A Genomic Balancing Act
by BradfordAn article by Professor Steve Jones, View From the lab: mutations suggests reasons for the utility of a front loading paradigm. Current approaches take note of an existing balance between the potential for change and the need to maintain genomic function by preserving stability.
Mutations are essential to an evolutionary process. If there are none, change is not possible. While too many leads to the demise of an organism, or a species, a balance allows for adapative changes. Mutations are kept in check by multiple DNA repair mechanisms tageting different types of damage. Jones describes the repair processes:
"The chances of physical error as each DNA molecule is copied are such that mistakes – mutations- should build up with great speed and stop most of the dividing helices in their tracks. Even those that make it would be so damaged that their carriers would not survive.
Fortunately, biological sums are never simple. The genetic material is indeed much damaged by the laws of chemistry, which work as inexorably in our cells as in a test tube. In cells, though, most of the mistakes are put right. The thousand natural shocks that life is heir to are fixed in many ingenious ways. Special enzymes clean up the mess as they snip out a mutated segment, join together broken bits of the molecule, or replace a faulty piece with the correct version. The process is like the spell-check in a word-processing program: make a mistake and the machine puts it right. More than 100 genes are now known to be involved in the DNA repair business. Without them we would not survive.
To check the spelling in a document, one needs a back-up based on the correct versions of words (a dictionary) – but where is the dictionary for DNA? In fact, the genome is built on back-ups, with repeat copies of genes that can be used to check when one has gone wrong. Even the double helix is a sort of spell-checker, for editorial enzymes can compare one DNA base with its opposite and undamaged number to check that it fits."
How did repair mechanisms evolve? This is another way of asking the question: How did a balance between change and stability evolve? Since genes coding for enzymes, enabling DNA repair, provide the needed stability and since they themselves had to evolve, the more basic question is: Is evolution possible without a means to limit damage to genomic sequences having selective value? What would have prevented the decay of the very coding sequences needed to confer selective value to enzyme repair genes or, for that matter, genes involved in the replication function? Evolution is required to attain the idealized balance between stability and change. Yet natural forces inhibit an evolutionary process until genomic repair systems are in place. More from Professor Jones:
"Damaged DNA is fixed with great efficiency, in many unexpected ways. Why, then – given that nearly all errors are put right – is it not repaired absolutely, with no mistakes at all? Why is the mutation rate not even lower than it is?"
That's an interesting question that will be left for comments. Jones of course knows why the rate cannot be zero. Why not proceed to the logical next step and hypothesize the front loading of the repair mechanisms needed to maintain the previously cited balance between genomic change and stability. Front loading by design not only explains balance, it explains how a natural barrier to it is overcome.
February 18th, 2007 at 9:51 pm
"Why is the mutation rate not even lower than it is?"
I assume that he asked this rhetorically, but I'll take a shot. It's because a species which had no mutation rate would be unable to adapt to environmental changes and changes to its ecological niche (for example, changes in its predator or its prey). Such a species is bound to go extinct eventually.
On the flip side, a species which mutates too rapidly loses the "ratcheting" effect of evolution — it is unable to accurately "save" the mutations which worked and pass them onto the next generation. Such a species would also be headed for extinction in due time.
This is just one explanation off the top of my head. Whether you agree with it or not, there are obviously other possible explanations in addition to "front-loading." That is, the "logical next step" isn't necessarily "front-loading."
But is this not the old argument, "We haven't completely nailed down the reason for X, therefore X is the result of an intelligent designer"
Comment by jeff_alexander — February 18, 2007 @ 9:51 pm
February 18th, 2007 at 10:46 pm
As I read the article, I would have thought a creationist wrote it if it weren't for the evolutionary dogma crammed into the patently creationist lingo used by Jones. It is so sad, and serves as a great evidence, that a belief in evolution has it's route in a lie from the enemy. Skeptics laugh if you will, but demons are real in my experience (and I'm a former skeptic) and will lie about whatever they can to steer people against the Word of God in the Bible. Feel free to email me or chat on my blog, I love to talk about this with people. Be blessed!
