ARCHIVE - The Science Behind Intelligent Design Theory-by Casey Luskin

[Valmoon]

To rebut Behe's claim it is only neccessary to show that the structures Behe alludes to could have arisen naturally. Not the easiest task. Looking at something as is and going back and trying to explain exactly how such a system arose is a daunting task. Much easier to take the Behe approach and claim divine interference.

There is nothing new to this approach. Behe simply applied an old approach to new subject matter. To people who have knowledge of the various god of the gap arguements that stand discredited Behe's claims probably seem slightly boring and his demands a little tedious.

But I am not the person to argue these fine technical points. (sorry Becky) The best I can do is point to people who have a greater knowledge in this area who have stepped up to the plate to counter Behe's claim. I couldnt even explain in technical terms how the image on my tv got there let alone explaining how blood clotting evolved naturally to where it currently is today.

I enjoyed reading this responce to Behe's Blood clotting claims.
http://www.talkorigins.org/origins/postmonth/feb97.html

Val

 

[Prisca]

Valmoon

Valmoon

You said, “To rebut Behe's claim it is only neccessary to show that the structures Behe alludes to could have arisen naturally.”

That is absolutely true. If we could demonstrate that these complex structures can arise naturally, step by step, then the idea of irreducible complexity would be severely damaged, if not destroyed. I’d like to say also, that ID theorists never say that naturalistic origins should not be researched, just that so far, no viable theory as to how this could have happened has been discovered. In the meantime, the public is force fed the theory of naturalistic evolution as though it were based on scientific fact.

You said, “Looking at something as is and going back and trying to explain exactly how such a system arose is a daunting task.

Yes it is, especially when the further we look, the more complex things appear. However, the technology is being developed and experiments continue in an attempt to examine the very building blocks of life, (the following links are non-ID sites):
http://www.lbl.gov/LBL-Programs/pbd/xl_research/molecMachines.html#movie
http://www.abc.net.au/science/news/stories/s55200.htm

You said, “Much easier to take the Behe approach and claim divine interference.”

Quite the contrary. It is very difficult for a scientist and researcher to make these claims when you consider the evolutionary bias in the scientific community today. I commend the bravery of the likes of Behe and other’s who, in the face of such a hostile environment, stick to their convictions and continue to challenge unproven evolutionary theories.

Thanks,
Becky

 

[Lion]

You've been watching too much TV.

You've been watching too much TV.

Valmoon
You said:

I couldnt even explain in technical terms how the image on my tv got there let alone explaining how blood clotting evolved naturally to where it currently is today.

I can tell you one thing, (using ID Theory), the image on your TV didn’t get there by evolving naturally.

 

[The Barbarian]

Evolution of irreducible complexity? Here ya go...

"For example, in the common bacteria E coli, there are three genes in the B-gal system : a permease (lacY), which allows B-galactosides into the cell; a B-galactosidase (lacZ), which digests the B-galactosides into usable sugars (galactose and glucose, through allo-lactose); and an enhancer (lacI), which increases production of the other two lac proteins about 500 to 1000x in the presense of B-galactosides. This is an 'irreproducbly complex' system - remove any one of the proteins (lacY, lacZ, or lacI), and the cell can't use B-galactosides as a carbon source.

Back in 1982, Barry Hall removed the lacZ gene from a strain of E coli, then plated them to see how long it would take the bacteria to re-develop lacZ function. It took less than 3 weeks.

The bacteria had another protein (completely unrelated to lacZ) that could catalyze the needed reaction, but at about one thousandth the needed levels (even if 100% of the protein in the bacteria were this, it wouldn't be enough). A mutation increased its ability to catalyze the reaction to usable levels. A second, later mutation altered the protein again, so that the end product could activate the lac system again - IT WAS NOW REGULATED (only active in the presence of substrate); the old lacI and lacY proteins were now part of a new system (which is now, again, irreproducibly complex)."

"Evolution on a Petri Dish : The evolved B-galactosidase system as a model for studying acquisitive evolution in the lab", Barry G Hall, Evolutionary Biology (1982) #15, pg 85-150.

Christians shouldn't be dismayed by this sort of thing. It merely shows that God is much greater and more intelligent than ID gives Him credit for.

Incidentally, I took one of Behe's "irreducibly complex" mousetraps and removed the bait tray. I put a bit of suet directly on the trigger. It caught a mouse.

"If I can't figure it out, then Godmustadunnit" is a loser of an argument. There's always someone out there a little smarter, who might know better.

 

[Prisca]

Thanks Barbarian. I am seriously going to consider the information you posted and go do some researching. I am not a microbiologist, so it may take me some time. What you have said appears to be a valid challenge to the theory of irreducible complexity and I am always in search of the truth. I'll report back as soon as I have a better grasp of the experiment you described.

