The Tangled Bank

#53744: charlie wagner — 12/14  at  10:14 AM
Facilitated Variation

For years I have been arguing that the neo-darwinian view of evolution, the slow accumulation of beneficial variations over time, has never had any empirical support. I have argued that science has failed produce any empirical evidence, either observational or experimental that supports a nexus between the trivial effects of mutation and natural selection and the emergence of highly organized structures, processes and systems.

I'm glad that people are beginning to notice this glaring defect.

"In the 150 years since Darwin, the field of evolutionary biology has left a glaring gap in understanding how animals developed their astounding variety and complexity. The standard answer has been that small genetic mutations accumulate over time to produce wondrous innovations such as eyes and wings. Drawing on cutting-edge research across the spectrum of modern biology, Marc Kirschner and John Gerhart demonstrate how this stock answer is woefully inadequate."

http://yalepress.yale.edu/yupbooks/book.asp?isbn=0300108656

Marc W. Kirschner and John C. Gerhart, The Plausibility of Life: Resolving Darwin’s Dilemma (Yale University Press, $30).*

(*just so there is no misunderstanding, these guys are opposed to intelligent design and have the misguided confidence that this new "patch" will somehow mitigate the growing belief that some sort of intelligent input is an absolute requirement for evolution.)

Now, just like Punctuated Equilibrium was proposed to explain the gaps in the fossil record, so a new "theory" has emerged to attempt to explain this glaring dilemma.

"The key is what they call “facilitated variation.” By this they mean that an organism does not merely tolerate environmental perturbations or developmental accidents, but in fact adjusts to the disturbances and incorporates them into its physiology or development. This buffering facilitates variation in traits by channeling environmental or genetic irregularities into integrated pathways of response. Furthermore, random inputs in the form of environmental perturbations or genetic mutations do not produce random outputs, because the outputs are shaped by the organism’s adaptive responses. Although genetic mutations may be random in their effects on the DNA sequence of an organism, facilitated variation implies that they may be far from random in how they affect the development of the organism. Facilitated variation therefore views the organism itself as playing a central part in determining how environmental and genetic variation is expressed

http://www.harvard-magazine.com/on-line/110512.html

"...random inputs in the form of environmental perturbations or genetic mutations do not produce random outputs, because the outputs are shaped by the organism’s adaptive responses."

That sounds an awful lot like "adaptive evolution", which sounds an awful lot like "directed evolution" (Barry Hall, are you listening? You were RIGHT!)

My, my, my....the organisms are rsponding to their environment, not just tolerating it? Now let me see, where have I heard THAT before?

http://makeashorterlink.com/?B1553205C

#53745: charlie wagner — 12/14  at  10:32 AM


Posted on talk.origins in 2002

"In her 1983 Nobel lecture, Barbara McClintock said "the genome is a highly sensitive organ of the cell, that in times of stress, can initiate it's own restructuring and renovation". This was in stark contrast to previously held beliefs that genetic change and the evolution that proceeds from it was the result of small, random mutations in individual genes.
Now, in 2002, we are beginning to realize, as Dr. McClintock did in 1983, that this perception is simply wrong. The "mutations" that lead to evolutionary change may not be totally random. For example, it has become clear that some parts of the genome are more likely to be duplicated than others, or moved to other places, depending on the
nature of their DNA sequences. Enzymes that copy the DNA and look after its integrity can selectively induce changes in certain parts of the genome, creating "hot spots" of mutation. What these new findings mean for evolution is still not yet clear, but it may not be too outrageous
to state what many bacterial geneticists are already saying: that cells can engineer their own genomes. This new thinking has resulted in a paradigm shift in which the old idea that genomes evolve to minimize mutation rates and prevent random genetic change is being replaced by the belief that the most successful genomes are those that are able to change quickly and substantially. In fact, this ability to change rapidly in the face of environmental stress may well be a dominant
feature of all genomes.
In some species, it's been discovered that genes have to undergo dramatic changes during reproduction, changes that involve not only removing the DNA bewteen coding regions, but also rearranging the order of the coding regions. Most organisms, at the very least, have enzmes
for cutting, splicing and rearranging their DNA. Apparently many genomes are not static entities, protected from coding errors by repair mechanisms and subject to random point mutations, but they actually use their dynamic flexibility to generate genetic variation, in effect, engineering their own genomes. DNA repair mechanisms are capable of repairing up to 99% of all coding errors, but this can vary, down to
only a few percent, depending on the sequence that needs repairing. All of these clues tell us that there's a lot more going on than we are currently aware of.
The transposons that Dr. McClintock described as early as 1948, may turn out to be crucial players in the evolution scenario. Many people still consider them to be "rogue" DNA's that are no different from random mutations, since they seemed to land just about anywhere in the genome. But this seemingly random, parasitic behavior may be an important part of the mechanism of evolution. Transposons may have played an important role in the evolution of the immune system and the incredible variety of antibodies may well be the result of transposons.
The enzymes Rag1 and Rag2, which play a key role in the assembly of the V, J and D sequences work just like transposases, which mobilize transposons. This may explain the sudden appearance of the immune system in vertebrates. The introduction of a transposon could easily have set
the stage for this evolutionary leap.
Transposons may even "capture" genes and move them in large chunks to new parts of the genome, reshaping the entire architecture of the genome. One can no longer merely suggest that transposable elements have a role in the evolution mechanism. It is now a fact. When species face
selective pressures and stresses, the genome is ready to react and respond. This is clearly demonstrated by the adaptive mutations that Cairns, Hall and Rosenberg are seeing. Bacteria can turn on response mechanisms under adverse conditions that are nothing at all like the
usual random mutations. The alarm sounds, and the cell responds by turning on systems that, among other things, activate repair mechanisms and promote DNA shuffling.
With more and more work being done, it's becoming clearer that genomes are capable of radically rearranging themselves, making use of mobile, transposable elements and stimulating specific stretches of DNA to mutate at high rates, helping themselves to adapt to challenging
environments. And as more and more biologists are adopting these new views of evolution and genomic function, the darwinian paradigm will fade peacefully into the sunset, to await the dawn of a new day for science as the capability of cells moves far beyond what Darwin ever dreamed possible."