Comment by Wayson — February 18, 2007 @ 10:46 pm
February 19th, 2007 at 3:55 am
Yes. Evolution is possible as long as the rate of uncorrected errors is sufficiently low. If the number of initial copying errors is high, then a really good repair mechanism is needed to keep the number of uncorrected errors down. If the rate of copying errors is moderate, then a moderately good repair mechanism will suffice. And if the number of copying errors is low enough, then no repair mechanism is needed at all.
The smaller the genome, the higher the allowable error rate under which evolution can still occur. (Another way to think of it is that it's not so much the error rate per nucleotide that matters, but rather the rate per organism.) Biologists believe that the repair mechanisms evolved when genomes were much smaller, and that in fact the repair mechanisms are what allowed genomes to get as large as they are today.
See Mark Ridley's book The Cooperative Gene (Mendel's Demon in the UK) for an excellent discussion of this.
Comment by keiths — February 19, 2007 @ 3:55 am
February 19th, 2007 at 4:19 am
Oh Bradford where is your faith in the infinite ability of evolution to solve any problem no matter how complicated. You poor deluded ID proponent, how can you possibily not understand something as obvious and simple as how such a mechanism evolved.
Comment by thesciphishow — February 19, 2007 @ 4:19 am
February 19th, 2007 at 8:35 am
It seems counter intutive to me that evolution evolved something that prevents evolution.
There are probably other explanations besides front-loading. For example, it could be the result of a very very lucky coincidence. However, I don't think that they are very likely.
We should just follow the evidence wherever it goes. ID can't really be proven, because just because something isn't very likely doesn't mean that it's not true. However it's a valid viewpoint.
Comment by WinglesS — February 19, 2007 @ 8:35 am
February 19th, 2007 at 9:32 am
WinglesS wrote:
Hi WinglesS,
The repair mechanisms don't prevent evolution; they simply limit the number of mutations.
As Jeff explained in his comment, too many mutations are just as bad for evolution as too few. The repair mechanisms keep the mutation rate within a safe range.
Comment by keiths — February 19, 2007 @ 9:32 am
February 19th, 2007 at 11:06 am
Hello Jeff. You wrote:
For the most part I agree with your analysis of the effects of a mutation range. The extremes of the range lead to extinction. The front loading concept is a recognition that a prebiotic process would initiate with no repair mechanisms available to remedy genomic corruption that would soon destroy any fortuitously acquired functional sequences in replicating RNA or whatever the theoretical choice may be. That's a novel condition for organisms and raises the reasonable question of whether such putative replicating entities could evolve. Uncontrolled genomic errors lead to demise.
To the contrary, the problem described leads to an open ended question which should not be resolved by the argument that since we have not nailed down the reason for X, therefore it is the result of a selective mutation process. IOW, testing should resolve the bone of contention.
Comment by Bradford — February 19, 2007 @ 11:06 am
February 19th, 2007 at 11:20 am
Keiths wrote:
You were doing OK until the last sentence. There is no scenario where the mutation rate is zero and as long as that is the case the results are cumulative. You also need to bear in mind that mismatch repair, which deals with mistakes of the type alluded to, are but one of multiple necessary mechanisms. The problem in maintaining genomic integrity is that causes of corruption are ubiquitous. They include all kinds of radiation effects, by-products of chemical reactions, including necessary metabolic ones, deamination and even hydrolysis.
What matters is the direction of change. If the arrow points toward increasing genomic instability, genomic catastrophe is inevitable. I'm less interested in what someone believes to have happened with small genomes evolving repair mechanisms than I am in evidence for this. Where is it?
Comment by Bradford — February 19, 2007 @ 11:20 am
February 19th, 2007 at 11:21 am
At least I'm willing to learn.:smile:
Comment by Bradford — February 19, 2007 @ 11:21 am
February 19th, 2007 at 11:27 am
I should add that the optimality of a non-zero mutation rate has implications for any front-loading hypothesis.
If front-loaded information is stored in the genome, then it too is subject to mutations at the non-zero rate. If the information isn't continually being expressed, then mutations will not be filtered out by selection and the front-loaded information will quickly be lost.
