Guided Pathways
by BradfordEvolution Under Intrinsic Control is a blog entry at Mike Gene's The Design Matrix. Mike begins by noting that "antibiotic resistant bacteria has long been used as a classic example of Darwinian evolution in action." He then focuses on a study by Floyd Romesberg and colleagues which puts a new twist on the resistence theme. Quoting Mike:
The twist is this: in this case, mutations don’t “just happen” – bacteria make sure they happen. That is, the evolution of antibiotic resistance is not simply the passive process of selection screening through the available variability. On the contrary, bacteria respond to the insult by making sure there is a plentiful source of variability to screen.
In this study, it was determined that bacterial input was essential to the evolution of antibiotic resistance. In other words, the cellular process of “making sure there is a plentiful source of variability to screen” is exactly what is needed to evolve antibiotic resistance.
A key component to adaptation appears to be LexA; a DNA binding protein which performs a regulatory function affecting multiple genes. There is an ingenius structural strategy involving LexA and damaged DNA. The DNA damage detection process leads to a series of biochemical events, the end result of which, is to release the repression of genes whose expression then initiates repair of damaged DNA. Mike links to a paper titled Inhibition of Mutation and Combating the Evolution of Antibiotic Resistance, published by PLOS Biology and authored by Ryan T. Cirz, Jodie K. Chin, David R. Andes, Valérie de Crécy-Lagard, William A. Craig, and Floyd E. Romesberg. Quoting from that paper:
The emergence of drug-resistant bacteria poses a serious threat to human health. In the case of several antibiotics, including those of the quinolone and rifamycin classes, bacteria rapidly acquire resistance through mutation of chromosomal genes during therapy. In this work, we show that preventing induction of the SOS response by interfering with the activity of the protease LexA renders pathogenic Escherichia coli unable to evolve resistance in vivo to ciprofloxacin or rifampicin, important quinolone and rifamycin antibiotics. We show in vitro that LexA cleavage is induced during RecBC-mediated repair of ciprofloxacin-mediated DNA damage and that this results in the derepression of the SOS-regulated polymerases Pol II, Pol IV and Pol V, which collaborate to induce resistance-conferring mutations.
Central to Darwinian views is the concept that mutations are random with respect to reproductive fitness. An efficient complex of genetic repair mechanisms ensures the integrity of cellular genomes. Mutations can be viewed as genetic changes which fall through existing DNA genomic integrity nets. Effective adaptation responses involve maintaining genomic integrity while allowing for some changes. That means maintaining stasis for functional and effective genes (most of them) while genetic tinkering occurs. Yet if genomic integrity is the consequence of a system, whose trigger mechanism ensures that only selective genes are expressed, then homeostatic capacity is intrinsically preprogrammed. When effective adaptive responses, resulting from genetic changes, act in concert with the types of mechanisms alluded to we have what Mike might describe as adjustments within homeostatic cellular environments. Quoting Mike:
While the teleological echo is faint, it is nevertheless there. We can begin to catch a glimpse of evolution as homeostasis. The integrity of the genome is threatened. Standard small scale feedback responses ensue as the cell attempts to reverse the change through repair and recombination mechanisms. But if the insult is too severe or too common, the next level of feedback response is…..evolution itself. The antibiotic is the stress that perturbs the homeostasis of the cells and evolution is the effector that reverses the effects of the change. Life fights back.
Mike concludes with the observation that DNA "may be plugged into an elaborate system that allows it act as sensor for its own continued perpetuation." Indeed. Or front loading DNA repair functions may be a sine qua non for cellular life forms.
January 21st, 2009 at 9:48 pm
Wrong. There's nothing special about the genetic system that sets it aside from evolutionary processes, so there's nothing odd or inconsistent with survival mechanisms being built into the system itself, including some that "direct" mutations in one way or another.
Random mistakes are an interesting and important characteristic of the replication system, but that doesn't mean that detecting something that isn't as random as you'd expect invalidates or undermines the theory.
