Evolution Evidence

[nstansbury]

Just read this article at NewScientist.com: http://www.newscientist.com/article/dn14094-bacteria-make-major-evolutionary-shift-in-the-lab.html

 

Aside from it being fascinating in its' own right, I thought it would be an interesting phenomenon for creationist to explain.

[Radical Edward]

the usual thing "no new information" "microevolutinary changes only - no goo to you via the zoo" "pre-programmed adaptivity"

 

and so on.

 

As a rule, creationsts don't explain things, they come up with crappy handwavy palm-offs and demand something stupid, like bacteria with legs.

[doG]

While this scientist can test and repeat his experiment I'll wager a creationist can't do the same Science, don't ya love it!

[CDarwin]

The will ignore everything mentioned above and demand angrily why you aren't talking about the holes in evolution and instead trying to attack Cdesignism.

[ydoaPs]

I reported the link to AiG. I wonder if it will be in this week's News To Note.

[CDarwin]

I reported the link to AiG. I wonder if it will be in this week's News To Note.

 

Oho, good idea.

[Radical Edward]

aah those pesky CDesign Proponentsists.

[Mr Skeptic]

Just read this article at NewScientist.com: http://www.newscientist.com/article/dn14094-bacteria-make-major-evolutionary-shift-in-the-lab.html

 

Aside from it being fascinating in its' own right, I thought it would be an interesting phenomenon for creationist to explain.

 

Well, when I found that article I decided to google up a more detailed explanation. Anyhow, I found it was discussed by Michael Behe. Behe claimed that it wasn't that big a deal -- E coli that can use citrate have been found elsewhere, and in any case E coli have the ability to metabolize citrate, but needed the ability to bring it into the cell. One of the proteins E coli have transports citrate, and it was overexpressed in one of the E coli that could eat citrate. In any case, Behe said it took a surprisingly long time to acquire the mutations needed in that experiment.

 

But then, you should know that Behe is strongly biased against evolution. It does seem what you were asking for, though be aware that he is one of the more reasonable ones. More info below:

 

http://www.uncommondescent.com/evolution/behes-multiple-mutations-needed-for-e-coli/

[lucaspa]

Well, when I found that article I decided to google up a more detailed explanation. Anyhow, I found it was discussed by Michael Behe. Behe claimed that it wasn't that big a deal -- E coli that can use citrate have been found elsewhere, and in any case E coli have the ability to metabolize citrate, but needed the ability to bring it into the cell. One of the proteins E coli have transports citrate, and it was overexpressed in one of the E coli that could eat citrate.

http://www.uncommondescent.com/evolution/behes-multiple-mutations-needed-for-e-coli/

 

Considering that the original researchers haven't found the change that allowed the E. coli to metabolize citrate, how does Behe know it is an overexpression of the citrate transport protein?

 

AH! He doesn't! He says that a known variant of E. coli that can use citrate has an overexpression of citrate permease, therefore he makes the leap (without data) that this is the case here.

 

Once again we see the pattern with creationism/ID: no experiments testing predictions of their own, just attempts to explain away data gathered by experiments testing evolution.

 

What Behe forgets is that natural selection is cumulative. He is still trying to say that you need several simultaneous mutations in the same individual, forgetting that you can have sequential slightly beneficial mutations such that each becomes fixed in the population before the next appears.

 

Also, Behe is forgetting that bacteria have the lowest mutation rate of all organisms. It's no wonder it took so many generations. It's about 0.00001 compared to 20 for humans.

[Mr Skeptic]

Considering that the original researchers haven't found the change that allowed the E. coli to metabolize citrate, how does Behe know it is an overexpression of the citrate transport protein?

 

AH! He doesn't! He says that a known variant of E. coli that can use citrate has an overexpression of citrate permease, therefore he makes the leap (without data) that this is the case here.

 

No, he makes no leaps. All he said is

It seems likely that Lenski’s mutant will turn out to be either this gene or another of the bacterium’s citrate-using genes, tweaked a bit to allow it to transport citrate in the presence of oxygen. (He hasn’t yet tracked down the mutation.)

