In a new post at UD, Denyse O’Leary quotes an article from The Scientist (which she misattributes to Science):
Populations of Escherichia coli grown in the lab quickly evolve tolerance when exposed to repeated treatments with the antibiotic ampicillin, according to a study published today (June 25) in Nature. Specifically, the bacteria evolved to stay in a dormant “lag” phase for just longer than three-, five-, or eight-hour-long treatment courses, before waking up and growing overnight until the next round of treatment began.
Denyse comments:
They don’t think, but something seems to be doing their thinking for them. Not natural selection acting on random mutation because they evidently choose to avoid it whenever possible. That is, they avoid direct conflict with antibiotics, whether natural or human-directed.
It’s fascinating. A simple non-teleological explanation is staring her in the face, but she manages to look right through it and latch onto a baroque and bizarre teleological explanation instead. Such is the tight grip of the teleological mindset.
Denyse, what is the “something” that is “thinking” these bacteria into antibiotic tolerance, and how does that work, exactly?
An environmentally sensitive genetic regulator. See the classic example of the Lac Operon. http://en.wikipedia.org/wiki/Lac_operon#Regulation
Putting, for example, duplicated and mutating genes under new different regulators is trivial for evolution. It happened in the Lenski experiment, get over it.
Now Phoodoo, what is YOUR explanation? How do the bacteria achieve this capability? Why does it take multiple rounds of selection to generate the result?
phoodoo,
No, what I said is that there is every reason to suppose (pending further actual research) that the switch has a genetic basis. And that there are sound mechanistic reasons for the ‘successful’ lag being at the lower end of the spectrum of possibilities – the ‘attractor’ for preserved genetic change being a resultant of long enough to evade the antibiotics but not so long as shorter lags don’t outcompete you.
Since I’m simply commenting on an article about a recent finding, not doing the research, what the hell else do you expect me to come up with? All answers to all questions you may decide to ask right now?
Every other switch directly investigated traces back to genetics, so why would this one be any different?
Horseshit. The genetic basis of antibiotic resistance is well-investigated. Your alternative hypothesis is to wave that silly non-explanation ‘information’, with no idea how to investigate that, pinpoint its location, or understand how the bacteria can anticipate their next dosage beyond the walls of their container. It’s laughable woo.
But if the Designer really has equipped bacteria to evade all our best efforts to combat disease, I wish he’d fuck off!
PaV @ UD
The teleological mindset is strong with that one. They talk about Darwinian fairy tales, but that takes the biscuit.
ID rejects it? Oh, I thought it was just PaV at this point.
ID says? Oh, I missed that research project.
It’s most likely? Oh, what other possibilities have you considered?
Intelligent intervention of some sort? Oh, any particular “sort” you had in mind?
And most ironic of all? PaV opens that comment with this:
*inserted for context.
Yeah, PaV, you’ve got nothing to be deriding anybody about here. An intelligent intervention of some sort? Snort!
phoodoo,
Let me join the chorus of commenters asking for your explanation of these experimental results. We’d like to compare it to the scientific explanation.
This is your chance to demonstrate the superiority of ID. Don’t blow it.
Seconded.
I too wish he made that up. It’s gibberish. Come on, fess up. Who introduced this nonsense notion of teleonaturalism?
Ah. I do. When a billiard ball hits the band, it isn’t to hit the other ball just right (whatever the intentions of the man with the stick may have been): it’s because the man with the stick hit the ball at such and such angle and speed. Phrasing this in teleological terms just happens because of the inadequacies of natural languages. There’s no need to go introducing philosophical notions in order to deal with the inadequacies of natural language.
Allan Miller,
First off Allan, I only respond to you more than others, because your posts make an effort at better quality than much of the rubbish here. I can’t imagine why anyone would respond to hotshoe.
I didn’t criticize your posts for not having details of the bacteria discovery, I was simply pointing out that from what we know so far, its another case of a very unusual way of life adapting to pressure. It certainly doesn’t look like a simple mutation in some of the random population, that just happens to be beneficial. That doesn’t mean it couldn’t be, but it looks too fast and too precise to be accidental. If it were such an obvious, simple random mutation, I don’t think many biologists would be surprised by it. The fact that they are, that it is newsworthy, again points to an unpredicted result.
Taken as just one bit of evidence it may not be so much, but if we keep adding up the discoveries that get uncovered everyday about life’s rapid adaptive powers, all combined together they show more and more patterns of intended adaptions, of clever life survival plans, of striving to survive, rather than happening to accidental stumble into a lucky niche.