Therefore, any viable front-loading hypothesis must assert that either
1. The front-loaded information is continually expressed, from the moment it is introduced until it is no longer needed; or
2. The front-loaded information is protected by a distinct, as of yet unknown near-perfect error-correcting mechanism, and is thus not subject to the normal non-zero mutation rate.
Option #2 would require that different repair mechanisms operate on different, segregated sections of the genome, and would also require that the near-perfect error-correcting mechanism itself be stored in the part of the genome it was protecting.
If I recall correctly, Krauze has indicated a belief that front-loaded information is continually expressed, and that it simply biases the direction of evolution (toward multi-cellularity, for example). I'm not sure what Mike believes.
Comment by keiths — February 19, 2007 @ 11:27 am
February 19th, 2007 at 11:34 am
Keiths, one can argue that the genomic repair mechanisms found throughout the living world are nearly perfect. Not quite but close.
Before I address a direction, I wish to ensure a possibility. That was the point of the balance paradigm.
Comment by Bradford — February 19, 2007 @ 11:34 am
February 19th, 2007 at 11:41 am
Bradford wrote:
Bradford,
You're neglecting the fact that death itself eliminates mutations from the gene pool. Deleterious mutations accumulate only if they are introduced faster than they can be eliminated through death (i.e. natural selection). No repair mechanism is needed as long as the mutation rate doesn't outstrip natural selection's ability to purge the mutations.
Comment by keiths — February 19, 2007 @ 11:41 am
February 19th, 2007 at 11:45 am
By why limit mutation? That kind of implies that a little mutation is good. A lot is bad. So a few errors are fine, because they are needed for evolution, too many are not? We do know that radiation causes mutations, but I haven't seen any studies that show that radiation is beneficial for evolution. For example, in http://www.livescience.com/hum...:
There must be some other mechanism that causes beneficial evoltion besides mutstion is there?
Comment by WinglesS — February 19, 2007 @ 11:45 am
February 19th, 2007 at 11:51 am
Keiths, the vast majority of mutations are eliminated in advance of their becoming fixed through repair mechanisms. It is DNA repair mechanisms that keep genomic damage in check. Eucaryotes even have a cellular suicide option (apoptosis) so that the entire organism need not perish. Death, leading to the extinction of species, would ensue without a means of DNA repair.
Comment by Bradford — February 19, 2007 @ 11:51 am
February 19th, 2007 at 11:58 am
Bradford wrote:
But if they are imperfect enough to allow the evolution of expressed genes, then they are much too imperfect to preserve unexpressed front-loaded information for significant periods.
Comment by keiths — February 19, 2007 @ 11:58 am
February 19th, 2007 at 12:13 pm
Keiths & Bradford,
Very interesting conversation.
I just have a question regarding an acceptable low rate of mutation and the potential unneeded mechanisms to repair these trivial genomic aberrations.
What if these seemingly irrelevant mutations impinge on the construction of the protein synthetic machinery? Wouldn't this lead to catastrophic problems for the cell?
Comment by Doug — February 19, 2007 @ 12:13 pm
February 19th, 2007 at 12:18 pm
The logic in this comment doesn't seem to support a naturalistic account for evolution. It seems to assume foresight on the part of the organism regarding the use or non-use of a genome that can experience mutations.
Regarding the first organism created/formed/whatever… I don't think there would be much concern over changes in its predator or its prey.
Comment by Doug — February 19, 2007 @ 12:18 pm
February 19th, 2007 at 12:21 pm
The relevant period of time is that which is needed for a cell to replicate.
Comment by Bradford — February 19, 2007 @ 12:21 pm
February 19th, 2007 at 12:28 pm
Yes, and how would genes coding for proteins in this process or any other necessary one, remain viable unless DNA repair mechanisms were already in place?
Comment by Bradford — February 19, 2007 @ 12:28 pm
February 19th, 2007 at 12:46 pm
I can understand what Keiths is saying when he states:
But then I think that some of these proteins being encoded will be performing tasks such as ensuring that the protein synthetic machinery accurately synthesizes proteins.
Or what about the discovery of parallel signals in the DNA? Touched on both here and at uncommondescent by DaveScot.
