good night
greatest show on earth
by unstopableravens 273 Replies latest watchtower beliefs
-
-
QC
@cofty
Here’s an opposing view to Dawkins’ citing Richard Lenski’s LTEE using E. coli
Excerpts from Evolution News:
Richard Lenski's Long-Term Evolution Experiments with E. coli
http://www.evolutionnews.org/2011/09/richard_lenskis_long_term_evol051051.html
ID readily allows that natural selection and random mutation can effect SOME changes in populations. The right question is not 'Can natural selection do anything?' but rather 'Can natural selection do EVERYTHING ?'
Behe's 2010Quarterly Review of Biology paper specificity:
By examining the DNA sequence of the E. coli in the neighborhood surrounding the IS [insertion sequence] elements, the investigators saw that several genes involved in central metabolism were knocked out, as well as some cell wall synthesis genes and several others. In subsequent work, Cooper et al. (2001) discovered that twelve of twelve cell lines showed adaptive IS-mediated deletions of their rbs operon, which is involved in making the sugar ribose. Thus, the adaptive mutations that were initially tracked down all involved loss-of-FCT.
Several years later, when the cultures had surpassed their 20,000th generation, Lenski's group at Michigan State brought more advanced techniques to bear on the problem of identifying the molecular changes underlying the adaptation of the E. coli cultures. Using DNA expression profiles, they were able to reliably track down changes in the expression of 1300 genes of the bacterium, and determined that 59 genes had changed their expression levels from the ancestor, 47 of which were expressed at lower levels (Cooper et al. 2003). The authors stated that "The expression levels of many of these 59 genes are known to be regulated by specific effectors including guanosine tetraphosphate (ppGpp) and cAMP-cAMP receptor protein (CRP)" (Cooper et al. 2003:1074). They also noted that the cellular concentration of ppGpp is controlled by several genes including spoT. After sequencing, they discovered a nonsynonymous point mutation in the spoT gene. When the researchers examined ten other populations that had evolved under the same conditions for 20,000 generations, they found that seven others also had fixed nonsynonymous point mutations in spoT, but with different substitutions than the first one that had been identified, thus suggesting that the mutations were decreasing the protein's activity.
The group then decided to concentrate on candidate genes suggested by the physiological adaptations that the cells had made over 20,000 generations. One such adaptation was a change in supercoiling density; therefore, genes affecting DNA topology were investigated (Crozat et al. 2005). Two of these genes, topA and fis, had sustained point mutations. In the case of topA, the mutation coded an amino acid substitution, whereas, with fis, a transversion had occurred at the fourth nucleotide before the starting ATG codon. The topA mutation decreased the activity of the enzyme, while the fis mutation decreased the amount of fis gene product produced.
If you weren't following all the technical language, here's what's going on: For the first 20,000 generations of Lenski's LTEE, very little happened. There were a few molecular adaptations observed, yet whenever we understood their molecular basis, they involved the knocking out of genes, or decreasing protein activity -- in essence, a decrease in specificity .
Behe summarizes:
The fact that multiple point mutations in each gene could serve an adaptive role -- and that disruption by IS insertion was beneficial -- suggests that the point mutations were decreasing or eliminating the protein's function.
Behe closes with another specific example that involved decreasing gene activity in Lenski's LTEE:
In an investigation of global protein profiles of the evolved E. coli, Lenski's group discovered that the MalT protein of the maltose operon had suffered mutations in 8 out of 12 strains (Pelosi et al. 2006). Several mutations were small deletions while others were point mutations, thus suggesting that decreasing the activity of the MalT protein was adaptive in minimal glucose media.
Looking at Table 3 of Behe's QRB paper, not a single example of an adaptive mutation in Lenski's LTEE entailed a gain of a new molecular function. In fact, over the course of his entire paper, Behe goes further and explains that most of our known examples of molecular adaptations in bacteria entail "loss-of-function" mutations.
E. coli used their normal metabolic pathways to use citrate as a food source. Behe made this point while commenting on these claims soon after they were first published in 2008:
Now, wild E. coli already has a number of enzymes that normally use citrate and can digest it (it's not some exotic chemical the bacterium has never seen before). However, the wild bacterium lacks an enzyme called a "citrate permease" which can transport citrate from outside the cell through the cell's membrane into its interior. So all the bacterium needed to do to use citrate was to find a way to get it into the cell. The rest of the machinery for its metabolism was already there. As Lenski put it, "The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions." (1)
Likewise, Behe's recent 2010 paper in Quarterly Review of Biology provided an extensive critique of claims that Lenski's LTEE showed the evolution of a new pathway that could metabolize citrate.
