Long Term Evolution Experiment

[Darwin123]

How did they test for the distant ancestors not having this ability at a low level?

I haven't read the Nature article. However, the newspaper article had a sufficiently complete description to infer what they did to infer.
The scientist kept frozen samples of the distant ancestors, i.e., the bacteria that were first placed in a flask. Samples were taken from the flask about every 5000 generations. I think that comes to about one sample every 2.5 years. They could check for the ability to digest citrate in the first and subsequent samples of frozen bacteria. I think they did that, although I have to check.
The frozen sample of stock culture showed no measurable ability to digest citrate. If you doubt it, ask them for samples of the stock solution. That is the entire reason that they are storing frozen samples.
If the original samples showed the ability to digest citrate at a very low level, then it still wouldn't matter. Finding that the original bacteria have a very small ability to digest citrate would merely show that the molecules were not really "fine tuned" to begin with.
We know that anyway. Actually, none of the chemical reactions require such precision that absolutely no other reactions can happen but the one. The specific shapes strongly bias the chemical reactions to one particular chemical reaction. However, they don't restrict other chemical reactions from occurring. Many metabolic diseases come about because the precise "correct" chemical reaction doesn't occur.
Mutations occur because the fidelity of the copying process is not totally specific. Cancer often starts because copying DNA is not so specific. Our digestive systems can handle lots of artificial chemicals, although not with perfect efficiency. The specificity comes because of natural selection and time, not because anyone designed the molecules for a specific task.
The fact is that the shapes of the molecules slowly changed, generation after generation, until they were specific to an entirely different chemical reaction. Complex changes in the molecules and the timing of gene expression were necessary to get the bacteria to digest citrate efficiently. Thus, the experiment shows that "fine-tuning" is the product of "time not design".
I doubt that the original bacteria had absolutely no way to digest any citrate. Even if the scientists couldn't find any such ability in any sample of bacteria, I would still suspect that there was a low level of citrate digestion. The reason that I would suspect this is because I know that no biochemical system is 100% specific to the one chemical reaction that it is "supposed to do". However, "supposed to do" is anthromorphizing. The specificity is due to generation after generation of random variation culled by natural selection.
At the beginning of the process, none of the bacteria had any metabolic chain of reactions that was specific to citrate digesting. The metabolic pathways were specific to something else, although they were never completely specific. This means that the shape of the molecules wasn't precisely "right" for digesting citrate, though it may have been mostly specific for something else. At the end of the experiment, the bacteria had a metabolic chain of reactions that seemed specific to citrate digesting. Hence, the fine-tuning of the citrate pathway is an illusion of time.
You wouldn't dismiss the evolution of ape to man by saying that the ape has a "small ability to reason". Saying that the bacteria had a small level of ability to digest citrate is like saying that nonhuman apes have a small ability to think, or that nonhuman apes have a small ability to determine when something is wrong. Or that dogs have a small ability to socialize. Natural selection is hypothesized to take the nonhuman apes small ability to reason and make it into a human ability to reason. That is how humans became human.
Specifically, the experiment knocks "irreducible complexity" on its rear. Whatever the metabolic pathway is now that digests citrate, that metabolic pathway has segments that were useful for something entirely different. Thus, the metabolic reaction for citrate has complexity that is reducible.

 

[Ygggdrasil]

Regarding the the Lenski long-term evolution experiment (LTEE), E. coli have the ability to digest citrate under anaerobic conditions, but not under aerobic conditions. In the LTEE, Lenski and colleagues identified a lineage of bacteria that had evolved the ability to metabolize the citrate under aerobic conditions (first described in a paper by them from 2008, http://www.ncbi.nlm.nih.gov/pubmed/18524956). In their latest Nature paper (http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11514.html), Lenski and colleagues sequence the ancestral bacteria that led up to the Cit⁺ population, and examine some of the mutations that underlie acquisition of the Cit⁺ pheotype. In particular, they find mutations that allow the citrate transporter to be produced under aerobic conditions and that increase the amount of citrate transporter produced.

