First paragraph of Lenski paper contains an error

_{June 25, 2008

Intelligent Design}

Share: Facebook; Twitter; LinkedIn; Flipboard; Print; Email

I started reading Lenski’s full paper myself to see what raw data was provided and I got no farther than the first paragraph beyond the abstract when I encountered a bias error that a chance worshipper would never notice. My emphasis:

At its core, evolution involves a profound tension between
random and deterministic processes. Natural selection
works systematically to adapt populations to their prevailing
environments. However, selection requires heritable variation
generated by random mutation, and even beneficial mutations
may be lost by random drift. Moreover, random and deterministic
processes become intertwined over time such that future
alternatives may be contingent on the prior history of an evolving
population.

The bold portion is patently wrong. Selection operates on any heritable variation whether random or not. That the authors would use the language they did (random variation) and the peer reviewers didn’t notice it is testimony to the chance worshipper bias that pervades evolution
research.

I would refer Lenski et al to a Scripps Institute experiment with E. coli that Bill Dembski blogged here on Uncommon Descent over 3 years ago:

To Stop Evolution: New Way Of Fighting Antibiotic Resistance Demonstrated By Scripps Scientists

The Scripps researchers, in a nutshell, discovered that E. coli, when stressed (such as running out of food as in Lenski’s experiment or in the presence of antibiotics in the Scripps experiment) selectively increases the mutation rate on certain genes. Thus the mutations in this case are not random but rather directed at a certain area in an attempt to solve a certain problem. Lenski should have have been aware of this but even if he weren’t he should have known just by definition alone selection can operate on any heritable change no matter how the change happened.

Chance worshipping causes science to have blind spots like this. Perhaps if they’d read the book:

Science’s Blind Spot: The Unseen Religion of Scientific Naturalism

written by my friend Cornelius G. Hunter they wouldn’t make these kinds of simple, obvious mistakes. But NOOOOOOO… Hunter and Dembski are both knuckle-dragging ID creationists so what would they know about any of this?

I believe the peanut gallery, in their latest fashion in phraseology, would summarize this as:

Lenski FAIL.

But they won’t because they’re living in denial of their own failings.

Comments

Dave, I haven't read through all the replies, but I believe you are wrong here. In order for selection to be the creative element in evolution, it must select from a pool of RANDOM variants. If variants are not random (that is, they arise nonrandomly in response to some cue) then these nonrandom variants are in themselves adaptive, and thus, selection becomes redundant as an adaptor.van_{June 26, 2008
June
06
Jun
26
26
2008
11:59 AM
11
11
59
AM
PDT}

Avonwatches said (#15) --
Someone also made the point (in another thread) that flipping a coin is not random - that is just how we describe the probability. In reality the coin toss determined by the side it was flipped from, strength behind the flick, rotation, etc etc.
But those factors -- the side it was flipped from, etc.. -- are themselves random, and there are other random factors, e.g., wind gusts and unevenness of the landing surface. If there is any bias in the results of the coin toss, the bias would show up in a very large number of tosses -- e.g., the result might be heads 55 percent of the time. The mathematics of probability and statistics is well understood -- for example, see this long list of topics on the subject -- http://en.wikipedia.org/wiki/List_of_probability_topics DaveScot said (#18) --
The most surprising thing is how LONG it took the bugs to find a way to digest citrate in an otherwise stress free environment.
I suspect that one of the reasons why it took so long is that probably many mutations were lost because (1) only one percent of the old populations were transferred to start the next populations and (2) there was an average of only six generations per population. IMO much more of the old populations -- maybe half -- should have been transferred to start the next populations. Bob O'H said (#19) --
Well, where would the genetic variation come from if not through random mutation?
The recombination of genes in sexual reproduction causes genetic variation without changes in the genes themselves (of course, this is just a general statement that does not apply to E. coli). BTW, Dave, my comment always show the message, "Your comment is awaiting moderation." Why, if I may ask? My comments are almost never censored here. Do all other commenters get that message? Does the message mean that my comment is not visible to other readers until the message disappears? Your history warrants screening your comments for foul and/or abusive language. -ds Larry Fafarman_{June 26, 2008
June
06
Jun
26
26
2008
11:26 AM
11
11
26
AM
PDT}