I'll say it's faint. Once again, we find "teleological" applied to what's already explained without teleology. It's just another learned response labeled "purpose".
Comment by don provan — January 21, 2009 @ 9:48 pm
January 21st, 2009 at 9:58 pm
Give us the ateleological explanation.
Comment by Bradford — January 21, 2009 @ 9:58 pm
January 21st, 2009 at 10:08 pm
Are you claiming that standard theory holds that mutations are not random with respect to reproductive fitness?
Comment by Bradford — January 21, 2009 @ 10:08 pm
January 21st, 2009 at 10:23 pm
If I understand it correctly, cleaving LexA simply increases the frequency of mutations. An increase in mutation frequency does not mean that those mutations are non-random with respect to a fitness function.
Comment by olegt — January 21, 2009 @ 10:23 pm
January 21st, 2009 at 10:47 pm
When DNA is damaged, the cell attempts a repair. This can lead to mutation. Some antibiotics attack DNA during replication, so there is an increase in repairs and an increase in the mutation rate. Suppressing the repair mechanism lowers the effective mutation rate. The mutations are still random with respect to fitness.
("Darwinian" is an ambiguous term, typically referring to evolution by natural selection. Darwin didn't know about genetic mutation.)
Comment by Zachriel — January 21, 2009 @ 10:47 pm
January 21st, 2009 at 11:45 pm
There is more to this. A consequence of the loss of LexA mediated repression is the expression of three enzymes required for mutation.
There is specificity with respect to the genes which must mutate:
Other expressed genes are involved in the repair of damaged DNA. An IC system with a threefold response: neutralizing a specific poison through mutation and delaying the cell cycle while maintaining a homeostatic environment through repair of damaged DNA.
Comment by Bradford — January 21, 2009 @ 11:45 pm
January 21st, 2009 at 11:52 pm
Zachriel:
The initial damage is effected through physical obstruction in the form of ciprofloxacin binding to a DSB and inhibiting topoisomerase induced rejoining. And studying the remedy:
Resulting in a find that:
Looking at this again:
The induced increase in the mutation rate, entailing 3 to 5 independent mutations, affects the genes coding for the enzymes. At the very least this looks like "programmed randomness."
Comment by Bradford — January 21, 2009 @ 11:52 pm
January 22nd, 2009 at 8:17 am
Can you clarify your position here, Bradford. Are you arguing that an intelligent agent is responsible for bacteria evolving resistance to anti-biotics?
Perhaps you could tell us if you think this is Gods handiwork though I have to wonder why God would do this; perhaps He thinks anti-biotics are evil, and this is his way of telling us to let nature run its course. After all, all those doctors are doing is delaying people getting to heaven.
Or is this evidence of aliens here on Earth right now, tinkering with bacteria DNA for their own dastardly purposes.
Perhaps you see this as evidence of front-loading; that a designer 4 billion years ago had the foresight to engineer in a latent resistence to antibiotics, that only now is becoming active.
Maybe you think the bacteria itself is clever enough to indulge in its own genetic engineering (I wonder if anyone posting on TT is as clever as bacteria, and knows how to modify DNA towards a certain end).
See if you want to argue foer teleology and purpose, you have to wonder what the purpose is. Who is it that wants bacteria to be resistant to anti-biotics. If Mike is right, then there is a huge amount of research to be done – and I think it would be very interesting.
But I doubt you would like the results.
Comment by The Pixie Again — January 22, 2009 @ 8:17 am
January 22nd, 2009 at 8:31 am
Are you suggesting that this "IC" system was front-loaded from the start?
Comment by Raevmo — January 22, 2009 @ 8:31 am
January 22nd, 2009 at 8:51 am
Not just mutations in the genes for those enzymes. Anywhere there is damage to DNA. LexA mediates a complex and multifaceted repair mechanism. If the system evolved, then we would expect LexA to be part of a family of related proteins.