Behe explains:
Recently, Lenski's group reported the isolation of a mutant E. coli that had evolved a Cit+ phenotype. That is, the strain could grow under aerobic conditions in a culture of citrate (Blount et al. 2008). Wild E. coli cannot grow under such conditions, as it lacks a citrate permease to import the metabolite under oxic conditions. (It should be noted that, once inside the cell, however, E. coli has the enzymatic capacity to metabolize citrate.) The phenotype, whose underlying molecular changes have not yet been reported, conferred an enormous growth advantage because the culture media contained excess citrate but only limited glucose, which the ancestral bacteria metabolized.
Thus, Behe explains that the precise genetic mechanisms that allowed E. coli to uptake citrate under oxic conditions are not known. But Behe goes further and points out that the citrate-metabolizing E. coli strains really aren't anything new, and that previous investigations suggest that the ability of the E. coli to uptake citrate under oxic conditions might result from molecular loss-of-function:
As Blount et al. (2008) discussed, several other laboratories had, in the past, also identified mutant E. coli strains with such a phenotype. In one such case, the underlying mutation was not identified (Hall 1982); however, in another case, high-level constitutive expression on a multicopy plasmid of a citrate transporter gene, citT, which normally transports citrate in the absence of oxygen, was responsible for eliciting the phenotype (Pos et al. 1998). If the phenotype of the Lenski Cit+ strain is caused by the loss of the activity of a normal genetic regulatory element, such as a repressor binding site or other FCT, it will, of course, be a loss-of-FCT mutation, despite its highly adaptive effects in the presence of citrate. If the phenotype is due to one or more mutations that result in, for example, the addition of a novel genetic regulatory element, gene-duplication with sequence divergence, or the gain of a new binding site, then it will be a noteworthy gain-of-FCT mutation.
Thus, previous research suggests that the adaptation which allowed these E. coli to uptake citrate under oxic conditions might be caused "by the loss of the activity of a normal genetic regulatory element."
Here's what is likely going on here:
Under normal conditions, E. coli can metabolize citrate; after all metabolizing citrate is an important step in the Krebs cycle, a pathway used by virtually all living organisms when creating energy . But under oxic conditions, E. coli lack the ability to transport citrate through the cell membrane into the cell. E. coli can do this under reducing conditions, but under oxic conditions E. coli can't normally uptake citrate .
If Lenski's citrate-using E. coli are like previous E. coli which were discovered uptaking citrate under oxic conditions, then it seems likely that the bacteria underwent a mutation that knocked out the regulation mechanism of a citrate-transport gene, causing over-expression, allowing the E. coli to uptake citrate under oxic conditions .
In other words, the machinery for both transporting and metabolizing citrate was already present in these bacteria. But a series of knockout mutations broke the regulation of pre-existing citrate transport mechanisms, causing over-expression of a citrate transport gene, allowing citrate to be transported under both oxic and anaerobic conditions. If this is the case, then clearly this example of Darwinian "evolution" entails the loss of a molecular function, not the gain of a new one .
In fact, as Behe notes, we don't really yet understand the precise molecular mechanisms that caused these E. coli to be able to uptake citrate under oxic conditions. So as far as we can tell, these changes entailed the origin of no new functional genes or proteins but might have resulted from a broken regulatory mechanism. We have not seen that natural selection and random mutation can produce functional, information-rich genes and proteins, and Venema is wrong to suggest otherwise.
This example hardly shows the Darwinian evolution of a "new function," especially since E. coli already had the ability to uptake and metabolize citrate.
What do Lenski's LTEE Really Tell Us?
Behe goes on to explain that to date, the known adaptations that have occurred in Lenski's LTEE are either modification-of-function or loss-of-function changes:
The results of future work aside, so far, during the course of the longest, most open-ended, and most extensive laboratory investigation of bacterial evolution, a number of adaptive mutations have been identified that endow the bacterial strain with greater fitness compared to that of the ancestral strain in the particular growth medium. The goal of Lenski's research was not to analyze adaptive mutations in terms of gain or loss of function, as is the focus here, but rather to address other longstanding evolutionary questions. Nonetheless, all of the mutations identified to date can readily be classified as either modification-of-function or loss-of-FCT .
Behe's paper further suggests that when there are several kinds of potential adaptive mutations that might occur, loss or modification of function adaptations will be far more common than gain-of-function adaptations.
He concludes:
Even if there were several possible pathways by which to construct a gain-of-FCT mutation, or several possible kinds of adaptive gain-of-FCT features, the rate of appearance of an adaptive mutation that would arise from the diminishment or elimination of the activity of a protein is expected to be 100-1000 times the rate of appearance of an adaptive mutation that requires specific changes to a gene .
The sort of loss-of-function examples seen in the LTEE will never show that natural selection can increase high CSI. To understand why, imagine the following hypothetical situation .