ecoli there’s no way to prove that [intelligent design] scientifically anyway I don't share your limited vision of what science can and cannot demonstrate. It appears I have more faith in science than you do. I tell you what. Describe an observation which, in principle, could NOT be understood by chance & necessity. Keep in mind a theory that explains everything explains nothing. In other words, it's not a theory unless it can, in principle, be falsified (Karl Popper - Philosopy of Science 101). To be fair, I'll offer you a falsifiable ID hypothesis. "Symbolic coding systems can be found in nature in two places. Incorporated in things invented by humans (example: morse code) and incorporated into all living cells (the genetic code). In all cases where the origin of symbolic coding systems can be determined with surety it was via intelligent agency. It is hypothesized that no unintelligent mechanism can produce a symbolic code because symbols are abstract and only an intelligence can create abstractions." This can be falsified by a single observation of an unintelligent process creating a symbolic code. DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
11:22 AM
11
11
22
AM
PDT}

DaveScot - I apologise and stand corrected on the point of the gene specific directed mutation. I didn't read subsequent papers, because the original news stories on the 'Scripps study' only referenced the one. However, this still does not point to the teleological: that E. coli are somehow deciding which gene locus to induce mutations. It is altogether possible that random mutation(s) produced a protein that, when under stress from a particular antibiotic, caused an increase in mutation rate in a gene specific region. Such random mutations would be selected for if the environmental pressures are present. The point being, if the source of proteins that can direct mutations are themselves produced by random mutations, then they can be understood by evolutionary theory. You're assumption that E. coli are purposefully directing this mutation has NOT been demonstrated by any of the studies you have brought up so far. Nor can I imagine how one could prove that E. coli are self-directing mutations... where did this unique inhibitory proteins come from? If the answer is intelligent design, then there's no way to prove that scientifically anyway, and I think you'll have a hard time proving that the ultimate source was not evolution. At any rate, it is of little consequence that Lenski was arguing against the notion of directed mutations 15 years ago. Our knowledge of science is expanding exponentially, but not every new discovery requires us to draft a completely new model to study it. I'm sure given new research, Lenski would revise his opinion of (it appears) proximate directed mutation.ecoli_{June 26, 2008
June
06
Jun
26
26
2008
11:16 AM
11
11
16
AM
PDT}

For example, directed mutation would shatter the belief that organisms are related to some ancestor if they share traits. Instead, they may simply share exposure to the same environmental cues. Cool. It certainly doesn't shatter my front-loaded ID hypothesis which requires trigger events for saltations into new (pre-planned) species. Nothing in evolution makes sense except in light of front loading.DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
11:12 AM
11
11
12
AM
PDT}

Directed vs. random mutation. There's no controversy in evolution. Move along people, nothing to see here. ROFLMAO!DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
11:04 AM
11
11
04
AM
PDT}