Comment by Zachriel — January 22, 2009 @ 8:51 am
January 22nd, 2009 at 11:52 am
While I am not certain it is necessary to label the system IC, the front-loading hypothesis seems plausible in this case.
In Chapter 7 of The Design Matrix, Mike discusses whether high- or low-information proteins would be used by a front-loading engineer (high-information meaning most or all of the amino acid sequence is required as-is for a specific function; low-information meaning a particular amino acid sequence is not necessary for a specific function). Mike answers this question by showing high- and low-information proteins would be "counterproductive to front-loading". Rather, Mike suggests mid-level information proteins to achieve the objectives of stasis and change.
Bradford extrapolates this in the OP:
And from Mike:
It would appear, IMO, that from a front-loading perpspective, preserving the integrity of the genome is the primary objective while the secondary objective is to tinker with the genome to achieve the overarching objective of preserving the organism.
Comment by JJS P.Eng. — January 22, 2009 @ 11:52 am
January 22nd, 2009 at 2:18 pm
Don P:
If LexA, and the repressed action of numerous genes, is so central to the viability of these cells…. so much so that the removal of the SOS response appears to be a death sentence for those cells.. in the event they stumble across some insult from without. How do you feel those proto-cells that would have lacked that ability faired when faced with similar insults?
Comment by GringoRoyale — January 22, 2009 @ 2:18 pm
January 22nd, 2009 at 2:20 pm
Can I beg the question for you, Don?
"well, they clearly faired well because here we are today, talking about it."
But why leave my criticism there?
Since you begged the question with that whole paragraph I quoted:
Comment by GringoRoyale — January 22, 2009 @ 2:20 pm
January 22nd, 2009 at 5:01 pm
JJS:
Perhaps Bradford can explain why he thinks the system is IC. The front-loading hypothesis doesn't seem that plausible to me (I must be using a different prior), but perhaps a phylogenetic analysis of the nonessential polymerases Pol II, Pol IV and Pol V might shed some light on it. If for example such an analysis would conclude that these polymerases were not present in LUCA, that would be evidence against the FL scenario. I don't know if such a study has been done, and I'm too lazy at the moment to investigate it.
Why? I thought the objective was the evolution of humans.
Comment by Raevmo — January 22, 2009 @ 5:01 pm
January 22nd, 2009 at 5:12 pm
I don't believe Mike was ever that ambitious with FLE as set out in DM.
Comment by JJS P.Eng. — January 22, 2009 @ 5:12 pm
January 22nd, 2009 at 5:16 pm
Duh. Maybe this is a clue:
How many genes are regulated by LexA?
Comment by Bradford — January 22, 2009 @ 5:16 pm
January 22nd, 2009 at 5:20 pm
JJS:
Of course not. That would be a little bit too unscientific. But I bet it's what many front-loading fans think anyway. Don't you agree?
Too bad you didn't respond to the serious part of my comment. Perhaps you have the time to investigate the phylogeny of polymerases?
Comment by Raevmo — January 22, 2009 @ 5:20 pm
January 22nd, 2009 at 5:22 pm
Bradford:
Why is this question relevant? I asked you to explain your claim that the system is IC.
Comment by Raevmo — January 22, 2009 @ 5:22 pm
January 22nd, 2009 at 5:23 pm
Raevmo, the Pols were a part of the response, not the whole package.
Comment by Bradford — January 22, 2009 @ 5:23 pm
January 22nd, 2009 at 5:24 pm
The system I had in mind involves the elements active in the adaptation.
Comment by Bradford — January 22, 2009 @ 5:24 pm
January 22nd, 2009 at 5:27 pm
You still didn't explain why it is IC in your opinion.
Comment by Raevmo — January 22, 2009 @ 5:27 pm
January 22nd, 2009 at 5:38 pm
An IC system is composed of multiple parts. Remove a part and the system is rendered dysfunctional. Disable the function of LexA and adaptive responses are disabled. Sounds IC.