That's a very reasonable guess; I can't see why you would think that unlikely.

 

Once again we see the pattern with creationism/ID: no experiments testing predictions of their own, just attempts to explain away data gathered by experiments testing evolution.

 

He is pointing out that the experiment is not such a big deal. When I read the report on NewScientist, I was very excited that they captured such a giant leap in evolution in such a short time. They made it sound as if E coli couldn't metabolize citrate, when it turn out it just couldn't ingest it in the presence of oxygen.

 

What Behe forgets is that natural selection is cumulative. He is still trying to say that you need several simultaneous mutations in the same individual, forgetting that you can have sequential slightly beneficial mutations such that each becomes fixed in the population before the next appears.

 

Also, Behe is forgetting that bacteria have the lowest mutation rate of all organisms. It's no wonder it took so many generations. It's about 0.00001 compared to 20 for humans.

 

I won't defend what he has to say about mutations and evolution though. More mutations needed for an ability drastically reduces the probability of that ability evolving, but more possible "correct" mutations for the ability drastically increases it again. I don't know enough about genetics to guestimate either of these.

[iNow]

Mr Skeptic,

 

If Mike Behe's comments were simply "guesses," how does he know how likely they are to be true? How has he discarded other possibilities? In my book, that guy has the academic honesty and integrity of a child molester, and I can't bring myself to take him very seriously.

 

He might be right. Sure. But I'm going to wait for someone else to show it if he is before I accept the assertion.

 

 

 

Fool me once, shame on you. Fool me twice, shame on me.

[MedGen]

Behe is the man that pointed at a bacterial flagellum and shouted Goddidit! I question his validity as a scientist on the grounds that he has discreditted himself merely by associating with the DI propagandists.

 

As for the 44,000 generation E.coli experiment, they actually took culture samples something like every 500 generations so they could backtrack and pinpoint the timings of the individual mutations that lead to the aerobic citrate metabolism.

 

Good blog by Grrlscientist

[ydoaPs]

Has E. coli evolved in front of our very eyes? A recent report in New Scientist claims that it has—and is a poke in the eye for creationists. But when we take a look at the facts' date=' is this actually the case? Or is this another example of the emperor trying on new clothes?[/b']

 

To get an idea of the evolutionary presuppositions and interpretations the article is filled with, take a look at the first web comment it inspired:

 

More proof, if any were needed, that Darwin is right, and the God squad wrong. But it won’t make any difference to them . . . the truth is to be found in the holy texts, and not laboratories.

 

The New Scientist article, “Bacteria Make Major Evolutionary Shift in the Lab,” starts off, “A major evolutionary innovation has unfurled right in front of researchers’ eyes. It’s the first time evolution has been caught in the act of making such a rare and complex new trait.” But let’s take a look at this “evolutionary innovation,” this “rare and complex new trait” that the evolution god has “created.”

 

The story starts 20 years back at Michigan State University. Evolutionary biologist Richard Lenski took a single E. coli bacterium and propagated it, using its descendants to “found” 12 laboratory populations that have continued to grow since then.

 

Lenski’s been watching in the meantime—perhaps not always literally, but nonetheless observing as 44,000 generations of the E. coli have come and gone. Every 500 generations, Lenski pulled a sample of each E. coli population and put it in the deep freeze.

 

During all this time, the bacteria has mutated (as expected) and “evolved”—and here, of course, is where the controversy begins.

 

According to Lenski, most of the evolution in the populations was the same: larger cells and faster growth rates, as well as lower “peak population densities,” occurred in each of the populations.

 

The most notable change happened in just one of the populations: around the 31,500th generation, the bacteria “suddenly acquired the ability to metabolise citrate,” which E. coli cannot normally process. The E. coli that developed the citrate-processing ability then increased in population size and diversity.

 

Lenski figures that this “citrate-plus” ability was an unusual circumstance. New Scientist explains, “either it was a single mutation of an unusually improbable sort, a rare chromosome inversion . . . or else gaining the ability to use citrate required the accumulation of several mutations in sequence.”