Oh my. I stumbled onto a huge controversy from decades past. Google Lenski and "directed mutation". It seems Lenski, 15 years ago, was arguing that directed mutation didn't exist. It's pretty much accepted now. Evidently he still can't bring himself to admit it and that's why he wrote that selection requires *random* mutations. It wasn't an innocent slip of tongue! This is why it was such a hot controversy:
Directed Mutation Dear reader, things have a way of working out serially. For several months, we have had in our possession a paper from Nature, by J. Cairns, of Harvard, plus some passionate correspondence stimulated by the paper. Now that the circle-forming sheep have provided a good introduction, we will jump into the fray, too. Basically Cairns (in Nature) and B. H. Hall (in Genetics) say that organisms can respond to environmental stresses by reorganizing their genes in a purposeful way. Such "directed mutation" shifts the course of evolution in a nonrandom way. Such a conclusion was like waving a red flag in front of the evolutionists. R. May, at the University of Oxford, complained, "The work is so flawed, I am reluctant to comment." On the other side, a University of Maryland geneticust, S. Benson, comments, "Many people have had such observations, but they have problems getting them published." Our template in this discussion is an article by A.S. Moffat in American Scientist. She says, "The stakes in this dispute are high, indeed. If directed mutations are real, the explanations of evolutionary biology that depend on random events must be thrown out. This would have broad implications. For example, directed mutation would shatter the belief that organisms are related to some ancestor if they share traits. Instead, they may simply share exposure to the same environmental cues. Also, different organisms may have different mutation rates based on their ability to respond to the environment. And the discipline of molecular taxonomy, where an organism's position on the evolutionary tree is fixed by comparing its genome to those of others, would need extreme revision." What sort of experiment did Cairns do to cause such a ruckus? In particular, he studied E. Coli bacteria. Normally, these bacteria cannot metabolize the sugar lactose. Cairns exposed the E. Coli to a sudden dose of lactose, demonstrating that if the bacteria must have lactose to survive, they quickly cast off the two genes that inhibit their metabolizing of lactose. Of course, the experiments were more complicated than this, but the fundamental finding was that the bacteria mutated so that they could use lactose much, much faster than chance mutation would permit, stastically speaking. The battle lines are forming. A sup-porter of directed mutation, J. Shapiro, of the University of Chicago, is quoted as follows in Moffat's article: "The genome is smart. It can respond to selective conditions. The signifi cance of the Cairns paper is not in the presentation of new data but in the framing of the questions and in changing the psychology of the situation. He has taken the question 'Are mutations directed?' which was taboo, and made it an issue that people will now do experiments on." (Moffat, Anne Simon; "A Challenge to Evolutionary Biology," American Scientist, 77:224, 1989.)
It seems I've reopened a big can of worms that I wasn't aware even existed. Fascinating.DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
11:00 AM
11
11
00
AM
PDT}

and more Mechanisms of directed mutation.Foster PL, Cairns J. Department of Environmental Health, Boston University School of Public Health, Boston University School of Medicine, Massachusetts 02118. Spontaneous mutants arise among nondividing populations of Escherichia coli in apparent response to selective conditions. In this report we investigate several hypotheses to account for the role of selection in the production of these "directed" or "adaptive" mutations. We found that the Lac+ phenotypes of some mutants that arise late after lactose selection are due to suppressor mutations that are unlinked to the mutant lacZ allele; thus the production of these Lac+ mutants does not require an information flow from successful proteins back to the DNA that encodes them. Transcriptional induction of the lac operon, even in the presence of another, utilizable carbon source, did not stimulate the occurrence of Lac+ mutants in the absence of lactose, indicating that the role of the selective agent is not merely to induce transcription. The absence of two DNA repair pathways-methyl-directed mismatch repair and alkylation repair-also did not result in an accumulation of Lac+ mutants in the absence of lactose, suggesting that these repair pathways are not normally responsible for correcting transient variants that might arise in the absence of selection. However, in one case the Lac+ mutation is likely to be due to a miscoding lesion occurring on the nontranscribed DNA strand, indicating that, at least in this instance, DNA replication is required before directed mutations can arise.DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
10:49 AM
10
10
49
AM
PDT}

imsds [even better] (everything below quoted, don't want to waste time formatting) Starvation-associated mutation in Escherichia coli: a spontaneous lesion hypothesis for "directed" mutation.Bridges BA. MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK. When stationary phase E. coli WU3610, carrying an ochre mutation in the tyrA gene, were incubated on plates lacking tyrosine, tyrosine-independent (Tyr+) mutants appeared from day 7 onwards in a time-dependent manner. These starvation-associated mutants did not contain either identifiable tRNA suppressors or reversions at the ochre site and are thus quite distinct from the mutants commonly found to arise during active growth. When an appropriate fluctuation assay protocol was employed slow growing Tyr+ mutants were also found to arise in growing cells, and their distribution was more characteristic of a replication-dependent than a time-dependent process. The rate of appearance of starvation-associated mutants at 37 degrees C was somewhat less than at 27 degrees C and this was attributed to a reduction in viability at the higher temperature. There was no evidence for the accumulation on the plates of mutations in other genes. Tyr+ mutants were, however, shown to arise during incubation of stationary phase cells under conditions where there was no selection for tyrosine independence, provided outgrowth was subsequently permitted on plates lacking tyrosine. This distinguishes the present system from those systems exhibiting genuine "directed" or "adaptive" mutation, should they exist. To explain the specificity which occurs, it is proposed that the appearance of stationary mutants in ochre strains reflects the time-dependent accumulation in the transcribed strand of a DNA lesion that has a high probability of miscoding during transcription and replication. A mutant RNA transcript permits protein synthesis which in turn triggers DNA replication. The mutation is then fixed in the DNA as a permanent heritable change. The apparent "directedness" of the process is, on this model, determined solely by the particular miscoding DNA lesion occurring in a transcribed strand at a site where a change in phenotype permits DNA replication to occur.DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
10:47 AM
10
10
47
AM
PDT}