Comment by Bradford — January 22, 2009 @ 5:38 pm
January 22nd, 2009 at 6:14 pm
Bradford:
LexA represses mutagenesis. Therefore, by interfering with the repression of LexA (i.e. by increasing LexA concentration), the mutagenic polymerases don't get expressed. So what you're saying is that any system with a crucial regulatory gene is IC, and that such a system therefore cannot evolve by natural selection.
Comment by Raevmo — January 22, 2009 @ 6:14 pm
January 22nd, 2009 at 6:20 pm
Raevmo:
You asked me why the complex was IC and I explained why. I made no claim as to how the system comes about but if you know the pathways then out with it.
Comment by Bradford — January 22, 2009 @ 6:20 pm
January 22nd, 2009 at 6:28 pm
Bradford:
You were saying the complex is IC because interfering with a regulatory gene (which codes for LexA) causes the complex to be disfunctional. Therefore any system whose function depends on a regulatory gene must be IC, right?
Comment by Raevmo — January 22, 2009 @ 6:28 pm
January 22nd, 2009 at 6:43 pm
Explain why critics niggle and haggle over IC. IC is a descriptive device. If a disabled regulatory gene renders a regulated system inoperable then we have constraints indicating how a multi-component system would have been generated. A would be in place before B and C etc.
Comment by Bradford — January 22, 2009 @ 6:43 pm
January 22nd, 2009 at 6:56 pm
Bradford:
You didn't answer my question:
By the logic you used to declare the LexA system IC, the answer must be yes.
IC is not just a descriptive device, as you very well know. It is also implied that an IC system must have been designed (i.e. poofed into existence by Mr Designer).
Comment by Raevmo — January 22, 2009 @ 6:56 pm
January 22nd, 2009 at 7:12 pm
To the contrary, it poses real questions which may not be welcome but are legitimate nonetheless. How do LexA inclusive genomes evolve? Any answer not gounded in rationality can be deemed a poof. Cells arose from… sounds poofy to me. It's all subjective. The objective part requires that you set aside your preconceptions and assess the origin of biosystems in light of what we know.
Comment by Bradford — January 22, 2009 @ 7:12 pm
January 22nd, 2009 at 7:36 pm
Apparently not. This new evidence points to bacteria being the ultimate objectives of the front-loaders. To be honest, I think this is a much more reasonable scenario. Imagining that four billion years of evolution to mankind can be built into single-celled organisms is not exactly credible. However, aliens seeding the plant with single-celled organisms designed to evolve into improved single-celled organisms is starting to sound realistic.
I guess we are just unwanted by-products of that process.
Comment by The Pixie Again — January 22, 2009 @ 7:36 pm
January 22nd, 2009 at 7:51 pm
Were you asleep in class when it was explained that reproductive capacity conjoined with an ability to adapt leads to an evolutionary process? Functional DNA would have both qualities. Who said you can't package evolution into a single cell?
Comment by Bradford — January 22, 2009 @ 7:51 pm
January 23rd, 2009 at 5:40 am
Ah, you are setting your sights lower. Now the front-loaders are only packaging the ability to evolve into the first life. Now that sounds entirely plausible, and something I can see mankind being capable of by the end of the century.
Comment by The Pixie Again — January 23, 2009 @ 5:40 am
January 23rd, 2009 at 12:02 pm
Establishing basic cellular capacities like the ability to reproduce and adapt has been my position on FL for some time. It is no simple task.
By working with DNA sourced from cells.
Comment by Bradford — January 23, 2009 @ 12:02 pm
January 23rd, 2009 at 1:20 pm
The atelic explanation is that the mechanisms convey a survival advantage to the genes that trigger them. I'm surprised you haven't heard about it.
Of course not. That would be silly, since anyone can observe for themselves that mutations tend to be random.
I said what I meant: the standard theory does not hold that all mutations must be entirely random. The standard theory is entirely consistent with adaptations to the replication system itself, including those that make advantageous mutations more likely under the right conditions. Certainly a mechanism that reduces the accuracy of replication is easy to understand within the standard theory. We can see the survival advantage right before our eyes.