Now the fact that the evolution of the Cit⁺ involves "merely" the repurposing of existing proteins and genetic elements may make the evolution of the Cit⁺ phenotype less impressive, but such an attitude misses the point of the study. These and other studies of the evolution of new traits often show that new traits do not arise out of thin air, and scientists can trace a very plausible sequence of mutations that introduce small changes allowing the new traits to emerge (for another example, see work on the evolution of the steroid receptor family http://www.ncbi.nlm.nih.gov/pubmed/16601189). Indeed, writing in a commentary on the recent Lenski paper, evolutionary biologists Heather Hendrickson & Paul Rainey write:

"Although E. coli can 'digest' citrate when oxygen is absent, it typically cannot do so under the aerobic conditions of this experiment. The fact that the microbe can use citrate under some circumstances raises an important point: new genes are not invented de novo. Quite the contrary — evolution builds on the raw material at its disposal. The bacterium has the building blocks necessary for the evolution of aerobic citrate utilization, but realization of this capacity requires a rewiring and refinement of regulatory connectivities. [...] The discovery of the Cit+ mutants in Lenski's experiment has been a mote in the eye for those suggesting that major phenotypic innovations cannot be explained by microevolutionary (gradual) processes."​

(http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11487.html)

 

[atyy]

Regarding the the Lenski long-term evolution experiment (LTEE), E. coli have the ability to digest citrate under anaerobic conditions, but not under aerobic conditions. In the LTEE, Lenski and colleagues identified a lineage of bacteria that had evolved the ability to metabolize the citrate under aerobic conditions (first described in a paper by them from 2008, http://www.ncbi.nlm.nih.gov/pubmed/18524956). In their latest Nature paper (http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11514.html), Lenski and colleagues sequence the ancestral bacteria that led up to the Cit⁺ population, and examine some of the mutations that underlie acquisition of the Cit⁺ pheotype. In particular, they find mutations that allow the citrate transporter to be produced under aerobic conditions and that increase the amount of citrate transporter produced.

Now the fact that the evolution of the Cit⁺ involves "merely" the repurposing of existing proteins and genetic elements may make the evolution of the Cit⁺ phenotype less impressive, but such an attitude misses the point of the study. These and other studies of the evolution of new traits often show that new traits do not arise out of thin air, and scientists can trace a very plausible sequence of mutations that introduce small changes allowing the new traits to emerge (for another example, see work on the evolution of the steroid receptor family http://www.ncbi.nlm.nih.gov/pubmed/16601189). Indeed, writing in a commentary on the recent Lenski paper, evolutionary biologists Heather Hendrickson & Paul Rainey write:

"Although E. coli can 'digest' citrate when oxygen is absent, it typically cannot do so under the aerobic conditions of this experiment. The fact that the microbe can use citrate under some circumstances raises an important point: new genes are not invented de novo. Quite the contrary — evolution builds on the raw material at its disposal. The bacterium has the building blocks necessary for the evolution of aerobic citrate utilization, but realization of this capacity requires a rewiring and refinement of regulatory connectivities. [...] The discovery of the Cit+ mutants in Lenski's experiment has been a mote in the eye for those suggesting that major phenotypic innovations cannot be explained by microevolutionary (gradual) processes."​

(http://www.nature.com/nature/journal/vaop/ncurrent/full/nature11487.html)

In Fig. 3 of the 2008 paper, Blount et al seem to favour the hypothesis that a sudden increase in mutation rate occured. Why is this taken to be in favour of something "gradual" when the schematic indicates a step change?

Incidentally, is there any serious hypothesis that major phenotypic innovations cannot be explained by microevolution? That's surely wrong even without Lenski's work. Take a bicycle, for example. We typically use words like "pedal" and "tire" to explain a bicycle, but no one says that a bicycle cannot be explained in terms of quarks, electrons and photons. So macroevolution and microevolution are not opposing views, rather views of the same processes on different scales, and the distinction between the two is only useful when there is a clear separation of scales.

Hmmm, I just looked at the commentary, their following sentence is "Indeed, for anti-evolutionists, lack of mechanistic detail has even allowed room for divine intervention." I find it dismaying that an article in Nature gives credence to such nonsense by considering it as something to be seriously addressed. I very much doubt Lenski's main point was to address anti-evolutionists. I would imagine more Eldredge and Gould, but I doubt they would have said that macroevolution cannot be explained by microevolution.