Consider an imaginary order of insects, the Evolutionoptera . Let's say there are 1 million species of Evolutionoptera, but ecologists find that the extinction rate among Evolutionoptera is 1000 species per millennium . The speciation rate (the rate at which new species arise) during the same period is 1 new species per 1000 years . At these rates, every thousand years 1000 species of Evolutionoptera will die off , while one new species will develop-- a net loss of 999 species . If these processes continue, in 1,000,001 years there will be no species of Evolutionoptera left on earth .
If Behe is correct, then Darwinian evolution at the molecular level faces a similar problem. If, all other things being equal, a loss or modification of function adaptation is generally 100-1000 times more likely than gain of function adaptations, then eventually an evolving population might run out of molecular functions to lose or modify. Neo-Darwinian evolution cannot forever rely on examples of loss or modification-of-function mutations to explain molecular evolution. At some point, there must be a gain of function.
But vague appeals to vast eons of time and huge population sizes are unconvincing. You just have to do the math. As David Abel reminds us:
Mere possibility is not an adequate basis for asserting scientific plausibility . A precisely defined universal bound is needed beyond which the assertion of plausibility, particularly in life-origin models, can be considered operationally falsified. But can something so seemingly relative and subjective as plausibility ever be quantified? Amazingly, the answer is, "Yes." ... One chance in 10 200 is theoretically possible, but given maximum cosmic probabilistic resources, such a possibility is hardly plausible. With funding resources rapidly drying up, science needs a foundational principle by which to falsify a myriad of theoretical possibilities that are not worthy of serious scientific consideration and modeling.
(David L. Abel, "The Universal Plausibility Metric (UPM) & Principle (UPP),"Theoretical Biology and Medical Modelling, Vol. 6:27 (Dec. 3, 2009).)
What is the probability for Evolution of one cell? (Use IE9)
-
cofty
QC - I am happy to explain Lensky's experiment later, I have to go out now.
It is groundbreaking work that shows exactly the sort of changes that "Ireducible Complexity" said was impossible.
The precise mutations are known and the generation numbers in which they occurred.
Could you explain exactly what it was about the article you copy-pasted above that you found interesting?
-
besty
What is the probability for Evolution of one cell? (Use IE9)
Watch the video to understand it all, and make sure you use the correct browser.
-
Thing
It's always hard with Dawkins, to know whether he is presenting information that all evolutionary biologists agree with, or whether some of the information is debatable. Ernest Mayr is considered one of the leading evolutionary biologist's of the 20th century. Consider what he says regarding Dawkins theory of the selfish gene. "An individual either survives or doesn't, an individual either reproduces or doesn't, an individual either reproduces very successfully or it doesn't. The idea that a few people have about the gene being the target of selection is completely impractical; a gene is never visible to natural selection, and in the genotype, it is always in the context with other genes, and the interaction with those other genes make a particular gene either more favorable or less favorable. In fact, Dobzhanksy, for instance, worked quite a bit on so-called lethal chromosomes which are highly successful in one combination, and lethal in another. Therefore people like Dawkins in England who still think the gene is the target of selection are evidently wrong. In the 30's and 40's, it was widely accepted that genes were the target of selection, because that was the only way they could be made accessible to mathematics, but now we know that it is really the whole genotype of the individual, not the gene."
-
Thing
sorry was using IE - lost all the formatting
-
cofty
Thing - The debate over the object of selection is a minor point. It does not change anything about the fact of common ancestry of all living things through unguided evolution over millions of years.
If you would like to read more about the specifics of this particular issue here is a useful article...
There is nothing in The Greatest Show on Earth that could be considered in the least controversial. It is a basic level popular science book.
If you have read the book it would be interesting to hear your thoughts about it.
-
jgnat
unstopableravens, I'll give you a paradox. Jesus is Truth. He and his Father are one. There are two accounts of creation in Genesis, giving a slightly different picture of how and when Adam and Eve were created. Which one is the Truth?
...
To get around these anomalies, bible apologists either try to reconcile the two accounts, or accept ambiguity. Not exactly hard and fast Truth.
Please show the same generosity when coming to terms with the findings of evolution.
-
cantleave
@QC - not sure of your argument here. The yellow highlights are hightlighting what exactly - are these your personal observations?
What is really confusing is what you have cut and paste is a critique of another IDM proponent, using the Behe's paper. What you need to do is go back to Behe's paper and as well as the Lenski Team's paper yourself.
-
cantleave
This is Behe's paper discussing the Lenski experiment.
From what I can make out the cut and paste is a critique of Dennis Venema's views(who in his own words is engaged in the conversation on evolutionary biology and evangelical Christianity through his role with the BioLogos Foundation) using Behe's critical paper of Lenski as the basis of the criticism.
For those unfamiliar with Behe http://en.wikipedia.org/wiki/Michael_Behe