 

But Lenski wondered: would that same ability have evolved again? He has since “replayed” the evolution from frozen samples, but only the original population of E. coli has supposedly re-evolved the citrate-processing capability, and only from generation 20,000 or later. Thus, Lenski and his team have concluded that something occurred in the single population after generation 20,000 that enabled the citrate processing around generation 31,500.

 

The New Scientist article closes:

 

Lenski’s experiment is also yet another poke in the eye for anti-evolutionists, notes Jerry Coyne, an evolutionary biologist at the University of Chicago. “The thing I like most is it says you can get these complex traits evolving by a combination of unlikely events,” he says. “That’s just what creationists say can’t happen.”

 

While Darwinists are quick to claim this experiment as support for “evolution” (in reference to full-blown, molecules-to-man evolution), let’s first take a step back and review what “evolution” is, along with the different narratives evolutionists and creationists tell.

 

“Evolution” (in a biological sense), strictly defined, is simply a change in a population’s gene frequencies over time (as generations come and go). Thus, even mutations that remove genetic information can spread if they confer some reproductive and survival advantage.

 

Thus, any time a biological population is observed undergoing any sort of heritable change—even a change that keeps genetic information constant or that reduces genetic information—it is “evolution” in action. This evolution “before our very eyes” is usually then touted as proof for molecules-to-man evolution, even though the latter would require a massive increase in genetic information. It’s the old “bait and switch” tactic, as “evolution” shifts meaning from experimentally shown change to unobservable molecules-to-man change.

 

So what’s really going on in Lenski’s experiment? Actually, nobody really knows! Lenski’s team is still working to understand “just what that earlier change was, and how it made the . . . mutation possible.” They will likely be analyzing the genome of the original E. coli parent and the genomes of its “evolved” offspring. The citrate-processing ability may be due to the activation of a latent function or a beneficial (but not information-gaining) mutation that allows citrate processing.

 

It’s important for us all to remember that when we read science news that seems to “confirm” evolution, it’s never a true threat to the biblical worldview and the creation account because God’s Word never changes but man’s fallible ideas do.

 

Furthermore, creationists are just as interested in figuring out how the citrate-processing ability came about in this batch of E. coli. AiG’s Dr. Georgia Purdom is studying the research for an upcoming semi-technical article in the journal Answers In Depth.

http://answersingenesis.org/articles/2008/06/14/news-to-note-06142008

[CDarwin]

I'll paraphrase: Anything you can see is micro-evolution!!! It's different!!! And We have scientists too, so we know!!!

[Edtharan]

I'll paraphrase: Anything you can see is micro-evolution!!! It's different!!! And We have scientists too, so we know!!!

They have some pimped out wheels on those goal posts. It makes them much easier to shift

[lucaspa]

That's a very reasonable guess; I can't see why you would think that unlikely.

 

In this context it is unreasonable. Behe is using it to lower the epistemic value of the discovery.

 

It's always good to go look at the primary article. Lenski isn't looking at demonstrating evolution in general but instead trying to delineate the relative contributions of contingency vs determinism.

 

"This potentiating change increased the mutation rate to Cit+ but did not cause generalized hypermutability. Thus, the evolution of this phenotype was contingent on the particular history of that population. More generally, we suggest that historical contingency is especially important when it facilitates the evolution of key innovations that are not easily evolved by gradual, cumulative selection. "

 

I won't defend what he has to say about mutations and evolution though. More mutations needed for an ability drastically reduces the probability of that ability evolving,

 

No, it doesn't. Because the "probability" is always calculated on the idea that the mutations must appear in the same generation. Thus, it is unlikely that all the mutations will appear in the same individual. But that isn't the case. The mutations can appear sequentially, with the first mutation having been fixed (present in all the individuals of the population) before the next mutation appears. Then the odds are much better because no matter what individual mutation #2 appears in, that individual will have mutation #1. Natural selection is a means to cut down odds.

 

Now, back to the article.