Edit: The 2008 paper definitely claims to provide evidence for the feasibility of a Gouldian hypothesis, but the stress is on Gould's historical contingency hypothesis, rather than punctuated equilibrium specifically. They have a really interesting note in the methods: "In the first replay experiment, populations evolved under the same conditions as the LTEE. In the second and third replay experiments, cells were incubated on MC plates. We started the first replay experiment on the 3rd anniversary of Stephen Jay Gould's death; we ended it on the 66th anniversary of his birth.".

 

[Darwin123]

“Lock and key theory”, I like that analogy. Thank you, I will study this.
I also think that there has to be a sequence in the assembling of the car. So highly specified part A must have just one right place B at moment C and highly specified part A’ must have just one right place B’ at moment C’ … etc.

I think this is demonstrably false. I know for a fact that different parts of the car can be put together in different sequences without affecting the final shape of the car. There are many sequences that don't work out. However, there is more than one way to build a car.
There are two types of random in your original question. One is the random of random motion in molecules. You mostly referred to that in your original post. The other is the random possibilities in history. This type of random is questioned in your current post.
The issue of random motion is more or less resolved by "lock and key" models. The shape and related properties of the molecule restrict the chemical reactions that are probable. However, there is also random in how the molecules got that shape. This is a question of natural history. The answer often given is that the random changes in the molecules were culled by natural selection. However, this makes sense only if the histories resulting in a certain morphology in shape. I will address the issue of history in this reply.
Just as there are many possible ways for an organism to evolve with the same general form. For example, you may hear about several "theories" regarding how the bird evolved.
These theories are usually comprised of sequences of events that led to the evolution of a modern bird. Some people is interpreted as an internal contradiction to the theory of evolution. However, there is nothing that fundamentally forbids any of these theories to be true. Given the morphology of any extant bird, and given only that morphology, there are any number of sequences that could result in the current bird.
Distinguishing between theories means looking for details not apparent in the morphology of the bird. Scientists look for fossils that may contradict any separate theory. They may also look at the genome of the bird. There can be more than one genome that results in the same morphology of the bird. One genome may be consistent with anyone theory of bird evolution than the other. However, the extra data merely narrows down the historical possibilities.
One thing not emphasized enough is that redundancy increases probability. If there is more than one history that can build a specific morphology, then the probabilities of those histories add up. They don't multiply. Therefore, the union set of sequences of events leading to a particular morphology or a particular shaped molecule can be probable because of historical redundancy, not because anyone sequence is probable.

 

[atyy]

Just as there are many possible ways for an organism to evolve with the same general form.

Doesn't the Lenski paper argue that this is not true in some circumstances?

He is trying to distinguish two scenarios:

"Stephen Jay Gould maintained that these historical contingencies make evolution largely unpredictable. Although each change on an evolutionary path has some causal relation to the circumstances in which it arose, outcomes must eventually depend on the details of long chains of antecedent states, small changes in which may have enormous long-term repercussions (13–15). Thus, Gould argued that contingency renders evolution fundamentally quirky and unpredictable, and he famously suggested that replaying the “tape of life” from some point in the distant past would yield a living world far different from the one we see today. Simon Conway Morris countered that natural selection constrains organisms to a relatively few highly adaptive options, so that “the evolutionary routes are many, but the destinations are limited” (16)."

And argues for the former in his experiment:

"A potentiated cell took the one less traveled by, and that has made all the difference."

 

[Darwin123]

Doesn't the Lenski paper argue that this is not true in some circumstances?

I never read his original article. I am still trying to find a link where I can get it for free.
As described in the abstract and in the newspaper article, his experiment did not address that point. This point could only be addressed if the experiment were repeated many times.

He is trying to distinguish two scenarios:

"Stephen Jay Gould maintained that these historical contingencies make evolution largely unpredictable. Although each change on an evolutionary path has some causal relation to the circumstances in which it arose, outcomes must eventually depend on the details of long chains of antecedent states, small changes in which may have enormous long-term repercussions (13–15). Thus, Gould argued that contingency renders evolution fundamentally quirky and unpredictable, and he famously suggested that replaying the “tape of life” from some point in the distant past would yield a living world far different from the one we see today. Simon Conway Morris countered that natural selection constrains organisms to a relatively few highly adaptive options, so that “the evolutionary routes are many, but the destinations are limited” (16)."