imsds I'll concede the point that Pol III and rDNA exclusion was my mistake in the SOS response but you're all still wrong that hypermutation in respones to stress is genome-wide. Hypermutation in bacteria and other cellular systems. B A Bridges MRC Cell Mutation Unit, University of Sussex, Brighton, UK. b.a.bridges@sussex.ac.uk
In bacteria there are numerous examples of transient mutator states, often occurring as a consequence of stress. They may be targeted to certain regions of the DNA, for example by transcription or by recombination.
DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
10:40 AM
10
10
40
AM
PDT}

Dave Scot ecoli is right and you are wrong. Obviously you are confusing DNA polymerase with RNA polymerase. DNA(!) Pol II, Pol IV, and Pol V are polymerases used by bacteria to replicate a damaged region of DNA and hence survive under adverse conditions. DNA polymerase III is part of the primary enzyme complex involved in bacterial DNA replication. "Pol III deals with rDNA..." Not really. That would be right for eucaryotic RNA (!) polymerase III which is required to synthesizes tRNAs, rRNA 5S and other small RNAs in eucaryotes.imsd007_{June 26, 2008
June
06
Jun
26
26
2008
09:55 AM
9
09
55
AM
PDT}

Bob No, the mutations are not randomly increased over the entire genome. They're targeted at where they are more likely to solve the problem versus making a bigger problem. See the comment to ecoli above. Is is even possible for you to admit when you're wrong? DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
04:32 AM
4
04
32
AM
PDT}

ecoli Sorry, but the mistake is yours not mine. http://lib.bioinfo.pl/pmid:9192894/pmid/cit We have recently shown that the evolution of resistance to ciprofloxacin in vivo and in vitro requires the induction of a mutation that is mediated by the cleavage of the SOS repressor LexA and the associated derepression of three specialized DNA polymerases (polymerase II [Pol II], Pol IV, and Pol V). These are specialized polymerases. The mutation rate of the entire genome doesn't increase, just the subsets of it that these particular polymerases work with. Nice try though. I suppose I can forgive you because the original Scripps paper made no mention of specificity in the mutation rate increase. I merely assumed by the mechanism they identified that it wasn't going to be a genome-wide mutation increase. That would be rather stupid of the designer to do it that way. For instance, it wouldn't be a good idea to start mutating the crap out of rDNA in response to stress. Some bits of DNA are far less tolerant of mutations than other bits. See, this is another example of science's blind spot. From a design theoretic view I wouldn't expect a designer to start mutating DNA that had no relation to the problem of toxins in the environment. Ribosomal DNA would be one example. Mutating that will almost certainly kill the organism and not solve the problem with the toxin. So we want to somehow protect that DNA from the increased mutation rate. As it turns out the assumption was correct and that was quickly discovered by Scripps about a year later. Pol III deals with rDNA and you'll note from the referenced article Pol III is not in the list of specialized polymerases found to part of the LexA cascade. Take off the blinders, man. Life was designed. It's a fruitful heuristic as I just demonstrated. DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
04:12 AM
4
04
12
AM
PDT}

Random mutations have no aim.
Yes, that's my point.
In the case of E.coli’s response to antibiotics the increased mutation rate is indeed aimed at something
Note what you wrote. it's the rate of mutation that is increased. But the actual mutations are still random: the only difference is that there are more of them.
But this is still tangential to the point of my article which was to say that Lenski was flat out wrong to say that selection requires random mutations.
Well, where would the genetic variation come from if not through random mutation?Bob O'H_{June 26, 2008
June
06
Jun
26
26
2008
03:53 AM
3
03
53
AM
PDT}

