The Hall-Hartl E. coli experiment. In a 1974 paper Barry Hall and Daniel Hartl identified a gene in the bacterium E. coli that is responsible for metabolizing lactose, using a complicated three-part process. They removed this gene, and then permitted the bacteria to multiply in a stressed environment containing lactose. Within 24 hours the bacteria had evolved a capability to utilize lactose, by means of a similar but distinct three-part biochemical pathway, involving two mutated genes [Hall1974; Miller1999, pg. 145-147]. Biologist Douglas Futumya described this discovery as follows: "One could not wish for a better demonstration of the neo-Darwinian principle that mutation and natural selection in concert are the source of complex adaptations." [Futumya1986]. Biologist Kenneth Miller points out that not only is it a valid example of evolutionary novelty, it is also an example of a multi-part biochemical system that intelligent design writer Michael Behe has insisted could not be produced by natural evolution [Miller2005]. See also the discussion of Complexity.
http://www.sciencemeetsreligion.org/evolution/novelty.php
Reality beats anyone's reasoning. And those papers you cited don't say what you seem to think they say.
This is the evidence to go with my previous post.
Here are some other possibilities they haven’t taken into consideration.
Hall’s work needs critical evaluation. Mutations in the Ebg system are clearly not an example of evolution but mutation and natural selection allowing for adaptation to the environment. Several possibilities for the function of the Ebg system are suggested. In addition, there is an assessment of the likelihood of these mutations in the
ebg operon occurring in a natural setting. An implication of this research is an understanding that adaptive mutation makes “limited” changes which severely restrict its use as a mechanism for evolution.
How is Dr. Miller defining evolution? Adaptive mutagenesis of the Ebg system is not creating a new system, nor does it even impart
E. coli with a new phenotype. Instead, the mutations, combined with selection, work on pre-existing genetic material. The wild-type
ebg ß-gal already possessed the ability to catabolize lactose. The mutations merely restored the Lac+ phenotype that the mutant strain of
E. coli had previously lost by a deletion of
lacZ. In addition, mutations at 92 and/or 977 in
ebgA simply allow the
ebg ß-gal system to utilize lactose better.
Hall’s work with the Ebg system is not an example of the evolution of a new system or even a new phenotype. Rather the process of adaptive mutagenesis (through mutation and natural selection) has allowed the bacteria to make a minimal number of changes in pre-existing systems to regain a previously lost function in order to adapt to adverse environmental conditions. More time and more beneficial mutations as achieved by adaptive mutagenesis still do not result in evolution, merely adaptation.
Another problem for adaptive mutagenesis as a mechanism for evolution is the net overall loss of functional systems. As discussed in the appendix, the proposed hypermutable state of bacteria under non-lethal selection leads to genome-wide mutations.
Although these cells possessed beneficial mutations which allowed them to utilize lactose, they also possessed deleterious mutations that resulted in the loss of the ability to utilize xylose or maltose. Hall also found auxotrophic mutations among Trp+ revertants. Mutations in enzymes typically alter their substrate specificity or interfere with their ability to interact with their natural substrate.
So if the organism is in the wild and continues to evolve it will eventually find it harder to survive because it will have a fitness cost overall.
As papers regarding the functionality of pseudogenes have only recently been published (last five years), it is possible that
ebgA is a pseduogene with an unknown regulatory function.
Another possibility is that the ebg operon represents a functionally redundant backup system for the lac operon.
Possibly
ebgA serves as a backup gene for several essential genes and the most flexibility within the system is achieved by altering
ebgA in accordance with the particular essential gene that has been inactivated. Further support of the idea that the
ebg operon is a backup system is implicated by the findings that adaptive mutagenesis of
ebgR is regulated.
Early findings by Hall and Foster/Cairns seemed to indicate that the only mutations that were occurring were those specific for dealing with the selective pressure that the bacteria were under. This would seem to contradict the randomness of mutations (or a mutation rate independent of the environment) required by Neo-Darwinian philosophy.