And argues for the former in his experiment:

"A potentiated cell took the one less traveled by, and that has made all the difference."

Lenski didn't really address the point of redundancy. The single experiment described can not distinguish between Conway's or Gould's theory.
1) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate by the same metabolic pathway, and if the frozen samples indicated a different historical path for each repetition, then that would prove Conway's theory. There was one destination, the aerobic citrate by that pathway. That would be like there were identical cities all over the world with different people in them and many roads passing through each. Like in some of the old SF novels, intelligent extraterrestial aliens would be all human but have different histories and cultures.
2) If only one of the experimental repetitions resulted in an E. coli that can aerobically digest citrate, and the other repetitions resulted in some completely different way to survive, then that would prove Gould's theory. There were dozens of survival options, and maybe dozens of ways to get to each final option. The aerobic digestion of citrate was only way to survive. It would be like there were lots of cities that are wildly different. There would be few if any intelligent extraterrestrials, and every planet would have wildly different organisms.
3) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate, and if the metabolic pathways were significantly different in each repetition, then the experiment would be prove the Star Trek model. Then there was only one adaptive option, which is the aerobic digestion of citrate. However, there were obviously dozens of destinations that are effectively the same. This would be as though there were nearly identical cities all over the world with different people living in them, and maybe one highway passing through each. Like Star Trek, it would imply that intelligent extraterrestrial aliens would have different anatomies but somehow have a similar culture and language.
4) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate, if the metabolic pathways were the same, and if the historical development were the same, then I would have to rethink my position as to evolution not being programmed. It would imply that there was only one niche that can survive in any given situation, only one organisms that can survive long term in that niche, and only one history that can lead to that organism. I don't see how that can occur without some type of programming.

I read some articles concerning antibiotic resistance that basically support the Star Trek theory. If a colony of bacteria is exposed to lowly increasing levels of antibiotic, then the colony always develops resistance to that antibiotic. However, the metabolic pathways that produce the antibiotic resistance are always different in each repetition of the experiment. If Gould were correct, then most colonies of bacteria would not develop a resistance. Most colonies would simply go extinct, some colonies would merely reproduce faster than the antibiotic could kill bacteria, and a bacteria in very few colonies would simply escape.

Resistance to a particular antibiotic is like being an intelligent alien on Star Trek. However, there are dozens of anatomies consistent with being an intelligent alien. Gould would say that being intelligent is a product of unlikely series of contingencies.

I will look for references concerning antibiotic experiments.

 

[atyy]

I never read his original article. I am still trying to find a link where I can get it for free.

Does this work for you: http://www.ncbi.nlm.nih.gov/pubmed/18524956 ? I was able to get it free from either of the two links at the top right of that page. The pnas site gives it nicely formatted, the pubmed site gives the "raw" version. This is the 2008 paper, not the latest.

 

[Ygggdrasil]

In Fig. 3 of the 2008 paper, Blount et al seem to favour the hypothesis that a sudden increase in mutation rate occured. Why is this taken to be in favour of something "gradual" when the schematic indicates a step change?

I think you're reading the figure incorrectly. The y-axis represents the probability that the Cit⁺ mutation would arise. In the historical contingency model favored by the Blount et al. the sudden increase in this probability occurs because the population acquires a "potentiating" mutation. This potentiation mutation, while it does not directly confer the Cit⁺ phenotype, is thought to be a prerequisite for the "actualizing" mutations to produce a Cit⁺.

This potentiation has been observed in other studies of protein evolution. For example, in the example of the evolution of steroid receptors I referred to earlier, the "actualizing" mutations that allowed the ancestral steroid receptor bind to a different steroid also happen to destabilize the structure of the receptor protein. Indeed, if these actualizing mutations are introduced directly into the ancient protein, the resulting mutant is not functional. Prior to the acquisition of the actualizing mutations, however, the protein acquired some neutral, "actualizing" mutations that help to stabilize the protein and enable the "actualizing" mutations to produce a functional protein (Ortlund et al. 2007. Crystal structure of an ancient protein: evolution by conformational epistasis. Science: 317 1544. PMID:17702911, note that the authors describe the potentiating mutation as a "permissive" mutation).