Link
Do we know how sensitive these parallel codes are to mutations? Even seemingly irrelevant ones?
Comment by Doug — February 19, 2007 @ 12:46 pm
February 19th, 2007 at 2:32 pm
Bradford wrote:
Perhaps I should have made this clear, but I presented the two extremes in order to put endpoints on a continuous scale of possibilities ranging from no-mutations to fast-mutations.
We know that a given replicator (such as DNA) is somewhere in that continuum. It is not hard to imagine that a competing replicator at a different point on that continuum might fare better because it has a more optimal mix of stability and mutation. It is not a novel idea that selection can work on a replicator's ability to reproduce itself.
It appears you are saying that you cannot fathom a continuous series of steps ranging from primitive replicators, to slightly better replicators, to pre-RNA-type replicators, to RNA-type replicators, to RNA, to DNA, and so fourth, with selection acting on each of these steps to produce the next step. Remember that it took a couple billion years for DNA to finally arrive on the scene.
So the question is, does that really seem so unreasonable? And if so, what shall we do about it? Shall we introduce an intelligent designer, or a front-loading designer, or a [insert favorite theoretical entity here] in order to explain it away? Or should we investigate further?
You are right, insofar as there is no widely accepted theory outside of replicator selection. At the moment, it's the best we've got. The limited test-tube experiments with RNA have been surprisingly fruitful, though they are still baby steps toward a greater understanding.
In order to give wings to the front-loading theory, all you have to do is design an experiment for which front-loading is more plausible than regular replicator selection. While this might in principle happen some day, at the moment there is no need to introduce an outside entity such as a front-loader.
Comment by jeff_alexander — February 19, 2007 @ 2:32 pm
February 19th, 2007 at 2:39 pm
I suspect that Professor Steve "Why Intelligent Design is Stupid" Jones is referring to (in the context of "Now comes news of a spectacular new talent in the world of biological proofreading"¦") this letter to Nature: Lolle, S.J., Victor, J.L., Young, J.M., and Pruitt, R.E. (2005). Genome-wide non-mendelian inheritance of extra-genomic information in Arabidopsis. Nature 434, 505"“509.
Computing anything involves error. Computing Mendelian ratios involves error (Notoriously so!) Could it be that the "error," the difference between the computed, predicted, results and the sampled, measured, results are not, as is usually done, attributable solely to the routine kinds of errors expected in computing and measuring anything? Could it be that errors are due to a systematic and theoretical error?
Maybe the difference is due to possibility that Mendelian and non-Mendelian systems of inheritance are operating in parallel. (Did I just question "Mendel's laws"! Golly, I don't want to do that because of the implications for a broader theory of evolution that accepts those "laws" as theoretical axioms. Moi?! I would never do that.)
But I'm not going to be very happy with a theory of evolution that does not (or cannot, by definition) consider all factors that contribute to evolution. (Which is just to say I expect on being unhappy for the rest of my life. LOL)
To me there is a far more interesting issue, usually treated as a "Nevermind": the problem of what an "error" might be. Is that just too obvious to have any question about? Why we speak of perfectly "natural" phenomena as somehow being in a state of "error."
What has always intrigued me about this topic is why the word "error" seems to occur so naturally to people. Does it make any sense at all to talk about "natural" phenomena somehow being in "error." I mean, how is that possible? Am I just being stupid here? I would suggest that the word "error" always implies the existence of an epistemic agent whose existence cannot be accounted for in purely "naturalistic" terms. Error never refers to "ontologically given" categories of existence"”It always refers life forms, whose existence cannot is not (should not) be accepted as ontologically given. Not on the "theory" of naturalism. Consider a simple experiment: I shine a light on a diffraction grating and observe the spectrum. I don't consider that those elements distributed to the left of the spectrum are in "error," as opposed to those that occur appositely, which are "correct." I accept the distribution as given. Why, unlike the physicist, does the biologist consider that some proportion of a certain phenomenological distribution of effects he observes are in "error"?
What's the conceptual difference between how an exposed photographic plate is interpreted and how a Northern blot is interpreted?