Although these cells possessed beneficial mutations which allowed them to utilize lactose, they also possessed deleterious mutations that resulted in the loss of the ability to utilize xylose or maltose. Hall also found auxotrophic mutations among Trp+ revertants. It is not known if the mutations at 92 and 977 in
ebgA affect the natural function of the Ebg system since its natural function is unknown. It is likely that these mutations do affect the natural function of
ebg ß-gal since they occur in the proposed active site. Mutations in enzymes typically alter their substrate specificity or interfere with their ability to interact with their natural substrate.
Hall, although not skeptical of evolution in general, does seem to conclude that his work on the Ebg system is not reflective of the experimental test or laboratory verification of evolution that Miller suggests. In a recent paper he recounted the history of his research on the Ebg system. Hall writes,
As a fresh young postdoc in 1972, I was pretty disdainful of evolutionary biology, dismissing it as just-so stories backed up by internally consistent, but experimentally untestable hypotheses. Underlying all of those questions was the big question: what did we have to know in order to predict both the evolutionary potential of an organism for a new gene function and the evolutionary potential of any particular ancestral gene?
Well, we pretty much lost sight of that question over the years of studying Ebg. We had started out wanting to be able to predict evolution but ended up, much like classical evolutionists, simply explaining what we had seen. Sure we had watched the events occur in the laboratory, but no effort to predict outcomes in advance had been attempted.
https://answersingenesis.org/geneti...of-barry-halls-research-of-e-coli-ebg-operon/
Estimating the prevalence of protein sequences adopting functional enzyme folds.
http://www.ncbi.nlm.nih.gov/pubmed/15321723
This paper talks about pre existing genetic info being turned on and activated rather than new genetic material evolving.
A Prescribed Evolutionary Hypothesis.
I propose that phylogeny took place in a manner similar to that of ontogeny by the derepression of preformed genomic information which was expressed through release from latency (derepression) by the restructuring of existing chromosomal information (position effects). Both indirect and direct evidence is presented in support of the Prescribed Evolutionary Hypothesis.
http://www.ncbi.nlm.nih.gov/pubmed/15889345
This is a paper by a prominent biologist in the journal in the journal of the US National Academy of Science. He acknowledges the simultaneous evolution of all components of a system are implausible.
Evolutionary layering and the limits to cellular perfection
Here, it is argued that random genetic drift can impose a strong barrier to the advancement of molecular refinements by adaptive processes.
http://www.pnas.org/content/109/46/18851
This paper below found evidence indicating that despite high mutation rates and generous assumptions favoring a Darwinian process, molecular adaptations requiring more than six mutations before yielding any advantage would be extremely unlikely to arise in the history of the Earth.
Estimating the prevalence of protein sequences adopting functional enzyme folds.
http://www.ncbi.nlm.nih.gov/pubmed/15321723
These papers talks about how adaptive evolution cannot produce all the changes we see in living things and that there is evidence of other processes that are more responsible such as HGT.
The frailty of adaptive hypotheses for the origins of organismal complexity
http://www.pnas.org/content/104/suppl_1/8597.full
The evolution of genetic networks by non-adaptive processes
http://www.nature.com/nrg/journal/v8/n10/abs/nrg2192.html
Darwinian evolution in the light of genomics.
http://www.ncbi.nlm.nih.gov/pubmed/19213802
Lastly this paper talks about the fitness cost of mutations, even beneficial ones.
Negative Epistasis Between Beneficial Mutations in an Evolving Bacterial Population
We analyzed the effects of epistasis on fitness for the first five mutations to fix in an experimental population of Escherichia coli. Epistasis depended on the effects of the combined mutations—the larger the expected benefit, the more negative the epistatic effect. Epistasis thus tended to produce diminishing returns with genotype fitness,
http://www.pnas.org/content/104/suppl_1/8597.full
That should just about cover all angles.