Bob my argument works no matter what I’m aiming at Your argument doesn't work if you're aiming, period. Random mutations have no aim. In the case of E.coli's response to antibiotics the increased mutation rate is indeed aimed at something - finding a way to stop the antibiotic from killing it. It's not a well targeted search but it is still targeted. If the increase in mutation rate occured randomly (for no particular reason) then your argument would work, but the increase in mutation rate is a response to a stimulus and that makes it not random. Let's try a different example. Suppose some stalking clown throws, monkey-like, a handful of his own poop aimed directly at your pointy little head, Bob. You might respond by dodging to the left, dodging to the right, ducking down, or any combination thereof. The particular direction you move to avoid becoming a poopyhead might be random but the act of dodging itself is not random (unless you're some kind of spastic that bobs and jinks around at random with no particular purpose). But this is still tangential to the point of my article which was to say that Lenski was flat out wrong to say that selection requires random mutations. I notice you haven't disagreed with that. Good boy. You're smarter than most of the peanut gallery which is why you continue to have a presence here. I note the peanut gallery is trying to say I'm pretending that this criticism of Lenski derails his whole paper. I made no such claim whatsoever. I merely pointed out that I didn't get farther than the first paragraph before encountering an obvious error. I seriously doubt that this single brain fart of Lenski's does much damage in an of itself to his methods or conclusions, it's merely an early indicator of the kind of sloppy, biased thinking that went into it. Or maybe not. Maybe it's an isolated error. Probably not, given the criticisms I've read and the basic sensationalist spin put on something that most bacteria are really good at - finding ways to eat things they normally don't eat. This is hardly a surprising result. The most surprising thing is how LONG it took the bugs to find a way to digest citrate in an otherwise stress free environment. They only had one single challenge in their little lives and that was how to avoid starving after eating the low hanging fruit in the agar. On the matter of no one rushing in to independently duplicate or validate Lenski's experiment I'll concede that not much time has passed but I'll still stand by the prediction that no one will bother no matter how much time passes. It's just not important and not surprising. There's nothing new or exciting about it. It's like announcing that after 20 years of observation he found dirt and water make mud. The Cold Fusion annoucement I contrasted this with had teams all over the world on it like flies on garbage the day after it was announced. THAT claim WAS important and surprising if valid. DaveScot_{June 26, 2008
June
06
Jun
26
26
2008
03:13 AM
3
03
13
AM
PDT}

Dave - my argument works no matter what I'm aiming at - I was just using hitting you as an example of something that might happen. The point is that the rate of mutation changes (so isn't random), but what mutations actually occur, and where they occur in the region with the higher mutation rate, is random. BTW Dave, I was actually aiming at the clowns that keep on stalking you.Bob O'H_{June 25, 2008
June
06
Jun
25
25
2008
11:12 PM
11
11
12
PM
PDT}

Ooooh. I also had a thought: At what point in our supposed 'ancestors' history did they (and all other animal species) develop a genetics system that actively INHIBITS random mutation? Because that makes it a whole lot harder to 'evolve new species'. Is DNA/RNA transcription protection prevalent in bacteria/protzoa (similar to our DNA protection/correction mechanisms)? Sorry, I have no clue.Avonwatches_{June 25, 2008
June
06
Jun
25
25
2008
10:46 PM
10
10
46
PM
PDT}

@10: Someone also made the point (in another thread) that flipping a coin is not random - that is just how we describe the probability. In reality the coin toss determined by the side it was flipped from, strength behind the flick, rotation, etc etc. Extrapolating, what ARE the actual mechanisms behind neo-darwinist evolution? They say 'chance/random mutations', but what are the supposed processes BEHIND the 'chance'? Knowing that, we can work out what neo-Darwinism is capable of theoretically (I'm aware this is discussed heavily in EdgeoEvo, and elsewhere). Just from basic genetics, I can think of: -point mutations -deletions -insertions ...what are the other Darwinistic processes that drive "chance/random mutation"?Avonwatches_{June 25, 2008
June
06
Jun
25
25
2008
10:37 PM
10
10
37
PM
PDT}

Excellent observations, DaveScot. Chance worshipers is also funny. Chance is their God of the gaps. Have you guys seen the Lenski dialog at conservapedia?William Wallace_{June 25, 2008
June
06
Jun
25
25
2008
10:20 PM
10
10
20
PM
PDT}