"Previous analyses of this experiment have shown numerous examples of parallel phenotypic and genetic evolution. All twelve populations underwent rapid improvement in fitness that decelerated over time (2, 3, 22, 23). All evolved higher maximum growth rates on glucose, shorter lag phases upon transfer into fresh medium, reduced peak population densities, and larger average cell sizes relative to their ancestor (22–26). "

 

AHA! Something Behe failed to mention: E. coli in the wild that can transport citrate got them from plasmids:

"Throughout the duration of the LTEE, there has existed an ecological opportunity in the form of an abundant, but unused, resource. DM25 medium contains not only glucose, but also citrate at a high concentration. The inability to use citrate as an energy source under oxic conditions has long been a defining characteristic of E. coli as a species (35, 36). Nevertheless, E. coli is not wholly indifferent to citrate. It uses a ferric dicitrate transport system for iron acquisition, although citrate does not enter the cell in this process (37, 38). It also has a complete tricarboxylic acid cycle, and can thus metabolize citrate internally during aerobic growth on other substrates (39). E. coli is able to ferment citrate under anoxic conditions if a cosubstrate is available for reducing power (40). The only known barrier to aerobic growth on citrate is its inability to transport citrate under oxic conditions (41–43). Indeed, atypical E. coli that grow aerobically on citrate (Cit+) have been isolated from agricultural and clinical settings, and were found to harbor plasmids, presumably acquired from other species, that encode citrate transporters (44, 45). "

 

But these guys can't get their citrate from another species; there isn't any. Behe misled everyone by implying that E. coli by themselves could be Cit+. Not true. The ones in the wild need plasmids from other species.

 

This is what Lenski tested:

"The long-delayed and unique evolution of the Cit+ phenotype might indicate that it required some unusually rare mutation, such as a particular chromosomal inversion, that does not scale with typical mutation rates. Alternatively, the occurrence or phenotypic expression of the mutation that generated the Cit+ function might depend on one or more earlier mutations, such that its evolution was contingent on the particular history of that population. Contingent adaptations should tend to be complex and require multiple steps, some of which might not be beneficial, at least not uniquely so given other advantageous paths. Otherwise, cumulative selection would predictably favor the same steps, and the evolutionary path should be repeatable (18). Contingent adaptations should thus display two characteristics. First, independent origins should be rare, because the same historical sequences would rarely recur (19). Second, significant time-lags should occur between the presentation of ecological opportunities or challenges and the evolution of those traits that confer adaptation to those circumstances (46). "

 

And Lenski concludes that he is looking at a contingent adaptation:

 

"These analyses compel us to reject the hypothesis that a rare mutation could have produced a Cit+ variant with equal probability at any point in the LTEE. Some unusually rare mutation might be involved, but its rarity does not provide a sufficient explanation for the unique and exceptionally slow evolution of this new function during the LTEE. Our results instead support the hypothesis of historical contingency, in which a genetic background arose that had an increased potential to evolve the Cit+ phenotype. "

 

"The evolution of the new Cit+ function represents a key innovation that involves multiple steps, and it provides an explicit demonstration of the importance of historical contingency in evolution. It also transcends the phenotypic boundaries of a diverse and well studied species, and led to an ecological transition from a single population to a two-member community. Our future research on this fascinating case of evolution in action will revolve around four themes: genetics, physiology, ecology, and speciation.

 

What is the genetic basis of this evolutionary innovation? The emergence of the Cit+ phenotype in population Ara-3 indicates at least two important genetic events: the origin of the function in its weak form, and its subsequent refinement for efficient use of citrate. "

 

The bolded part is very important. This is the first instance of E. coli itself being able to use citrate in the medium as a food source. All other cases say E. coli got the ability from a plasmid from another species.

 

"A more likely possibility, in our view, is that an existing transporter has been coopted for citrate transport under oxic conditions. This transporter may previously have transported citrate under anoxic conditions (43) or, alternatively, it may have transported another substrate in the presence of oxygen. The evolved changes might involve gene regulation, protein structure, or both (61). "

[Mr Skeptic]

In this context it is unreasonable. Behe is using it to lower the epistemic value of the discovery.