Is evolution slow or fast? In Darwin’s time he assumed it would have to be very slow to make any sense. but we keep seeing instances where it is not slow. Where the results are surprisingly fast. Where the results seem to be predictive or organized in nature.
If one is just constantly saying, well, its not a problem, without looking at the fact that all added together it starts looking like a problem, then it seems that person is not really willing to entertain any alternative ideas. They have decided they don’t like the idea that life is guided, or that life was intended, because it is an interference to what they want to believe in, much like you would be dismayed by a God that would allow bacteria to thrive. Its hurts your sensibilities, so of course its better to not let the evidence pile up in your mind.
Just like you say epigenetics is easy to arise through simple mutations, without really giving that a thorough run through. Its not easy in the slightest.
Obviously its your choice to have a mindset which will simply overlook new ideas everyday, because you prefer the ones you already accept. But I think it is naive to suggest this in not an agenda driven mindset, even if it is completely sub-conscious.
phoodoo,
I appreciate the change in tone. Though I would take exception to the idea that my position is down to a ‘mindset’. There are some hard-won facts in there as well! I have no objection to the possibility of intelligent intervention per se, I just see no evidence for it.
On the other hand, irrespective of any factual basis for such intervention, living organisms do make replication and other errors, and they do prove to be beneficial some of the time, counter-intuitively. Where not beneficial, they tend to be eliminated; where beneficial, they tend to become the ‘new normal’. So unless the Designer is intervening constantly, this process is an inevitable background, and must be responsible for a certain amount of organic change, and adaptation.
It’s true that the general opinion among professionals is that this ‘certain amount’ is 100%. Some people have a somewhat understandable difficulty with the capacity of such change to make wings, hearts or genetic switches, but with these bacteria we are at a much lower level. Trying to deny any explanatory power to evolutionary mechanisms is trying too hard IMO, because these obviously exist, and obviously have the capacity to do work. It’s a bit of a ‘foot in the door’, I guess, if you are strongly resistant to evolution, but my perspective is more informed by what I know than what I hope for.
No, actually, it’s just that there is no evidence for it apart from, well, hope, from people like you.
Simply provide actual evidence that life is guided and you’ll win over the people who live by evidence. They call them scientists round these parts.
And you suppose that’s the reason why people don’t accept the idea that life is guided? Perhaps it’s because you’ve not shown that to be the case? Perhaps?
Then all you can do is put the evidence out there and hope the next generation is more open, no?
Yet all you have to offer as evidence is your incredulity
Yes, in the same what that life “looks” designed. This, to you, looks too fast and too precise so you decide “it must be design”.
Yet you have the gall to say
It’s your mindset that is overlooking new ideas, the idea that something might not be designed. That you jump to design on the basis of nothing at all other then a feeling shows that you are doing exactly what you accuse others of doing. i.e. having a previously set idea and casting anything you see into support of that idea.
Write an OP then where you add up the discoveries. Try to convince (positive evidence) rather then attack.
phoodoo,
What are you basing that on, other than wishful thinking?
I’ve read the Nature letter, and the mutations involved are quite simple. The researchers identified three genes involved with the lag time trait. Each of the five evolved strains had one distinct mutation affecting one of these three genes. The mutations were all simple: four of the five were point mutations, and the fifth was an inversion.
Why would you invoke teleology to explain this when a mechanistic explanation is sufficient?
Only it wasn’t fast, nor precise, and it wasn’t accidental – Well, okay, it is accidental, but not random.
The sweet spot wasn’t hit in one go. It took many generations. Certainly no less than many other instances of adaptation due to molecular evolution witnessed in the lab.
It took the death of a large part of each generation for the first and then the second and then subsequent improvements to become fixed in the population.
Each strain in the experiment had a unique way of adapting to the cycle, caused by mutations unique to that strain. The different strains, of course, all having originally been cloned from the same ancestor.
None of which would be necessary if evolution was somehow intelligently guided.
Gral and keiths, those are very good posts. They show quite well what every colloquy with phoodoo shows–his fallacy of argumentum ad ignorantium. “Evolution by design” so-called has no explanation for anything whatever–other than “intelligence” or “organization” or “design”–catch-all terms that don’t mean anything precise and can’t be tested, Actual evolutionary theory can and has explained many many things in our world. However, any time a scientist cannot explain some feature of the living world–or is even surprised by something he or she discovers–that is seen as some sort of evidence for “evolution by design.”