Good find Davy, I concur. Random mutation is a patently false umbrella to lump all mutations under. One of the main conceptual difficulties with using the word "random" to refer to beneficial mutations is the fact that under the Darwinian version of evolutionary theory, human beings are merely “evolved creatures” of and by natural selection and random mutation universally. The obvious problem here is that human beings do things "purposively" and hence are a contradictory example of Darwinian evolution “universally” acting in a "random" fashion on all life forms and things. The point is we can easily see, if from self phenomenological reflection alone, that oftentimes evolution is NOT heuristically random at all and hence the universal umbrella of random mutation thus becomes a question of "when is evolution acting purposively and when is it acting randomly?" Of course if we cannot explain a given event or structure via the virtue of a purely stochastic algorithm, then the word "random" as a descriptive designation for mutations must disappear from the gamut of possible explanatory tools. It just so happens that this is quite often the case. Human beings are not random- natural selection is not random- the mutations, as easily exemplified by the high ratio of negative to positive advantages passed onto living creature are not “random” either. Ergo, neither is the core driving force/s behind evolution. Here's a not so random word of advice for all you Darwinists out there It’s about time you got another theory. I say, “The only thing random about life’s design is, perhaps, the theory of evolution itself.”Frost122585_{June 25, 2008
June
06
Jun
25
25
2008
08:19 PM
8
08
19
PM
PDT}

todd said (#8) --
Looking at the first paragraph you quoted, Lenski writes “Natural selection works systematically to adapt populations to their prevailing environments.” I don’t want to be picky, but isn’t ’selection’ something only performed by intelligent agency?
I think that you are being too "picky." The term "natural selection" uses the word "selection" in a figurative sense. Also, I think that the statement “Natural selection works systematically to adapt populations to their prevailing environments” is wrong. Natural selection often does not "adapt populations to their prevailing environments" but often causes extinctions or decimations of populations because of those populations' failure to adapt to their environments. Anyway, I am bothered much less by inaccurate statements in the paper than I am by principal author Zachary Blount's failure to give straight answers to simple, basic questions about the research.Larry Fafarman_{June 25, 2008
June
06
Jun
25
25
2008
06:48 PM
6
06
48
PM
PDT}

I am sorry to tell you, DaveScot, that the error is yours. You misrepresented the work done in the Scripps Institute's research. They did not find that E. coli was able to cause the mutation of a specific gene or even gene locus. What they found, was that E. coli can, when experiencing periods of stress, influence DNA repair machinery to increase the general mutation rate. The mutations are still random, but by allowing the rate (key word) of mutations to remain high, bacterial populations have more diversity so that, when in the presence of antibiotics (or other stresses) some of the individuals that happen to have evolved resistance can be selected for. It is a common mistake to associate evolution with the teleological. E. coli don't choose to evolve any more than the earth chooses to revolve around the sun. The simple fact is that a behavior is beneficial to reproduction (and spreading of genes) than it can be selected for. If you have further comments or questions about your mistake (which I hope you will correct in the interest of academic integrity) please visit my blog and post a comment (I have recently made a post about this very entry) http://blogs.scienceforums.net/ecoliecoli_{June 25, 2008
June
06
Jun
25
25
2008
05:20 PM
5
05
20
PM
PDT}

I don't understand the controversy. Is there something special about this mutation that contradicts Behe's hypothesis regarding mutations rates and the need for multiple simultaneous mutations to reach novel beneficial functions? It certainly doesn't appear so.Jehu_{June 25, 2008
June
06
Jun
25
25
2008
03:45 PM
3
03
45
PM
PDT}

DaveScot said in the original post,
The Scripps researchers, in a nutshell, discovered that E. coli, when stressed (such as running out of food as in Lenski’s experiment or in the presence of antibiotics in the Scripps experiment) selectively increases the mutation rate on certain genes. (emphasis added)
How does running out of food increase the mutation rate on certain genes? I think that running out of food has the opposite effect. Errors in gene duplication during reproduction are a major source of mutations, and running out of food prevents reproduction. It appears to me that the glucose cycling (giving the bacteria insufficient glucose so that there are alternating periods of glucose feeding and glucose starvation) favored the evolution of citrate-eating bacteria in Lenski's experiment in the following ways: (1) The glucose feeding period allows "silent" (unexpressed) mutations during reproduction in the bacteria that can eat only glucose, and (2) The glucose starvation period gives an advantage to Cit+ (citrate-eating) bacteria because they can continue to reproduce while the glucose-eating-only bacteria cannot. On Carl Zimmer's "The Loom" blog, I asked Zachary Blount, the lead co-author of the paper, if a purpose of the glucose cycling was to favor Cit+ evolution, and he refused to answer. IMO when an author of a paper refuses to give straight answers to simple, basic questions about it, the paper has no credibility.Larry Fafarman_{June 25, 2008
June
06
Jun
25
25
2008
02:54 PM
2
02
54
PM
PDT}