 

But saying he is wrong is also a guess, that you were using to reduce the believability of his argument. So his argument is based on a guess, and later when we find out whether he is wrong or not we can see whether it was a good guess or not.

 

It's always good to go look at the primary article. Lenski isn't looking at demonstrating evolution in general but instead trying to delineate the relative contributions of contingency vs determinism.

 

Well, it certainly was an interesting experiment. That kind of thing must take a lot of patience. However, it would take several different experiments with several different types of abilities to properly determine contingency vs determinism. The more "irreducibly complex" that an ability is, the more it would depend on contingencies whereas the type of ability that is easy to do incrementally would be very deterministic. Some of both of these were observed in his experiment, but more would be needed to get a feel for how long or easy a trait would be to evolve.

 

No, it doesn't. Because the "probability" is always calculated on the idea that the mutations must appear in the same generation. Thus, it is unlikely that all the mutations will appear in the same individual.

 

Yes, that is a horrid assumption.

 

But that isn't the case. The mutations can appear sequentially, with the first mutation having been fixed (present in all the individuals of the population) before the next mutation appears. Then the odds are much better because no matter what individual mutation #2 appears in, that individual will have mutation #1.

 

Still, what I said was true, including the part where I don't know enough biology to guestimate any of these odds. In any case, this is irrelevant to what I said.

 

Natural selection is a means to cut down odds.

 

Only for beneficial traits, of course

 

AHA! Something Behe failed to mention: E. coli in the wild that can transport citrate got them from plasmids:

 

Yes, people who leave out facts or exaggerate are much more annoying to deal with than those who just outright lie

 

"... were found to harbor plasmids, presumably acquired from other species, that encode citrate transporters (44, 45). "

 

But these guys can't get their citrate from another species; there isn't any. Behe misled everyone by implying that E. coli by themselves could be Cit+. Not true. The ones in the wild need plasmids from other species.

...

This is the first instance of E. coli itself being able to use citrate in the medium as a food source. All other cases say E. coli got the ability from a plasmid from another species.

 

Well, in the link I gave you, Behe references (reference #3) a journal article where the citrate carrier called CitT was in the chromosome (not plasmid) of a strain of E. coli. So, looks like Behe just taught you something! :D:D

 

"A more likely possibility, in our view, is that an existing transporter has been coopted for citrate transport under oxic conditions. This transporter may previously have transported citrate under anoxic conditions (43) or, alternatively, it may have transported another substrate in the presence of oxygen. The evolved changes might involve gene regulation, protein structure, or both (61). "

 

It seems likely that Lenski’s mutant will turn out to be either this gene or another of the bacterium’s citrate-using genes, tweaked a bit to allow it to transport citrate in the presence of oxygen. (He hasn’t yet tracked down the mutation.)

 

So Behe's guess is a bit narrower than your source's guess, which also includes the possibility that it originally transported a substance other than citrate but under oxic condidtions.

[Element 007]

Reading the tone and attitude in some of these responses, it is apparent that a lot of people take a highly ideological position on this stuff. What is truely behind the need to defend evolution? A truely scientific attitude anxiously explores possible falsifying aspects as much as affirming aspects within experiments. Thats objectivity. In that spirit, I would love to see an evolutionist write a critique of the Lenski research, one that honestly examines possible falsifying factors. Are there any evolutionists that are also not ideologues?

 

Mr. Skeptic, your posts are sobering and a joy to read.

[Mr Skeptic]

Thanks, Element.

 

Just for the record, I'm also an evolutionist. I was dragged kicking and screaming by the evidence, so I don't think I'm one of your ideologues. Sill, I will defend people who believe otherwise against accusations of being complete idiots (since I am just as smart as when I didn't believe evolution), and also some general ideas.

[iNow]

I will defend people who believe otherwise against accusations of being complete idiots (since I am just as smart as when I didn't believe evolution), and also some general ideas.

 

I think you are smarter now than then, but that's just me.

[Mr Skeptic]

Not smarter. Less ignorant.

