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Jhud -> RE: Documented evolution of new functions and behaviors in bacteria (4/15/2008 12:34:28 PM)
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I wanted to jump in here before the thread gets too far off topic.
I would have responded earlier, but I wanted to take a little time to read through the relevant literature, see exactly what has been found, and what were the factors that lead to it.
Part of the problem with the OP as it is stated is that it is based on a two page very generalized NYT story, which briefly refers to three different studies dealing with three different species, Escherichia coli, Pseudomonas, Myxococcus Xanthus.
Of course, as is typical with such articles, it refers to all the changes that occurred to the organisms in the various experiments as ‘evolution’ without providing particular details about the actual causes of those changes. Indeed, the article briefly acknowledges that the mechanisms that actually caused the changes are at this point unknown:
But Dr. Velicer has no idea at the moment how the mutation brought about the remarkable transformation in behavior. The mutated segment of DNA actually lies near, but not inside, a gene. It is possible that proteins latch on to this region and switch the nearby gene on or off. But no one actually knows what the gene normally does.
Mutations like this one, Dr. Velicer said, “make for a much more complicated story.” It is a story he and other scientists are looking forward to revealing.
So to simply place them under the rubric of ‘evolution’ or claim they contradict Behe is premature at best, somewhat disingenuous at worst.
That being said, a brief primer, utilizing another recent find dealing with change in a bacterium and antibiotic resistance that I have posted previously. It will become evident why this is relevant in a short while.
In this paper we are dealing with antibiotic resistance Escherichia coli, one of the bacterium being considered in the NYTs article.
Antibiotic resistance is often depicted as a ‘classic’ evolutionary case. You have a population of bacteria, you apply an antibiotic which acts as a selective factor, the bacteria which survive convey that resistance to their progeny, and viola! One evolves a population of resistant bacteria.
The causes of this resistance from a genetic perspective have been little known. In typical evolutionary fashion, it is often assumed to derive from a genetic mutation which conveys a novel capability to the organism which has it.
The paper here chronicles something quite different. Rather than a novel characteristic, the effect of the antibiotic on the population seems to promote enhanced regulation of already extant capabilities, or in this case, a structure called an efflux pump. The purpose of this pump is to (surprise, surprise) pump toxins the organism encounter in the environment out of the cellular membrane.
In the presence of antibiotic, the genes that control the pump increase the activity of the pump, which in turn pumps more of the toxin (in this case the antibiotic) out of the cell, and create ‘resistance’ to the antibiotic. As the paper details, it is a non-mutational environmental response:
Living organisms have the capacity to adapt to changing environments without the need to rely on mutations, which are infrequent and thereby slow, to be incorporated into a population in a given environment. In the case of the efflux of toxic compounds, physiological adaptation of a cell to a given substance in a given environment begins with an event that takes place at or within the cell envelope and results in a sensor type of stress response. This eventually results in genetic activity that encodes for additional units of that same efflux pump that extrude a broad range of substrates. The addition of more efflux pumps into the cell envelope increases the survival of the organism.
Now, what relevance does this have to the topic at hand?
Well, the author of the OP wants a quick and easy means of looking at what are rather sophisticated suite of biological capabilities; namely ‘mutations did it’. I would suggest that upon further investigation, the researchers will find complex regulatory process that better explain the response of these organisms to the various environmental stressors that they have been subjected to.
Indeed, I think the answers would be apparent faster if they were inclined to consider them as the researchers considering bacterial resistance did. Indeed, I would say this rises to the level of a prediction, based on an ID paradigm.
And this is one of my problems with evolutionary thinking; it undermines actual understanding of biological processes by presuming, as the author did, that they are primarily Neo-Darwinian in nature – and that is detrimental in a much greater way when one considers that much of this research impacts the health of humans and environments. Following rabbit trails only hurts us.
Now, as I said I read through some of the more detailed literature concerning the cases the NYTs reports, something I don’t think the author of the OP bothered to do. In my brief reading I would say that the changes are less ‘evolutionary’ than the OP supposes.
In fact, it seems to be the case in terms of Lenski’s ‘heat resistant’ bacteria that we are dealing with more of these sorts of changes. His paper, Evolutionary changes in heat-inducible gene expression in lines of Escherichia coli adapted to high temperature chronicles what seem to be modifications to currently existing genes as a stress response:
Genes encoding molecular chaperones and ATP-dependent proteases, key components of the cytoplasmic stress response, exhibit relatively little expression change; whereas genes with periplasmic functions exhibit significant expression changes suggesting a key role for the extracytoplasmic stress response in the adaptation to high temperature. Following acclimation at 41.5°C, two of the three lines exhibited significantly improved survival at 50°C, indicating changes in inducible thermotolerance. Thus evolution at high temperature led to significant changes at the molecular level in heat-inducible gene expression and at the organismal level in inducible thermotolerance and fitness.
So I would say that no, this isn’t indicative of the evolutionary change one should expect if neo-Darwinism is true.
Another paper (Long-term experimental evolution in Escherichia coli. XI. Rejection of non-transitive interactions as cause of declining rate of adaptation) , again by Lenski, demonstrates how, over time, adaptation actually declines, and the rate of change actually plateaus. This would seem to verify Behe's contention that there is a limit to mutational evolutionary change.
So I would say that while the NYTs article presents intriguing possibilities, on closer inspection it provides little support for Neo-Darwinism. Indeed, it doesn't even proffer that any of the organisms speciated, much less followed unique evolutionary paths.
Just a few short thoughts on the subject.
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