Comment by don provan — January 23, 2009 @ 1:20 pm
January 23rd, 2009 at 1:27 pm
Presumably they would have been wiped out. No wonder we see that ability in the survivors.
Comment by don provan — January 23, 2009 @ 1:27 pm
January 23rd, 2009 at 1:43 pm
Hand-wave alert! Hand-wave alert!
Comment by JJS P.Eng. — January 23, 2009 @ 1:43 pm
January 23rd, 2009 at 2:20 pm
You don't think they would have been wiped out?
Comment by don provan — January 23, 2009 @ 2:20 pm
January 23rd, 2009 at 2:26 pm
don, your explanation amounts to "those that survive are fit and the fit are those that survive."
It's also very similar to hand-waving arguments against fine-tuning (well, it's what we expect if there are observers to observe it).
My objection was more to the second sentence of your response. Too simple. Too just-so. Too meh!
Comment by JJS P.Eng. — January 23, 2009 @ 2:26 pm
January 23rd, 2009 at 2:52 pm
JJ,
No, my explanation is that the this configuration of mechanisms enhanced survival over other mechanisms, and that's why we see it and not others. You may think that's a tautology, but it's really just undeniable, which is why it's so popular.
The second sentence just follows from the first. I'm sorry if you don't like its simplicity. Scientists like it because it's so simple. That, and the fact that it hasn't been refuted.
I'm a little surprised to find you arguing with me about this. In the other thread, I thought you were suggesting that front loading could leverage this process, but now you're questioning it.
Comment by don provan — January 23, 2009 @ 2:52 pm
January 23rd, 2009 at 2:59 pm
I'm hardly surprised by verbiage that conveys no specificity. This explains the origin of the LexA repression system? "Hey Joe. It has some survival advantage. Know what I'm sayin?"
Comment by Bradford — January 23, 2009 @ 2:59 pm
January 23rd, 2009 at 4:11 pm
It is equally as specific as the front loading explanation, but has the advantage of invoking mechanisms we've observed for ourselves.
I have to admit, I didn't bother reading the paper itself, but I don't think the exact nature of the survival advantage is in question. I'm doing nothing here beyond invoking exactly those evolutionary mechanisms that I'm repeatedly assured IDist accept.
Comment by don provan — January 23, 2009 @ 4:11 pm
January 23rd, 2009 at 5:07 pm
dp:
Not so. You do not observe that any mechanisms generated the LexA complex. What we observe is the disablement of adaptive responses when LexA function is disabled; the classic confirmation of an IC system.
Comment by Bradford — January 23, 2009 @ 5:07 pm
January 23rd, 2009 at 6:08 pm
Do you observe that any mechanisms generated the LexA complex? No. OK, we're past that. Now, do we observe the postulated mechanisms generate other changes? Yes, of course. Even IDists don't deny this. Do we observe front loading generate other changes? No, we have not observed any such mechanism for ourselves.
Comment by don provan — January 23, 2009 @ 6:08 pm
January 23rd, 2009 at 6:17 pm
Those observed changes are of a totally different order.
That's exactly the point. We have no non-telic mechanisms identified as responsible for generating the genetic repair mechanisms in question. Front loading otherwise unexplainable features allows us to explain what subsequently occurs.
Comment by Bradford — January 23, 2009 @ 6:17 pm
January 23rd, 2009 at 9:05 pm
We've never seen any changes of any order caused by front loading.
Comment by don provan — January 23, 2009 @ 9:05 pm
January 23rd, 2009 at 9:16 pm
That's your personal view. There is no way to know, based on an empirical approach, whether what we see descended from a front loaded initial genome or otherwise.
Comment by Bradford — January 23, 2009 @ 9:16 pm
January 24th, 2009 at 1:43 pm
It is? Are you saying we have see changes caused by front loading? Or have we only conjectured that some changes might have been caused by front loading?