It is fallacious reasoning through and through. I recommend to anyone who can’t see this the substitution of the word “Dumbledore” for “Design” anywhere it turns up in any “argument” undertaken by an IDer. The result will be just as good as such “argument” was prior to this change. If there is ever to be a sensible discussion about this matter between the parties (something I sincerely doubt), there would have to be both agreed-upon definitions of such terms as “design” and “accidental,” and criteria of experimental success and failure that are acceptable to both sides. Without those, any question that science can’t answer–whether it’s shape of some breed of dog’s snout or the truth or falsity of Goldbach’s Conjecture–will be trotted out as solid evidence for the existence of Dumbledore.
What is the point, exactly? phoodoo, if every person who posts here were to admit with no hesitation, that in its present state, science cannot explain every single thing in the universe (evento such poster’s own satisfaction), would you consider this a complete victory of your viewpoint? An affirmative answer to that signifies the fallacy of your argument.
You think. truly, I believe, that scientists have the responsibility to continue to make discoveries; what you don’t get is that Dumbledore theorists have the equal onus to make discovery number one. Provide just one sensible explanation for….you know…..anything at all. Then a comparison might be made. But this “Yeah but you don’t understand THIS” or “How can you explain THAT” when your side can’t explain anything whatever isn’t quite fair, is it? I repeat: saying “Dumbledore” over and over isn’t a theory and does not explain anything at all.
Which will undoubtedly be responded to by phoodoo with words like “saying ‘evolution‘ over and over doesn’t explain anything at all“. At which point we’re going to have to go back to explaining about what evolutionary theory states in such cases, what we’ve learned about the molecular mechanisms involved, how observations substantiate this or that – and we’ll have come full circle again.
And in fact, phoodooo sez
Ignoring, as predicted, that even the paper in question details precisely what the experimental setup was, what was observed, and what the relevant mutations were.
Gralgrathor,
OK, that’s a good point. But so far as I understand it, contemporary “evolutionary theory” doesn’t just mean “anti-designism.” It at least grew out of natural selection and random variation (where the meanings of those terms are precise and widely understood. Now if changes have or have had to be made since Wallace, that’s life in the empirical world. As you say above, saying “evolutionary theory” actually means something other than “Hah! it’s not design!” So far as I can tell, that’s the main difference here. Saying “design” (or “Dumbledore) amounts to nothing more than “You’re theory can’t explain this!” or “Your theorists are surprised by that!” It’s like the Algonquins in “Black Robe” pontificating about the clock that they believed to be the big boss of the Frenchmen since these latter could be predicted to do things when the clock’s bell rang. Amazing, the Algonquins thought, that such a small man would be put in charge of men with guns.
“Exploring the genetic basis of this adaptation, the researchers identified three genes that seemed to play a functional role in antibiotic tolerance. While the exact mechanism of how mutations in these genes may have lengthened the bacteria’s lag time is not yet known, two of the genes are part of pathways that were previously implicated in bacterial persistence,,,”
Where does that say the mutations are quite simple? Perhaps you should tell the researchers the mechanisms then, since they don’t seem to know.
And we still have yet to answer, where is the clock in a bacteria.
The mutations are quite simple. The actual pathway from gene to lag-cycle is somewhat more involved.
Likely the “clock” in such organisms is based around the buildup of some product or byproduct of cellular chemistry. Once a certain concentration of this or that compound is achieved, the balance tips and the organisms goes into replication mode.
I recommend you go read the wikipedia article on the Lac Operon I linked you earlier. It explains how an environmentally sensitive regulation mechanism can function. Yes, it can even be used to show how you can get a chemically based clock.
Exactly as Gralgathor alludes to above, it has to do with the slow build-up of certain compounds. In the case of the Lac Operon, the concentrations of Lactose and Glucose determines various stages of Lactose metabolism and transport in E Coli. And in that case we know how.
Similar such mechanisms have been elucidated in both bacteria and eukaryotes.
Why do you keep reveling around in your ignorance about this subject, instead of actually picking up a textbook on cell biology and gene regulation? No, we still don’t know how THESE bacteria regulate their dormant state, but what we DO know is that such mechanisms exist and are therefore eminently possible. There’s no need to start positing that invisible agents from Hogwarts are involved.
Rumraket,
It is a very typical evolutionist cop out strategy to say, go read something, and claim that the answers are there. However when pressed to say where in there the answer lies, the evolutionist just say, well, don’t expect me to find it….
In fact if one reads all that is involved in lac operon, the one thing that becomes clear is that believing this whole operation is a result of accidental copying errors, is about as dumb as something gets.
But here, let’s let the readers decide:—————–
phoodoo,
Explanation of diauxie depended on the characterization of additional mutations affecting the lac genes other than those explained by the classical model. Two other genes, cya and crp, subsequently were identified that mapped far from lac, and that, when mutated, result in a decreased level of expression in the presence of IPTG and even in strains of the bacterium lacking the repressor or operator. The discovery of cAMP in E. coli led to the demonstration that mutants defective the cya gene but not the crp gene could be restored to full activity by the addition of cAMP to the medium.