Sincerely,
Becky

 

[Nathon Detroit]

Barbarion you said...

Incidentally, I took one of Behe's "irreducibly complex" mousetraps and removed the bait tray. I put a bit of suet directly on the trigger. It caught a mouse.

That's weird! The mouse traps I have.... (the traditional wood type) have a trigger mechanism that also functions as the bait holder - which is why it springs closed when the mouse eats the bait. If I removed my bait holder on my mousetrap there would be nothing to keep the spring holder in place. Just my two cents.

Maybe we have different types of mousetraps???

I am encouraged that you are not against killing mice!

 

[Prisca]

Barbarion

Barbarion

Just a couple of comments before I start researching:

You said, "Incidentally, I took one of Behe's "irreducibly complex" mousetraps and removed the bait tray. I put a bit of suet directly on the trigger. It caught a mouse.'

Even if your trap could successfully function without a bait tray, you are ignoring an important point. The irreducible complexity of a thing does not necessarily pertain to every part of a structure. It only pertains to those parts that are crucial to the successful operation of that system. The bait tray you described would have only been added for convenience, not fuction.

"If I can't figure it out, then Godmustadunnit" is a loser of an argument. There's always someone out there a little smarter, who might know better.”

But what if God did really did do it and we as humans continue to deny His wonderful workmanship? How foolish man is when he attributes the work of God to the mere actions of natural processes and chance.

 

[Prisca]

What I've found so far...

What I've found so far...

Barbarion, here is a summary of what I have found so far. Does this sound like an accurate understanding of the Barry Hall experiment?

Step 1. The gene for beta-galactosidase was deleted from E. coli.
Step 2. An artificial lactose permease inducer - IPTG - was added to get lactose to into the cells.

Result:
A gene that already metabolized lactose mutated at a single base pair to function like the deleted gene. This gene metabolized lactose at 10% the rate of the deleted gene. A regulatory gene mutated at a single base pair to turn on the new beta-galactosidase gene in the presence of lactose. These double mutants could now synthesize some allolactose (a natural lactose permease inducer) so they no longer required IPTG.

I’m still trying to learn so give me time. Please correct any part of the above if necessary.

 

[Prisca]

I'm still researching Barry Hall's experiment, but in the mean time, I found the following description and quote on a microbiology website (sorry, the quote was not referenced):

E. coli has cryptic gene, ebgA, that can hydrolyze lactose if lacZ has been deleted. Activation of ebg requires two mutations, one in repressor (ebgR) and one in coding region of ebgA. Neither mutation by itself will allow a lacZ mutant to use lactose. Each mutation occurs at frequency of less than 10-8. But yet will see Lac+ colonies of lacZ strain that has been grown to stationary phase on medium containing lactose (these colonies arise through mutations in both ebgR and ebgA).

Now known that the mutation in ebgR arises first that allows the cells to grow very slowly on lactulose. The second mutation (in the ebgA gene) then arises and allows the double mutants to grow very rapidly.

"It is difficult to imagine how bacteria are able to solve complex problems like these - and do so without, at the same time, accumulating a large number of neutral and deleterious mutations - unless they have access to some reversible process of trial and error."
http://www.science.siu.edu/microbiology/micr460/460 Pages/460.SPAM.html

The following is just a little more backup info:

The Lac Operon

The "operon" model of gene regulation was first proposed by Monod and Jacob in the 1960's and there are two general types: inducible and repressible. Figure 1 shows the basic configuration (omitting the cAMP/CAP complex) of the inducible operon for the sugar lactose

The repressor molecules are continuously being produced and in the absense of lactose derived substrate molecules are able to bind to the "operator" site of the operon. 

This prevents the RNA polymerase that recognises and binds to the "promotor" site from moving along and transcribing the structural genes (the "OFF" state).

When the substrate molecules are present (figure 2) they bind with the repressor molecules and by changing their shape prevent them from occupying the "operator" site. 

RNA polymerase is now able to move along from the "promotor" site and transcribe the structural genes. Subsequent translation produces the enzymes necessary to break down the lactose into glucose and galactose (the gal operon eventually converts the galactose into glucose). The "ON" state.

Repressible operons that are normally "ON", such as those specifying particular amino acids, can be switched "OFF" by a homeostatic feedback loop. If, for example, a bacterium is supplied with a particular amino acid then the amino acid itself (or "end-product") binds to the associated co-repressor molecules and by changing their shape enable them to occupy the "operator" site on the gene. Transcription of the gene is thus inhibited until concentrations of the amino acid fall back to more optimum levels.
http://www.btinternet.com/~johnlatter22/bac.html
Hope I didn't put you all to

 

[Prisca]

Barbarion,

Barbarion,

You said, “Back in 1982, Barry Hall removed the lacZ gene from a strain of E coli, then plated them to see how long it would take the bacteria to re-develop lacZ function. It took less than 3 weeks.”