[iNow]

A worthy clarification, but I'll keep calling you smarter if you don't mind.

[lucaspa]

What is truely behind the need to defend evolution? A truely scientific attitude anxiously explores possible falsifying aspects as much as affirming aspects within experiments.

 

What you are missing is that creationism/ID has already been falsified. The ideology is on the side of creationism/ID that refuses to admit that the theory has been falsified. It ignores the massive amounts of data and instead only tries to discredit the data supporting evolution.

 

In that spirit, I would love to see an evolutionist write a critique of the Lenski research, one that honestly examines possible falsifying factors. Are there any evolutionists that are also not ideologues?

 

That assumes that there are valid criticisms of the paper. Experimentally, the approach is straighforward and simple. The assay for use of citrate is simple and all they are doing is thawing out previous generations to see where in those generations the ability to use citrate appeared.

 

All in all, for the hypothesis the paper is stating and the conclusions the paper is reaching, the paper is very well written. I have a few minor quibbles with some of the figures.

 

It is the soundness of the paper (and the study) that contributes to the ineffective and silly criticisms of it by creationists. There aren't any major valid criticisms. So Behe resorts to false witness about the nature of the use of citrate by E. coli in the wild.

 

But saying he is wrong is also a guess, that you were using to reduce the believability of his argument.

 

You should have read the rest of my post before you said this. As it turns out, the smoking gun that Behe is wrong is present in the paper!

 

Well, it certainly was an interesting experiment. That kind of thing must take a lot of patience. However, it would take several different experiments with several different types of abilities to properly determine contingency vs determinism.

 

Oh yes. This is merely the latest salvo in the debate. It will continue. The argument, if you noticed, has already settled not on whether there is only determinism or contingency, but rather on how much contribution each makes.

 

The more "irreducibly complex" that an ability is, the more it would depend on contingencies whereas the type of ability that is easy to do incrementally would be very deterministic.

 

There is no such thing as "irreducibly complex" in the meaning that Behe uses. All"irreducibly complex" structures can be reached by one of the 4 modes of Darwinian evolution: http://www.cbs.dtu.dk/dave/JTB.html

 

Some of both of these were observed in his experiment, but more would be needed to get a feel for how long or easy a trait would be to evolve.

 

What standard would you use for "easy"? Evolution is constrained by history, so some structures or traits are not at all accessible to particular genomes. For instance, no tetrapod is going to be able to evolve a hexapodal structure. Once a trait is under 2 or more positive selection pressures, it is essentially unchangeable: G Wagner, Complexity matters. Science, 279, Number 5354 Issue of 20 February 1998, pp. 1158 - 1159

 

Yes, that is a horrid assumption.

 

But that is the assumption made by Behe and other creationists.

 

I won't defend what he has to say about mutations and evolution though. More mutations needed for an ability drastically reduces the probability of that ability evolving,

 

As you said, you don't know enough biology. This isn't true because the mutations appear sequentially. Also, more than one mutation will do the same basic job. As long as the first mutation confers any advantage (even if the advantage is not what the final product is going to be) then it will be fixed. This negates the idea of lower probability for the later mutations: they have the same probability of appearing as they always did.

 

[Only for beneficial traits, of course

 

But that's what we are talking about, right?

 

Yes, people who leave out facts or exaggerate are much more annoying to deal with than those who just outright lie

 

It's more difficult to track them down. But leaving out relevant facts is an outright lie. This is the smoking gun that made Behe's "wild guess" a lie.

 

Well, in the link I gave you, Behe references (reference #3) a journal article where the citrate carrier called CitT was in the chromosome (not plasmid) of a strain of E. coli. So, looks like Behe just taught you something!

 

The reference is: "3. Pos, K.M., Dimroth, P., and Bott, M. 1998. The Escherichia coli citrate carrier CitT: a member of a novel eubacterial transporter family related to the 2-oxoglutarate/malate translocator from spinach chloroplasts. J. Bacteriol. 180:4160-4165."