The cya gene encodes adenylate cyclase, which produces cAMP. In a cya mutant, the absence of cAMP makes the expression of the lacZYA genes more than ten times lower than normal. Addition of cAMP corrects the low Lac expression characteristic of cya mutants. The second gene, crp, encodes a protein called catabolite activator protein (CAP) or cAMP receptor protein (CRP).
The dual regulation causes the lactose metabolism enzymes to be made in small quantities in the presence of both glucose and lactose (sometimes called leaky expression) due to lactose (the inducer) inhibiting LacI (the repressor protein) from binding to the operator, but at high cAMP concentrations and in the presence of lactose there are high levels of expression (Phase II in Figure 2). Leaky expression is necessary in order to allow for metabolism of some lactose after the glucose source is expended, but before lac expression is fully activated.
In summary:
When lactose is absent then there is very little Lac enzyme production (the operator has Lac repressor bound to it).
When lactose is present but a preferred carbon source (like glucose) is also present then a small amount of enzyme is produced (Lac repressor is not bound to the operator).
When glucose is absent, CAP-cAMP binds to a specific DNA site upstream of the promoter and makes a direct protein-protein interaction with RNAP that facilitates the binding of RNAP to the promoter.
The delay between growth phases reflects the time needed to produce sufficient quantities of lactose-metabolizing enzymes. First, the CAP regulatory protein has to assemble on the lac promoter, resulting in an increase in the production of lac mRNA. More available copies of the lac mRNA results in the production (see translation) of significantly more copies of LacZ (β-galactosidase, for lactose metabolism) and LacY (lactose permease to transport lactose into the cell). After a delay needed to increase the level of the lactose metabolizing enzymes, the bacteria enter into a new rapid phase of cell growth.
The diagram below summarizes these statements.
lac operon in detail
Two puzzles of catabolite repression relate to how cAMP levels are coupled to the presence of glucose, and secondly, why the cells should even bother. After lactose is cleaved it actually forms glucose and galactose (easily converted to glucose). In metabolic terms, lactose is just as good a carbon and energy source as glucose. The cAMP level is related not to intracellular glucose concentration but to the rate of glucose transport, which influences the activity of adenylate cyclase. (In addition, glucose transport also leads to direct inhibition of the lactose permease.) As to why E. coli works this way, one can only speculate. All enteric bacteria ferment glucose, which suggests they encounter it frequently. It is possible that a small difference in efficiency of transport or metabolism of glucose v. lactose makes it advantageous for cells to regulate the lac operon in this way.[10]
Use in molecular biology
The lac gene and its derivatives are amenable to use as a reporter gene in a number of bacterial-based selection techniques such as two hybrid analysis, in which the successful binding of a transcriptional activator to a specific promoter sequence must be determined.[6] In LB plates containing X-gal, the colour change from white colonies to a shade of blue corresponds to about 20-100 β-galactosidase units, while tetrazolium lactose and MacConkey lactose media have a range of 100-1000 units, being most sensitive in the high and low parts of this range respectively.[6] Since MacConkey lactose and tetrazolium lactose media both rely on the products of lactose breakdown, they require the presence of both lacZ and lacY genes. The many lac fusion techniques which include only the lacZ gene are thus suited to the X-gal plates [6] or ONPG liquid broths
That’s what I’ve been saying!
Jesus did it!
With a little help from Johnny.
I scanned up and didn’t see Phoodoo’s alternate explanation. Please correct me if I missed it.
You didn’t. He’s engaged in evasive manoeuvres.
You might have missed it, after all what’s it going to be other then “it was designed”?
If the evolutionists argument is that accidents did it, an alternative explanation is not required to counter that.
If someone in a wheelchair claimed they climbed Mount Everest by waiting for asteroids to hit them in the back randomly and propel them upwards, a reasonable person doesn’t have to accept the argument of—Well, can you prove that it is impossible. We know there are asteroids, and we know that impacts move things, so there is no reason to say it didn’t happen.
However, if you see a bunch of species and somebody tells you that a guy with a beard who could walk on water and had no human father made them, you should rush to accept it. And this rush should be made in spite of the fact that the so-called accident theory is quite capable of explaining countless things (even though not the Everest ascent–something for which it never actually claimed responsibility), and the bearded guy theory has never been able to explain anything whatever.
Excellent.