What you didn’t say was that, “All of the other functions for lactose metabolism, including lactose permease and the pathways for metabolism of glucose and galactose, the products of lactose hydrolysis, remain intact, thus re-acquisition of lactose utilization requires only the evolution of a new B-galactosidase function.”(Hall 1999) In other words, a complete multi-part system was not wiped out in this case, as you implied. As Behe put it, “only one component of a multipart system was deleted.”

You said, “The bacteria had another protein (completely unrelated to lacZ) that could catalyze the needed reaction, but at about one thousandth the needed levels (even if 100% of the protein in the bacteria were this, it wouldn't be enough). [Hall called this protein evolved B-galactosidase or "ebg"] A mutation increased its ability to catalyze the reaction to usable levels. A second, later mutation altered the protein again, so that the end product could activate the lac system again - IT WAS NOW REGULATED (only active in the presence of substrate); the old lacI and lacY proteins were now part of a new system (which is now, again, irreproducibly complex)."

However, “the ebg proteins--both the repressor and B-galactosidase--are homologous to the E. coli lac proteins and overlap the proteins in activity. Both of the unmutated ebg proteins already bind lactose. Binding of lactose even to the unmutated ebg repressor induces a 100-fold increase in synthesis of the ebg operon.” (Hall 1982a)

Even so, the experiment generated some controversy. Why? As Behe said, “Because there were two separate mutations in different genes--neither of which by itself allowed cell growth. (Hall 1982a)” “The odds against the mutations appearing randomly and independently were prohibitive (Hall 1982b). Hall's results and similar results from other laboratories led to research in the area dubbed "adaptive mutations." (Cairns 1998; Foster 1999; Hall 1998; McFadden and Al Khalili 1999; Shapiro 1997).”

These further investigations led to the "Directed Mutation" hypothesis. Eventually, these mutations were later re-named “Stationary-Phase Mutations” Apparently, the idea of “Directed Mutations” did not sit well with researchers. It has even been referred to as "the mutation whose name one dare not speak" by Dr. Susan Rosenberg, (http://www.btinternet.com/~johnlatter22/direct.html)

So, after all my research, I have to agree with Behe's conclusions:

The admirably-careful work of Hall involved a series of micromutations stitched together by intelligent intervention. He showed that the activity of a deleted enzyme could be replaced only by mutations to a second, homologous protein with a nearly-identical active site; and only if the second repressor already bound lactose; and only if the system were also artificially supported by inclusion of IPTG; and only if the system were also allowed to use a preexisting permease. Such results are exactly what one expects of irreducible complexity requiring intelligent intervention, and of limited capabilities for Darwinian processes.
Michael Behe, "A True Acid Test": Response to Ken Miller

 

[Stratnerd]

Becky,

Please interpret this "a series of micromutations stitched together by intelligent intervention".

Is he saying that the mutations in Hall's experiment were directed by God?

Thanks!

 

[Prisca]

Stratnerd

Stratnerd

You said, “Please interpret this "a series of micromutations stitched together by intelligent intervention".

I thought the quote I posted from the Department of Microbiology At Southern Illinois University said it pretty well…

"It is difficult to imagine how bacteria are able to solve complex problems like these - and do so without, at the same time, accumulating a large number of neutral and deleterious mutations - unless they have access to some reversible process of trial and error."

Of course, I would rephrase the quote something like this:

It is difficult to imagine how bacteria are able to solve complex problems like these - and do so without, at the same time, accumulating a large number of neutral and deleterious mutations – unless they were designed to do so.

You said, “Is he saying that the mutations in Hall's experiment were directed by God?”

I believe Behe is saying that the mutations in Hall’s experiment were designed by some form of intelligence. Whether or not he believes this “intelligence” is from God, I do not know.

 

[Stratnerd]

Sorry if I come across partially dense (I am) but is Behe saying

1. God designed bacteria with certain mechanisms of mutations (sort of a theistic view) or

2. God was at work in the lab in the best interest (inferred) of the microbes to mutate their DNA.

What do you think?

 

[Prisca]

Stratnerd

Stratnerd

You said, “Sorry if I come across partially dense…

No, you didn’t, I just misunderstood. In fact, the first time I read your post, I read it the way you meant it. Unfortunately, I was interrupted before I could post and when I came back I took the wrong track. Sorry about that.

You had asked, (regarding the quote from Behe’s article), “Is he saying that the mutations in Hall's experiment were directed by God?”