 

Here's the abstract. Look at what I bolded:

"Under anoxic conditions in the presence of an oxidizable cosubstrate such as glucose or glycerol, Escherichia coli converts citrate to acetate and succinate. Two enzymes are specifically required for the fermentation of the tricarboxylic acid, i.e., a citrate uptake system and citrate lyase. Here we report that the open reading frame (designated citT) located at 13.90 min on the E. coli chromosome between rna and the citrate lyase genes encodes a citrate carrier. E. coli transformed with a plasmid expressing citT was capable of aerobic growth on citrate, which provides convincing evidence for a function of CitT as a citrate carrier. Transport studies with cell suspensions of the transformed strain indicated that CitT catalyzes a homologous exchange of citrate or a heterologous exchange against succinate, fumarate, or tartrate. Since succinate is the end product of citrate fermentation in E. coli, it is likely that CitT functions in vivo as a citrate/succinate antiporter. Analysis of the primary sequence showed that CitT (487 amino acids, 53.1 kDa) is a highly hydrophobic protein with 12 putative transmembrane helices. Sequence comparisons revealed that CitT is related to the 2-oxoglutarate/malate translocator (SODiT1 gene product) from spinach chloroplasts and five bacterial gene products, none of which has yet been functionally characterized. It is suggested that the E. coli CitT protein is a member of a novel family of eubacterial transporters involved in the transport of di- and tricarboxylic acids."

 

They had to put CitT in a plasmid and transfect the E. coli before E. coli could use citrate in an aerobic environment. These E. coli were NOT in the wild and the ability to aerobically metabolize citrate comes from a human constructed plasmid. So there is nothing in this paper to contradict Lenski.

 

As you said: " people who leave out facts or exaggerate are much more annoying to deal with than those who just outright lie "

 

So Behe's guess is a bit narrower than your source's guess, which also includes the possibility that it originally transported a substance other than citrate but under oxic condidtions.

 

Behe limited his possibilities in order to attack the paper and try and say the paper did not show evolution. Like you said above: "people who leave out facts ... are much more annoying to deal with than those who just outright lie" Behe made it appear that his guess was the only valid guess.

Edited June 20, 2008 by lucaspa
multiple post merged

[PhDP]

As you said, you don't know enough biology. This isn't true because the mutations appear sequentially. Also, more than one mutation will do the same basic job. This negates the idea of lower probability for the later mutations: they have the same probability of appearing as they always did.

 

I'm not sure you know enough about evolution, what on earth is that;

 

As long as the first mutation confers any advantage (even if the advantage is not what the final product is going to be) then it will be fixed.

[Mr Skeptic]

You should have read the rest of my post before you said this. As it turns out, the smoking gun that Behe is wrong is present in the paper!

 

Oh. How do you know which mutations are responsible for Lenski's strain's ability to use citrate when even he doesn't, though? If you don't, then how can you say whether Behe's guess is wrong or not?

 

Oh yes. This is merely the latest salvo in the debate. It will continue. The argument, if you noticed, has already settled not on whether there is only determinism or contingency, but rather on how much contribution each makes.

 

Gee, I hadn't noticed Guess that makes my previous talk about which type of ability would require more contingency and which would be more deterministic look silly.

 

As you said, you don't know enough biology.

Woah! You're tripping all over yourself trying to disprove a true statement, and it only makes you look silly.

I won't defend what he has to say about mutations and evolution though. More mutations needed for an ability drastically reduces the probability of that ability evolving, but more possible "correct" mutations for the ability drastically increases it again. I don't know enough about genetics to guestimate either of these.

For the record, I don't believe any scientist knows enough about biology either, else Lenski wouldn't have needed to do his experiment. Anyhow, since you invited some harsh criticism, here's your first helping.

 

This isn't true because the mutations appear sequentially.

 

For one thing, mutations don't necessarily appear sequentially. Various mutations can happen and develop in parallel. In species with sexual reproduction or other genetic transfer, the mutations can develop in parallel in multiple individuals.

 

Also, more than one mutation will do the same basic job.

 

Yup, that's what I said. How does that disprove me?