I'd say there is a profound difference. One that is casually ignored in the common acceptance and usage of a term like "error" (and "correction).
Comment by Rock — February 19, 2007 @ 2:39 pm
February 19th, 2007 at 2:49 pm
Some of this can be empirically explored if we disable error correction mechanisms. It will give us a good hint of how evolvable the systems are withoug error correction, although I suspect most systems will be DOA.
Comment by Salvador T. Cordova — February 19, 2007 @ 2:49 pm
February 19th, 2007 at 2:52 pm
Jeff wrote:
Doug wrote in response:
I don't understand your point. The species is extinct, so obviously it didn't have foresight. A related species may have had a more useful mutation rate and thus survived.
Comment by jeff_alexander — February 19, 2007 @ 2:52 pm
February 19th, 2007 at 3:05 pm
For the purpose of this blog, an error is that which corrupts coding sequences that enhance reproductive fitness.
Comment by Bradford — February 19, 2007 @ 3:05 pm
February 19th, 2007 at 3:51 pm
I knew that, Bradford. I've said exactly the same thing. The biological concept of "fitness" is what engineers often call an "error function."
Evolutionary theory is a based on the fit of two independently given patterns. One pattern we call a life form and the other the environment. Two independently given patterns. Think about it, Bradford. Two independently given patterns. (Am I repetitive or what?)Two independently given patterns.
Of course, its not an error function (or any other kind of "function") if there is not some predefined specification, pattern, to which a rule does not apply and to which any sampled instance must conform. (Accordingly, biophilosophers should never talk about "functions," and according to biophilosophers, biologists shouldn't either!)
How is it possible for life forms to err and correct errors, Bradford? It is not possible. LOL An "impossibility" result based on a "proof of existence"! Life is impossible, but here we are! Life forms must, like everything else, conform to an existing pattern and the very idea that they may diverge from the pattern ("error") is a fundamental problem for"¦ not just philosophical naturalism, but its progenitor, theological naturalism!
I want to know how it is possible for a life form to make an "error."
Comment by Rock — February 19, 2007 @ 3:51 pm
February 19th, 2007 at 3:55 pm
It's difficult to restrain a teleological perspective on life. You have to constantly remind yourself that you are looking at a purposeless process even if this is untrue.
Comment by Bradford — February 19, 2007 @ 3:55 pm
February 19th, 2007 at 4:05 pm
Biology is teleology, Bradford. As opposed to physics, which I attempted to highlight.
Comment by Rock — February 19, 2007 @ 4:05 pm
February 19th, 2007 at 4:56 pm
Bradford:
Ah, but the mechanisms in question "correct" the "errors" that would help the organism survive and reproduce too. So "a change to the genome that reduces reproductive fitness" is not a sufficient definition of "error" to provide a description of what error-correcting mechanisms do. Rather, you need a norm, something the genome is meant or intended to adhere to, such that anything that departs from this norm is in error, in order to provide a sufficient definition of "error" for use in describing error-correcting mechanisms.
Of course, if someone thinks that design is an illusion that we're imposing on biology, and if they are consistent, then they must hold that such norms are also illusions that we're imposing, and by extension, that errors and hence error-correcting mechanisms (and all other biological functions for that matter) are illusions – concepts that we're constructing and imposing on the world rather than facts we're discovering about the world that actually need an explanation.
It's a good thing that most ateleologists are not consistent! The whole biological enterprise would cease to exist if they suddenly agreed that they were speaking incoherently by denying and accepting teleology at the same time, and chose to consistently deny it in order to rectify the situation. Or at least it's a good thing until you try to convince them of it, at which point it becomes annoying
Comment by Deuce — February 19, 2007 @ 4:56 pm
February 19th, 2007 at 5:16 pm
Bradford wrote:
I suppose you are free to use words as you wish, but that is not how a molecular biologist would define error. An error is a simply a mistake in the copying of a sequence of molecules. It may or may not enhance reproductive fitness, or it may be a neutral mutation which has no effect.
Comment by jeff_alexander — February 19, 2007 @ 5:16 pm
February 19th, 2007 at 5:23 pm
Salvador wrote:
Salvador,
It makes as much sense to disable the genomic error-correcting mechanisms to learn about their evolvability as it does to disable the genes that build the heart to learn about its evolvability.