Unfortunately, in the 2012 Nature study, Blount et al. are unable to identify nature of the the potentiating mutations for the Cit⁺ phenotype. Hopefully future studies will reveal the identify of and molecular mechanisms for these potentiating mutations.

Incidentally, is there any serious hypothesis that major phenotypic innovations cannot be explained by microevolution?

No, but it is always nice to have more examples where the molecular mechanisms behind the evolution of new phenotypes have been worked out.

Lenski didn't really address the point of redundancy. The single experiment described can not distinguish between Conway's or Gould's theory.
1) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate by the same metabolic pathway, and if the frozen samples indicated a different historical path for each repetition, then that would prove Conway's theory. There was one destination, the aerobic citrate by that pathway. That would be like there were identical cities all over the world with different people in them and many roads passing through each. Like in some of the old SF novels, intelligent extraterrestial aliens would be all human but have different histories and cultures.
2) If only one of the experimental repetitions resulted in an E. coli that can aerobically digest citrate, and the other repetitions resulted in some completely different way to survive, then that would prove Gould's theory. There were dozens of survival options, and maybe dozens of ways to get to each final option. The aerobic digestion of citrate was only way to survive. It would be like there were lots of cities that are wildly different. There would be few if any intelligent extraterrestrials, and every planet would have wildly different organisms.
3) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate, and if the metabolic pathways were significantly different in each repetition, then the experiment would be prove the Star Trek model. Then there was only one adaptive option, which is the aerobic digestion of citrate. However, there were obviously dozens of destinations that are effectively the same. This would be as though there were nearly identical cities all over the world with different people living in them, and maybe one highway passing through each. Like Star Trek, it would imply that intelligent extraterrestrial aliens would have different anatomies but somehow have a similar culture and language.
4) If all the experimental repetitions resulted in an E. coli that can aerobically digest citrate, if the metabolic pathways were the same, and if the historical development were the same, then I would have to rethink my position as to evolution not being programmed. It would imply that there was only one niche that can survive in any given situation, only one organisms that can survive long term in that niche, and only one history that can lead to that organism. I don't see how that can occur without some type of programming.

Actually, Lenski did perform the experiment you proposed. In 1988, Lenski founded 12 populations with genetically identical bacteria. Only one of these populations (population #3) acquired the Cit⁺ phenotype. Now, one might contend that if they did not run the experiment long enough to observe the other populations evolve a Cit⁺ phenotype, but the replay experiments in the 2008 PNAS paper argues against this point. Thus, Lenski's work on the Cit⁺ experiments support Gould's theory and may even provide evidence for the importance of neutral drift in opening new adaptive pathways.

Of course, other studies support other models of evolution. There are various studies that argue for highly constrained pathways for the evolution of new traits (for example, see this paper on the evolution of antibiotic resistance: Weinreich et al. 2006. Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins. Science 312:111. doi:10.1126/science.1123539), while others seem to support the existence of multiple adaptive pathways (for example, see Toprak et al. 2012. Evolutionary paths to antibiotic resistance under dynamically sustained drug selection. Nature Genetics 44: 101. http://dx.doi.org/10.1038/ng.1034 ). So, the situation probably depends on the exact nature of the adaptation required. Of course, this question is still very much an open and active area of research.

 

[atyy]

I think you're reading the figure incorrectly. The y-axis represents the probability that the Cit⁺ mutation would arise. In the historical contingency model favored by the Blount et al. the sudden increase in this probability occurs because the population acquires a "potentiating" mutation. This potentiation mutation, while it does not directly confer the Cit⁺ phenotype, is thought to be a prerequisite for the "actualizing" mutations to produce a Cit⁺.

That is my understanding. I don't have any major problems with the Lenski paper, except possibly the alternative hypotheses should be points on a continuum, but it's clear they knew it. What I don't understand is the commentary by Hendrickson and Rainey. Overall Blount (2008) cites Gould and says that his results show the feasibility of Gould's hypothesis, but the commentary cites Gould to oppose his hypothesis. Is there a conflict between the points of view of Blount (2008) and the Nature commentary?