 

As long as the first mutation confers any advantage (even if the advantage is not what the final product is going to be)

 

But here you are assuming that the mutation will be one of the needed mutations. It could just be another completely unrelated mutation.

 

then it will be fixed.

 

Whether a mutation gets fixed or not depends both on the extent of its effect, and the population size it occurs in.

 

This negates the idea of lower probability for the later mutations:

 

I never said anything about later mutations. Just that more required mutations means more unlikely for all of them to happen. If you like I can explain that further: in statistics, the probability of multiple unrelated events occurring is the product of their individual probabilities. Since probabilities for random events are always less than 1, more of them decreases the probability of them all happening. For multiple slightly related events, the probability of all of them happening is more complicated than just multiplying, but is still lower the more events there are.

 

they have the same probability of appearing as they always did.

 

Not really. Since the previous mutations can have an effect on what the result of additional mutations would be, the later mutations can have a higher or lower chance of developing than before the previous mutations had happened.

 

But that's what we are talking about, right?

 

What I said will be true for any ability, whether it is beneficial or not.

 

---

 

PS: When I say that I am not defending someone's crap, attacking what I say as if I were is not a good idea.

 

 

It's more difficult to track them down. But leaving out relevant facts is an outright lie. This is the smoking gun that made Behe's "wild guess" a lie.

 

Since when is a guess a lie? And like I said, there's not too much wild about it since it is also other researcher's guess.

 

The reference is: "3. Pos, K.M., Dimroth, P., and Bott, M. 1998. The Escherichia coli citrate carrier CitT: a member of a novel eubacterial transporter family related to the 2-oxoglutarate/malate translocator from spinach chloroplasts. J. Bacteriol. 180:4160-4165."

 

Here's the abstract. Look at what I bolded:

"Under anoxic conditions in the presence of an oxidizable cosubstrate such as glucose or glycerol, Escherichia coli converts citrate to acetate and succinate. Two enzymes are specifically required for the fermentation of the tricarboxylic acid, i.e., a citrate uptake system and citrate lyase. Here we report that the open reading frame (designated citT) located at 13.90 min on the E. coli chromosome between rna and the citrate lyase genes encodes a citrate carrier. E. coli transformed with a plasmid expressing citT was capable of aerobic growth on citrate, which provides convincing evidence for a function of CitT as a citrate carrier. Transport studies with cell suspensions of the transformed strain indicated that CitT catalyzes a homologous exchange of citrate or a heterologous exchange against succinate, fumarate, or tartrate. Since succinate is the end product of citrate fermentation in E. coli, it is likely that CitT functions in vivo as a citrate/succinate antiporter. Analysis of the primary sequence showed that CitT (487 amino acids, 53.1 kDa) is a highly hydrophobic protein with 12 putative transmembrane helices. Sequence comparisons revealed that CitT is related to the 2-oxoglutarate/malate translocator (SODiT1 gene product) from spinach chloroplasts and five bacterial gene products, none of which has yet been functionally characterized. It is suggested that the E. coli CitT protein is a member of a novel family of eubacterial transporters involved in the transport of di- and tricarboxylic acids."

 

They had to put CitT in a plasmid and transfect the E. coli before E. coli could use citrate in an aerobic environment. These E. coli were NOT in the wild and the ability to aerobically metabolize citrate comes from a human constructed plasmid. So there is nothing in this paper to contradict Lenski.

 

Hm, I had missed the part where the original was anaerobic before it was put into a plasmid. In any case, it still counters what you said:

But these guys can't get their citrate from another species; there isn't any. Behe misled everyone by implying that E. coli by themselves could be Cit+. Not true. The ones in the wild need plasmids from other species.

These plasmids were made from E coli, rather than other species. So I still think that Behe taught you something

 

Behe limited his possibilities in order to attack the paper and try and say the paper did not show evolution. Like you said above: "people who leave out facts ... are much more annoying to deal with than those who just outright lie" Behe made it appear that his guess was the only valid guess.

 

I thought he made it appear that his guess was a guess? Why should everyone's guess be the same?