Dave, This post hits right at the center of the problem with most Science® and Reason™ zealots - this isn't 'A' blind spot, it is 'THE' blind spot. The chance crowd is generally unaware of nor can elucidate the epistemological underpinnings of the arguments they make. It never ceases to amaze when chest thumpers bray about their devotion to the Truth© through Reason™ and Science® while displaying such fundamental ignorance of basic logic. That the question "What is Science?" cannot be answered scientifically is the first clue Science® is not an ultimate in understanding our experience in space & time. Ever try to get a Science® zealot to see their own philosophy? Looking at the first paragraph you quoted, Lenski writes "Natural selection works systematically to adapt populations to their prevailing environments." I don't want to be picky, but isn't 'selection' something only performed by intelligent agency? Did the Colorado river 'select' its path which led the formation of the Grand Canyon? Even laying that aside, isn't systematic work a product of teleology? The wording also seems backward - is it more correct to say populations adapt to environments?todd_{June 25, 2008
June
06
Jun
25
25
2008
02:36 PM
2
02
36
PM
PDT}

Congregate Bob mentioned me by name and associated me with Texas. That is foreknowledge. That's beside the point in any case as I explained in the article. Even if Lenski wasn't aware of the Scripps research he should know that selection can operate on mutations whether they are random or directed. Do you disagree with that? DaveScot_{June 25, 2008
June
06
Jun
25
25
2008
12:29 PM
12
12
29
PM
PDT}

Dave- Maybe that kindergarten teacher could help you with reading comprehension. Bob O'H said he was throwing paper airplanes at Texas, not that he was trying to hit you. Compare Bob O'H's original:
Now, if I started throwing paper aeroplanes at Texas, in Might hit Dave.
with your inadvertent misrepresentation:
The mere fact that you’re throwing paper airplanes at Texas instead of New Jersey when it’s me you want to hit makes it something less than random throws.
congregate_{June 25, 2008
June
06
Jun
25
25
2008
12:05 PM
12
12
05
PM
PDT}

Bob The mere fact that you're throwing paper airplanes at Texas instead of New Jersey when it's me you want to hit makes it something less than random throws. You are using foreknowledge of how to better your odds of hitting me. Is there something about that you don't understand? If so I'll see if I can find a kindergarten teacher to explain it to you as I have too little patience at explaining to adults what should be obvious even to a young child. DaveScot_{June 25, 2008
June
06
Jun
25
25
2008
11:52 AM
11
11
52
AM
PDT}

Or like Moran and McNeill and all the other chance worshippers know very well that mutations of an ultimately random nature are all their dogmatic view of organic evolution allows them to consider. They're lying through their teeth when they say that random mutations are not the ultimate source of all variation and casual mistakes like Lenski made that I spotted betray their belief system to attentive readers not indoctrinated in their pseudo-religious evolutionary narrative.DaveScot_{June 25, 2008
June
06
Jun
25
25
2008
11:49 AM
11
11
49
AM
PDT}

Hmm. Now, if I started throwing paper aeroplanes at Texas, in Might hit Dave. I'm sure I we would all agree that that would be random. Now, if I doubled the rate at which I threw paper aeroplanes, would hitting Dave now be non-random? The bacterium is doing the same thing: it increases the rate of mutation. It's only non-random for a narrow definition of random that would exclude everything except rolled dice, tossed coins and possibly radioactive decay.Bob O'H_{June 25, 2008
June
06
Jun
25
25
2008
11:44 AM
11
11
44
AM
PDT}

Prev 1 2 3 Next

You must be logged in to post a comment.

Leave a Reply