Now we've come back to where I said, "It is equally as specific as the front loading explanation, but has the advantage of invoking mechanisms we've observed for ourselves." If you want to label something "a different order", be my guest, but it remains true that the accepted explanation invokes mechanisms we've observed at work. That gives it an advantage even if you think those mechanisms are insufficient.
Comment by don provan — January 24, 2009 @ 1:43 pm
January 24th, 2009 at 2:00 pm
Bradford:
What makes you think that such questions are not welcome? Evolutionary biology tries to answer such questions all the time. It is rather the opposite: you do not welcome such questions because you prefer to believe that The Designer poofed the "IC" stuff into existence, so you can feel more confident about your religious beliefs.
Comment by Raevmo — January 24, 2009 @ 2:00 pm
January 24th, 2009 at 2:20 pm
We have not observed any mechanisms which generate the basic replicating unit for life- cells. At a foundational level you have no way of distinguishing FL from a non-FL mechanism.
Comment by Bradford — January 24, 2009 @ 2:20 pm
January 24th, 2009 at 2:24 pm
I know you like repeating that lie. But my beliefs hinge on what happened 2,000 years ago; about which objective evidence is notably poor at refuting. Abiogenesis is poof science. You simply have a different deity named chance and ignorance but your blind faith is unswerving nonetheless.
Comment by Bradford — January 24, 2009 @ 2:24 pm
January 24th, 2009 at 5:13 pm
Bradford:
Your beliefs hinge on hearsay, fabrications, wishful thinking and self-delusion.
Where is the "poof" in abiogenesis?
Comment by Raevmo — January 24, 2009 @ 5:13 pm
January 24th, 2009 at 6:09 pm
Start with a short nucleic acid polymer and poof, you end up with a cell grounded in beliefs hinged on wishful thinking and self-delusion.
Comment by Bradford — January 24, 2009 @ 6:09 pm
January 24th, 2009 at 6:31 pm
Bradford:
You obviously misunderstand the important poof concept. Who do you think you are fooling with your ridiculously dishonest caricature of scientific research into abiogenesis?
Comment by Raevmo — January 24, 2009 @ 6:31 pm
January 24th, 2009 at 6:45 pm
Rarvmo,
Eyewitness accounts are not hearsay
Fabrications and wishful thinking demand an expectation of resurrection before the end of the world.
That leads you with self delusion and such a charge demands evidence.
What evidence do you have for insanity in the witnesses or in Bradford?
How so poof is poof is it not?
Peace
Comment by fifth monarchy man — January 24, 2009 @ 6:45 pm
January 24th, 2009 at 7:51 pm
Exactly fmm. Poof is poof. Raevmo has his own sacred cows and a different perspective on herasy.
Comment by Bradford — January 24, 2009 @ 7:51 pm
January 26th, 2009 at 1:45 pm
That's what I said to begin with. It's front loading's biggest problem.
I thought we were discussing variations in replication, and we've already agreed that mainstream theory does explain some variations. My original point was that these variations don't seem significantly different that any we agree about, they just happen to be variations in the very mechanisms that causes variations. You said, "Those observed changes are of a totally different order," but they just seem like more changes of the same kind to scientists.
On the other hand, if we are talking about "generating the basic replicating unit for life- cells," then both theories are, as I said, quite unspecific: "it is natural processes" vs. "it is front loading". But the explanation that says, "it's probably more of the same" has an inside track over a theory that says, "it's something entirely different that we don't see anywhere else." I agree that doesn't make front loading wrong, but it gives it a longer row to hoe.
Comment by don provan — January 26, 2009 @ 1:45 pm
January 26th, 2009 at 2:03 pm
We have not observed any mechanisms which generate the basic replicating unit for life- cells.
I'm more interested in research results than what it is you think scientists believe. My above statement is correct. You and others are free to think a ribonucleic acid "mutates" en route to a cell if you wish. We all have our cherished beliefs after all.