That’s a good question. I have not read much of Behe’s work, but I did come across the following statement in an article he wrote titled Intelligent Design Is Not Creationism:

”In fact, my own views fit quite comfortably with the 40% of scientists that Scott acknowledges think ‘evolution occurred, but was guided by God.’”

I suppose, with the above quote in mind, Behe would most likely agree with statement #2 from your above post (although I can’t say that with 100% certainty). I, on the other hand, would be most likely to agree with statement #1.

 

[Stratnerd]

Becky,

I think we might be able to test the hypothesis that God direct mutations. I haven't really thought about this one but if God is directing mutations then we should find that if we try to kill bacteria in several independent colonies then there should be

1. The same answer to the antibacteria in all colonies

2. The mutation rate that "fixes" the problem succeeds that of all other areas.

I'm not sure this rules out the hypothesis that areas that are important for resistance are naturally more prone to mutation. That could be tested by not adding a biotic and looking at the background mutation rate at that gene(s).

What bugs me about suggesting that God directs mutations is the suggestion that he's behind the mutations that give the nasty bacteria/viruses resistance... then whos best interest is He looking after?

 

[Warren]

Behe is not saying that the mutations in Hall's experiments are guided by God.

 

[Stratnerd]

Warren & Becky,

What I'm driving at is finding something about ID that is testable. I admit that I haven't read all 100-something posts but is there?

 

[Prisca]

Warren

Warren

You said, “Behe is not saying that the mutations in Hall's experiments are guided by God.”

I personally haven’t read enough of Behe’s work to know for sure what he believes about these mutations. Do you have any information showing that Behe does not believe the mutations in Hall's experiments are guided by God?

Thanks,
Becky

 

[Warren]

Becky>>I personally haven’t read enough of Behe’s work to know for sure what he believes about these mutations. Do you have any information showing that Behe does not believe the mutations in Hall's experiments are guided by God? <<

I have read a lot of Behe's articles. I can't give you a direct quote right now but I can assure you that neither Behe or any other scientist in the ID movement believes that God intervenes in scientific experiments. That's not to say, however, that Hall's experiments might not strenghten the ID inference.

 

[Warren]

Stratnerd>> What I'm driving at is finding something about ID that is testable. I admit that I haven't read all 100-something posts but is there?<<

The inductive sciences (by which we might understand physics, chemistry, and the other primarily experimental sciences) are motivated by the question "How does nature normally operate?" The historical sciences (by which we might understand cosmology, geology, paleontology, evolutionary theory and biological systematics), on the other hand, are motivated primarily by the question "How did this system or object come to be?" These are logically distinct questions. In the latter case, when we ask how something came to be, we explain by invoking causal narratives or patterns of events -- employing methods often termed "abductive" or "retroductive" -- to find that set of events that best accounts for the features of what we observe in the present.

This is detective-style reasoning and while such reasoning certainly employs natural laws (the bread-and-butter of the inductive or experimental sciences), those laws are insufficient tools for answering the questions posed in the historical sciences. In evolutionary theory, says Stephen Jay Gould, "we infer history from its results."

This means that testing, or theory evaluation more generally, will also differ in important ways between the inductive and historical sciences. As Darwin often argued to his correspondents, the theory of common descent by natural selection had to be weighed comparatively, "vis-a-vis its competitors." Explanations are judged by their relative power, and by their consistency with what we know from the present.

Can a theory of design be formulated to meet these standards? Yes: the theory is attempting to answer a "What happened?" question, and does so by postulating the past action of an intelligent agent. That's a perfectly appropriate answer to a perfectly appropriate historical question. Starting with distinctive features of living systems, design attempts to account for those features by referring them to a sufficient cause, namely, an intelligence. In every respect design as a theory is logically fully consonant with the types of answers, and methods of evaluation, common to the historical sciences.

The purpose of inductive science is to most accurately describe natural processes--the regular and repeatable patterns found in nature. The sudden appearance of 65 phyla during the cambrian era is not regular, predictable, or repeatable. One might ask why the sudden appearance of the major groups (e.g., new phyla in the Cambrian explosion) is even considered natural at all.

Design and Darwinian macroevolution are historical theories. Historical theories make claims about events that occurred in the past and that cannot be directly verified and may never recur. Yet like other historical theories, these theories can be tested after the fact by reference to their comparative explanatory power. To impose stricter standards ignores the limitations inherent in all historical inquiry.

An openness to design arguments is a necessary condition of a fully rational historical biology. In my opinion, a rational historical biology therefore must address not only the question, "Which materialistic evolutionary scenario provides the most adequate explanation of biological complexity?" but also the question, "Does a strictly materialistic evolutionary scenario, or one involving intelligent agency, or some other, best explain the origin of biological complexity, given all relevant evidence?" To insist otherwise is to insist that materialism holds a metaphysically privileged position.