It’s EVERYWHERE in there. The entire article explains how the Lac Operon functions, thereby telling you how an environmentally sensitive gene regulator functions in principle.
This is the question I set out to address. You asked a related question, (where one would find a “clock” inside a bacterium?) I pointed you in a direction that actually answers your question. It’s not an actual clock, because an actual clock isn’t needed to achieve the effect you find mysterious. What is sufficient is a regulation mechanism that is sensitive to environmental conditions. So that could be how the bacteria achieve this effect.
Genetically controlled “clocks” based on either variations in concentration, or oscillating chemical reactions are also known and candidate mechanisms have been elucidated through experiment.
So, do you really think we need someone to sit around and “think” for the bacteria? Do you think someone had to design a clock and put it inside them? Why did it then take multiple rounds of selection to achieve the observed effect?
What is your explanation?
How do you derive that conclusion? Lay out the argument with all the appropriate premises you find established in that article and derive the “clear” conclusion you allude to (and include selection this time). By the way, what happened to natural selection?
That’s cute but at least we have a bit more than “accidents did it”. A number of key genes were elucidated to be implicated. How do genes change, phoodoo? An actual experiment was set up, which involved multiple consequtive rounds of selection.
What are they selecting, phoodoo? Designed mutations? Why didn’t the very first generation of bacteria already have these designed systems in place? Does the designer have a lag-period too?
No, you don’t get to just handwave away the fact that an actual experiment was done which hints at a bit more than just simplistic caricatures like “accidents did it”. They might not yet have elucidated in detail how the changes happened, but on the surface of it it looks like textbook evolution: It took time to achieve the effect (implying that mutations had to happen over multiple generations), many bacteria died in the process (implying that many of the mutations were indeed deleterious), and it took multiple rounds of selection (implying that some of them were beneficial). This is a hell of a lot more than just “accidents did it”.
Now, what is YOUR explanation?
Rumraket,
The answer is in Shakespeare’s The Lamentable Tragedy of Titus Andronicus.
Go read a book and you will understand, instead of always being so ignorant.
That’s lucky because “it was designed” is not an explanation.
If you are the alternative to ignorance, I’ll keep on being ignorant thanks.
Talking to ourselves, are we? 😉
Aha, phoodoo’s explanation for descent, etc., can all be found in _Titus Andronicus_. I wonder why he waited so long to divulge that tidbit! It’s like playing Zork!
Rumraket,
I liked phoodoo’s “happy meteorite” comment. It reminded me of Climbing Mount Improbable. A book that would help anybody understand natural selection – unless their mental processes are dedicated to evading understanding.
Uh-oh, I just realized, maybe we have to read it backwards or in an Urdu translation or something. Or maybe we have to be high on some special “designer drug.” (I know HE’LL say we just have to be smart enough to “get it”–but that’s not really so helpful to us lesser beings. You’d think he’d exercise a smidge of benevolence and just, you know, tell us.)
🙁
heh, indeed! What makes it worse is that sometimes we disagree!
Your reply does not contain an answer to any of my questions.
Also, none of the works of Shakespeare contain anything of relevance to evolution vs design, or anything about cell biology.
In contrast, the link I gave you, and actual books on cell biology, do contain the answers you are ignorant about.
Sorry, you lose. 😛
I think that many IDists just want to keep all the “evolutionists” busy so they have less time to spread their “poison”.
A poor plan, but when your position is as unfounded as theirs, what else is there?
Rumraket and OMagain, you guys seem really sure of yourselves, but have you actually ever read Titus Andronicus looking for clues to questions regarding the evolution of bacteria?
And have you read the text both frontwards and backwards, inverting certain letters (like “m” and “w”) where necessary to preserve biological sense?
Hah. I didn’t think so.
Rumraket,
Get an education first then get back to me. Why do you keep reveling in your ignorance? After you have read some then maybe you can come here and ask questions. We are here to help you, but if you refuse to even get an education, how can people explain things to you so you can understand.
Heh, funny.
He means bible.
Submitted for evidence case 9146232568:
There is no theory of ID, just anti-evolutionary flailing.
phoodoo,
Point mutations are simple. One nucleotide replaces another at a particular location.
Inversion mutations are simple. The order of a sequence of nucleotides (24 base pairs, in this case) is reversed.
I ask again: Why would you invoke teleology to explain this when a mechanistic explanation is sufficient?
Oh, I see now – this thread is about your personal pride and being butthurt for being called out on making silly statements based on your ignorance.
Fine, be like that.
Ooh, you’re so cute.
I just want to tickle your cute little sense of humor.
C’mon, please, just one little smile. You’re so cute when you smile.
Intelligent Failing.