Comment by Bradford — January 26, 2009 @ 2:03 pm
January 26th, 2009 at 2:17 pm
I'll keep repeating this until you kiddies get it right: there is NO mechanism for design. Engineers make use of mechanisms in their designs. The design action of an engineer cannot be reduced to a mechanism. IMO, FLE concerns itself with investigating the (potential) manipulation of natural mechanisms to achieve a desired result (design objective).
No, it is not. The lack of a front-loaded mechanism is a non-issue.
Comment by JJS P.Eng. — January 26, 2009 @ 2:17 pm
January 26th, 2009 at 2:21 pm
Thanks Poppa.
Comment by Bradford — January 26, 2009 @ 2:21 pm
January 26th, 2009 at 2:25 pm
JJS:
This kiddie respectfully disagrees. There are computers that design stuff — even "unexpected" designs since the computers use random number generators. Are you saying that there is no mechanism for design in that case?
Comment by Raevmo — January 26, 2009 @ 2:25 pm
January 26th, 2009 at 2:37 pm
Let me address the two cases you presented separately:
1. Computers "designing" stuff: This "design" is based on a program that was developed by software engineers who programmed the parameters of the search of options so that a human engineer can eliminate various options in a workable timeframe. The computer ends up being a tool to examine different design directions. It's really no different than me creating a spreadsheet to go through the myriad of different steel section options in the time span of a few minutes instead of hours.
At the end of the day, it is a human engineer that must check the details of the design to ensure it functions in the real world properly. Thus you have human engineer(s) at both the start and the finish of the design process. The computer merely facilitates the search for options. It does not design.
2. Accidental design: this sounds a lot like "designoids" as expressed by Dawkins and Gene. This is not design, but tinkering or evolutionary noise. In order for tinkering to occur, it needs something to tinker with. In most cases, that something is purposely designed.
Comment by JJS P.Eng. — January 26, 2009 @ 2:37 pm
January 26th, 2009 at 2:58 pm
JJS:
I would say it does. The human (or computer) who checks the design merely evaluates it, it doesn't do the designing. In case of front-loading: the environment checks the design.
Again, I disagree. Evolutionary algorithms can design stuff, and they rely on (pseudo) random numbers to generate new designs. Perhaps in your brain there is also a (pseudo) random design generator, and another part of your brain selects the one that meets certain requirements.
Comment by Raevmo — January 26, 2009 @ 2:58 pm
January 26th, 2009 at 3:07 pm
So should we listen to JJ or to Bradford? And why?
Comment by don provan — January 26, 2009 @ 3:07 pm
January 26th, 2009 at 3:21 pm
Raevmo:
To an extent. But that interaction raises some interesting points about FLE; a subject matter to be explored in an upcoming blog entry.
Raevmo to JJS:
Or perhaps in his mind there exists a capacity for analysis which makes assessments independently of brain biochemical determinism and that is further evidence of design.
Comment by Bradford — January 26, 2009 @ 3:21 pm
January 26th, 2009 at 3:28 pm
Design theories such as front loading offer no mechanisms. We agree. That was my point. Bradford argued that the prevailing theory offers no observable mechanism for the structure being studied, and I was pointing out that this is an extreme case of the kettle calling the pot black since front loading offers no mechanisms whatsoever, while the prevailiing theory offered mechanisms that simply haven't been observed in this specific case.
As it happens, I was just saying that I never see any mechanisms suggested, but thank you for confirming that an inability to propose any mechanism, observed or not, is actually a logical consequence of the theory.
Comment by don provan — January 26, 2009 @ 3:28 pm
January 26th, 2009 at 3:39 pm
Bradford:
Looking forward to that then.
Further?
Comment by Raevmo — January 26, 2009 @ 3:39 pm
January 26th, 2009 at 4:18 pm
Please direct all further responses to my comment to this thread.
My apologies for taking your thread off-track, Bradford.
Comment by JJS P.Eng. — January 26, 2009 @ 4:18 pm
January 26th, 2009 at 4:24 pm
No need to. I respect my elders.
Comment by Bradford — January 26, 2009 @ 4:24 pm