 

[Ygggdrasil]

Since the commentary was written by a different set of authors and based on new data from the 2012 Nature paper, one would probably expect the two pieces to have different points of view on the subject. However, I see the two articles as citing two different concepts that Gould contributed to evolutionary theory. Blount et al. 2008 cite Gould's work on the role of historical contingency in evolution and show how historical contingency (through the potentiating mutations) played a role in the evolution of the Cit⁺ phenotype. Hendrickson and Rainey 2012, however, cite Gould in relation to the idea that incremental mutational change may not adequately explain some phenotypic innovation. Perhaps this is related to the Gould's work on gradualism vs punctuated equilibrium. On this subject, Hendrickson and Rainey say that Lenski's work does not support Gould as the 2012 Nature paper identifies a clear set of incremental changes that lead to the acquisition and refinement of the Cit⁺ phenotype (of course, if the authors of the commentary are trying to cite Lenski's work in opposition to punctuated equilibrium, I do not think they have a strong argument. In fact, that Lenski's work supports the role of historical contingency in evolution could probably be seen as supporting a proposed mechanism for how puncutated equilibria may come about. So, I do agree with your general point that the focus of the Nature commentary seems misguided. Whereas Hendrickson and Rainey focus too much talking about whether or not incremental mutation can produce major phenotypic change, the focus of the Lenski article is on the mechanisms by which incremental mutations produce phenotypic change).

Anyway, just because the papers support one aspect of Gould's hypotheses on evolution does not mean that they support all aspects of Gould's hypotheses on evolution.

 

[Pythagorean]

To put it plainly, we are talking about creeps vs. jerks right? Why should they be mutually exclusive? Can't a series of creeps lead to a jerk or a jerk lead to a series of creeps? Aren't particular types of evolution (change in signaling molecules vs. change in bone structure) going to lend themselves more to a jerk or a creep?

What's the line between a creep and a jerk? How many incremental changes per time step is each defined at and how's the magnitude of the "change in position" defined? Is there examples of a rate somewhere between creep and jerk?

 

[Ryan_m_b]

Thread split to avoid derailing original.

 

[atyy]

Since the commentary was written by a different set of authors and based on new data from the 2012 Nature paper, one would probably expect the two pieces to have different points of view on the subject. However, I see the two articles as citing two different concepts that Gould contributed to evolutionary theory. Blount et al. 2008 cite Gould's work on the role of historical contingency in evolution and show how historical contingency (through the potentiating mutations) played a role in the evolution of the Cit⁺ phenotype. Hendrickson and Rainey 2012, however, cite Gould in relation to the idea that incremental mutational change may not adequately explain some phenotypic innovation. Perhaps this is related to the Gould's work on gradualism vs punctuated equilibrium. On this subject, Hendrickson and Rainey say that Lenski's work does not support Gould as the 2012 Nature paper identifies a clear set of incremental changes that lead to the acquisition and refinement of the Cit⁺ phenotype (of course, if the authors of the commentary are trying to cite Lenski's work in opposition to punctuated equilibrium, I do not think they have a strong argument. In fact, that Lenski's work supports the role of historical contingency in evolution could probably be seen as supporting a proposed mechanism for how puncutated equilibria may come about. So, I do agree with your general point that the focus of the Nature commentary seems misguided. Whereas Hendrickson and Rainey focus too much talking about whether or not incremental mutation can produce major phenotypic change, the focus of the Lenski article is on the mechanisms by which incremental mutations produce phenotypic change).

Anyway, just because the papers support one aspect of Gould's hypotheses on evolution does not mean that they support all aspects of Gould's hypotheses on evolution.

I agree completely.

To put it plainly, we are talking about creeps vs. jerks right? Why should they be mutually exclusive? Can't a series of creeps lead to a jerk or a jerk lead to a series of creeps? Aren't particular types of evolution (change in signaling molecules vs. change in bone structure) going to lend themselves more to a jerk or a creep?

What's the line between a creep and a jerk? How many incremental changes per time step is each defined at and how's the magnitude of the "change in position" defined? Is there examples of a rate somewhere between creep and jerk?

