself was bothered by the implicit personification in “natural selection”). Some mutations are random, for sure. No cell can anticipate where a cosmic ray will hit. How, then, can cells regulate mutations, turning on a “low mutation rate phenotype” under stress? In Current Biology, McDonald and team experimented with E. coli response to mutations. Their paper featured these 4 highlights:
The evolution of low mutation rates in mutator-founded populations � Nonmutators do not only evolve due to reduced genetic load compared to mutators; they can invade � Diploidy is found to be closely associated with reduction of the impact of the mutator phenotype � Genomes may influence mutation rates by initiating more high-fidelity replication early in S phase.
The authors believe that mutations are the source of “beneficial adaptive variation,” but cannot deny they also produce “deleterious genetic load.” When a cell invades a novel environment, it is able to switch on a “mutator phenotype” with a 10- to 100-fold increase in mutation rate. The fact that this “mutator allele” switches on is an indication that there’s a functional purpose behind it. It’s risky, because mutational load is likely to drive many of the cells extinct.
We find that after ?6,700 generations, four out of eight experimental mutator lines had evolved a decreased mutation rate. We provide evidence that the accumulation of deleterious mutations leads to selection for reduced mutation rate clones in populations of mutators. (Emphasis added.)
The authors did not give any examples of a beneficial mutation. All they proved is that populations tend to “evolve” a decreased mutation rate, thereby cutting off the source of “beneficial adaptive variation” while saving themselves from “deleterious genetic load.”
Defensive Block and Tackle
“Researchers demonstrate how ‘interfering’ RNA can block bacterial evolution” is the headline of a news release from Rockefeller University. As expected, the pro-Darwin press release speaks of “evolutionary tricks” and “instant evolution,” but a close reading shows a designed mechanism for surviving under stress:
Bacteria may be simple creatures, but unlike “higher” organisms they have a neat evolutionary trick. When the going gets tough, they can simply pick up and incorporate a loose bit of genetic material from their environment. It’s instant evolution, no time-consuming mutations required. This process, known as horizontal gene transfer, is an important reason why nasty bacteria like pneumococci are often able to evade immune system attacks and antibiotic drugs.
Needless to say, “evolution” without “time-consuming mutations” is not the neo-Darwinian way. By picking up existing genetic information from the environment through horizontal gene transfer, the bacteria give evidence of design for surviving storms of misfortune:
“Transformation is something that bacteria use as a last resort,” says Luciano Marraffini, head of Rockefeller’s Laboratory of Bacteriology. “In a desperate attempt to stay alive under hostile conditions, they start incorporating whatever genes they can find into their chromosome in the hopes that they can quickly evolve out of trouble.“
Michael Behe described in The Edge of Evolution how a cell under stress, like a city under siege, will do whatever it can to survive, throwing whatever is available at the enemy or accepting weapons from allies. If it survives, it has not become something better. It just avoided dying. The ability of a cell to accept or reject existing foreign DNA shows evidence of design for disaster preparedness.
Epistasis and Stasis
Mutating a gene affects other genes. Genes belong to networks that can absorb shocks. That appears to be the message in a PNAS paper about epistasis, or “nonlinear genetic interactions between polymorphic loci.” Do epistatic interactions promote speciation — the kind Darwin needs — or do they promote canalization, the ability of a genotype to vary and yet still produce the same animal?
Whatever the hope, the researchers found that “Epistasis dominates the genetic architecture of Drosophila quantitative traits.” By comparing two pools of fruit flies, they found a lot of genetic variation that the networks apparently absorbed, because both populations remain fruit flies. “Knowledge of epistatic networks will contribute to our understanding of the genetic basis of evolutionarily and clinically important traits,” they said, indicating evolutionists don’t have that understanding yet.
Neo-Darwinism: Reality vs. Hype
With these anti-Darwinian processes in mind, let’s examine some of the recent claims in the news from the world of science.
Michigan State University went over the top again in its hype about Lenski’s lab with its E. coli population that “evolved” the ability to digest citrate. “Evolution is as complicated as 1-2-3” the MSU press release blares. We might ask why his research assistant Zachary Blount is sitting under a pyramid of petri dishes. Maybe he is meditating on new ways to blow the data out of proportion.
Casey Luskin and Michael Behe unmasked this hype last year so there is no need to repeat it, since nothing new is added by the press release.
Gain of function?
A paper claiming to find a “gain of function” was published in Science magazine, announcing, “A Gain-of-Function Polymorphism Controlling Complex Traits and Fitness in Nature.” Prasad and team realize the obvious: that neo-Darwinism can’t afford to lose money on every sale:
Few studies have identified the genes that underlie complex trait variation in nature and the evolutionary processes that influence these polymorphisms. Most such work has focused on loss-of-function mutations that lead to adaptive phenotypes, likely because novel gain-of-function changes occur infrequently and require persistent natural selection to be maintained in populations. Nonetheless, new functional mechanisms are crucially important for adaptive evolution. To understand the adaptive consequences of complex trait variation, we must establish a direct relationship between genetic polymorphisms and phenotypic traits, and investigate the fitness consequences of this variation in natural environments.
This is amazing: the Darwin Bicentennial was three years ago, but hardly anyone has yet tied genes to fitness! Most of the actual lab work has identified loss of information that allowed organisms to adapt. But evolutionists need to tie genes to fitness gains, they said. It’s important. Neo-Darwinism must establish that relationship. Read that paragraph again and let the import of the confession sink in.
That was the build-up to their announcement of a gain-of-function mutation: the ability of a certain plant to ward off pests a little more effectively with a slightly modified chemical defense gene. Again, though, as with the citrate claim, they were talking about an existing polymorphism in one of the populations of similar plants. Despite their pride in showing how a particular gene location “affects plant chemistry and insect resistance, and thus fitness, in a quantitative manner,” the fitness gain they came up with was only 1.3%. Whether a subjective notion like “fitness” can be quantified to two significant figures is highly suspect.
What’s more, numerous other factors could confuse the conclusion. The populations were separated by many miles, one in Colorado and another in Montana, where ecological differences (weather, type of pests and their ratios) could be more important than the similarities. The researchers’ courageous attempts to attribute this slight benefit to modest changes in existing complex pathways is overshadowed by their admission that “few studies have identified the genes that underlie complex trait variation in nature.”
Reviving the old icon of Darwin’s finches, some evolutionists at Harvard Medical School, publishing in PNAS, peeked into beaks and gleaned genes for insight into evolution. From the abstract, it appears all they found was that finches in the Caribbean and finches on the Galapagos grow bigger beaks in a slightly different order. Darwin’s finches develop the prenasal cartilage first, then the premaxillary bone, whereas the Caribbean finches do both at the same time.
“Together, our results demonstrate high flexibility in the relationship between morphology and underlying developmental causes, where different developmental programs can generate identical shapes, and similar developmental programs can pattern different shapes.” This appears to be just another case of canalization with not much to speak of in terms of real evolutionary change. In fact, since the beaks of Darwin’s finches have been shown to oscillate between big and small depending on the climate, this flexibility in developmental programs (note that word “programs”) is arguably a good design feature, providing robustness to perturbations, not a pathway to better things.
In short, the claims by evolutionists for neo-Darwinian progress are modest at best and unsupported at worst, while evidence mounts that life is designed to resist neo-Darwinian mechanisms in its requirement to survive stress and adapt to change.