Yes, I think there should be a model class with some parameter(s) interpolating between the extremes, and more properly the experiments should constrain the range of the parameter. But I haven't got a concrete formulation. I suspect that Blount et al have this in the back of their heads, and they just wrote it in very abridged form. Maybe you can work it out in your spare time, and show it to us (I'm sure you wouldn't, because you'd want to publish it then wouldn't you?:tongue:)

 

[Darwin123]

Does this work for you: http://www.ncbi.nlm.nih.gov/pubmed/18524956 ? I was able to get it free from either of the two links at the top right of that page. The pnas site gives it nicely formatted, the pubmed site gives the "raw" version. This is the 2008 paper, not the latest.

Thank you. I downloaded a copy. I will read it.
I immediately Emailed a copy to a Creationist buddy, along with a rebuttal by Behe. Of course, I rebutted Behe's rebuttal. Would you believe that Behe has never heard of Dollo's Law?

 

[Pythagorean]

Yes, I think there should be a model class with some parameter(s) interpolating between the extremes, and more properly the experiments should constrain the range of the parameter. But I haven't got a concrete formulation. I suspect that Blount et al have this in the back of their heads, and they just wrote it in very abridged form. Maybe you can work it out in your spare time, and show it to us (I'm sure you wouldn't, because you'd want to publish it then wouldn't you?:tongue:)

I'd only just need to standardize the definition of evolutionary state in a way that I could scrape, data-mine, and integrate all original experimental research into a hierarchy of spatiotemporal scales. Simple!

 

[Darwin123]

I'd only just need to standardize the definition of evolutionary state in a way that I could scrape, data-mine, and integrate all original experimental research into a hierarchy of spatiotemporal scales. Simple!

This job will be even more difficult in experiments that include gene transfer. Gene transfer can be lateral or sexual. Most strains of E. coli can perform bacterial conjugation resulting in lateral gene transfer. Lenski's experiment used a special variety of E. coli that could not perform bacterial conjugation. He called this strain without conjunction asexual E. coli. The other E. coli were called sexual bacteria. Although conjunction is not really the same a sex, it can be considered a prototype of sex. So I will use the same terminology.
Lenski chose the asexual bacterium so that it would be easier to track changes in individual lineages. That way, he could draw dendritic cladograms with no reticulation. By doing so, Lenski seriously limited the evolutionary potential of the E. coli.
We generally learn that evolution is enhanced by sex because of gene transfer. Gene transfer combines genes different cells to be associated in the same individual. Some genes can perform are only useful, or can perform certain functions, together with other genes in the same cell.
The bacteria in Lenski's experiment accumulated a lot of deletion mutations. Behe deduced from that fact that evolution could never result in added function. This conclusion was wrong. However, it brings up an interesting possibility.
If Lenski had chosen a sexual bacteria, then the bacterium could have acquired additional genes from other bacteria. Deleted genes could be "replaced". In fact, the genome could have grown. Gene networks could have formed. There could have been even more evolution. It would be more difficult to track the changes. Instead of dendritic cladograms, Lewinski may have been force to draw reticulated cladograms. However, there would be more evolutionary change. Just as important, the experiment would have been a better simulation of natural conditions.
All viruses and bacteria perform lateral gene transfer. Doing this experiment with castrated bacteria can lead to a severely restricted type of evolution. It would be better to study it in a laboratory, though interpreting results would be slightly messier.
I conjecture that Lenski and Brout would have seen even more extreme changes if a strain of sexual bacteria were used. I hope Lenski repeats the experiment with a strain sexual bacteria. Or maybe some other scientist could repeat the experiment with sexual bacteria. I would like to see what would result with bacteria that exchange genes.
Also, I wonder if these neutered bacteria will ever redevelop the ability to conjugate. Or maybe they can develop some other method of gene transfer. Maybe the environmental conditions can be varied to encourage the bacterium to redevelop lateral gene transfer.
The experiment can be tried with some type of sexual microbe like yeast. It may be easier to track changes in the genome with an organism that practices true sex. True sex is a bit more selective than conjugation.
Perhaps some people here would like to conjecture on how Lenski's experimental results would be different if gene transfer were allowed.

 

[Evo]

Darwin, please start using proper spacing between paragraphs, it would make reading your rather lengthy posts much easier!