Once error-correcting mechanisms are in place, an organism's evolution will move in directions which take advantage of the possibilities opened up by the ability to correct errors, including larger genomes.
Similarly, once the genes are in place to build a heart, evolution can proceed in directions unavailable to an organism with a passive circulatory system.
In both cases, the organism's descendants come to depend completely upon a feature that was originally just a bonus, but this dependence in no way indicates that the feature could not have evolved.
Comment by keiths — February 19, 2007 @ 5:23 pm
February 19th, 2007 at 5:25 pm
One of the difficulties of a discussion of a genome that encompasses putative, precursor types is the inability to nail down what the other side is referring to. Consequently I can be only as specific as theories allow. Clearly experimental results do not document the evolution of an RNA based genome to the point where errors are easily defined much less corrected.
Comment by Bradford — February 19, 2007 @ 5:25 pm
February 19th, 2007 at 5:33 pm
The concept of error is not fully consistent with the idea of reproductive fitness, but more consistent with a teleological viewpoint.
There are endless debates and very good peer reviewed articles and books over why fitness is a poor way to characterize engineering metaphors. The error metaphor is one of them.
Unless one has a conception of the "correct" architecture, one has no concept of error. It is possible natural selection favors errors, like blind cave fish or moles. The error was decay in the eye. It's like a sinking ship or airplane having to jettison functional systems to survive. It is still a broken object and error.
That's why natural selection is such a poor way to view everything in biology, it leads to meaningless or non-sequiter statements.
Much of that gets cleared up when one adopts engineering metaphors with no reference to reproductive success. Allen Orr came to the same conclusion when he ripped apart Daniel Dennett's Darwin's Dangerous Idea.
If an engineer had to identify systems in terms of reproductive fitness alone, he'd go ballistic. The way systems are identified and evaluated is their analogy to known or hypothesized systems. Natural Selection being imposed on the engineering discipline is distasteful. And if study biology in the modern way is like reverse engineering, the lense of natural selection has to be removed from our eyes because it is totally distorting the reverse engineering process.
Comment by Salvador T. Cordova — February 19, 2007 @ 5:33 pm
February 19th, 2007 at 5:34 pm
Thanks for that Jeff but errors that do not decrease reproductive fitness are irrelevant to the issue addressed by the blog; namely the evolution of a balance between change and stability. The stabilization of genomes reflects a capacity to retain functional sequences. It's about the utility of function in the end.
Comment by Bradford — February 19, 2007 @ 5:34 pm
February 19th, 2007 at 5:39 pm
That's an opinion that should be subject to testing. When it is not it becomes dogma. BTW, how could genomic repair mechanisms ever be just a bonus? That's the matter that must be tested rather than assumed.
Comment by Bradford — February 19, 2007 @ 5:39 pm
February 19th, 2007 at 5:45 pm
I won't dispute this but NS is the reigning paradigm and if change is to come about it seems to me you have to challenge the one sitting on top of the hill.
Comment by Bradford — February 19, 2007 @ 5:45 pm
February 19th, 2007 at 5:48 pm
Bradford wrote:
I thought I addressed that issue in my post which said, among other things, "It is not a novel idea that selection can work on a replicator's ability to reproduce itself."
Comment by jeff_alexander — February 19, 2007 @ 5:48 pm
February 19th, 2007 at 5:52 pm
The question I am raising is whether or not sequences that would confer a capacity for self-replication would be retained in the absence of genomic repair mechanisms.
Comment by Bradford — February 19, 2007 @ 5:52 pm
February 19th, 2007 at 6:12 pm
Orr says no such thing in that review, nor anywhere else to the best of my knowledge. Orr certainly criticises Dennett's naive and outdated pan-selectionism, as would any evolutionary biologist. But his alternative is not "adopt[ing] engineering metaphors": instead, he points to the well-accepted role of random genetic drift as a major player (along with selection) in evolutionary change. He emphasises, though, that "[e]volutionists are essentially unanimous that, where there is apparent "Design" in organisms, it is caused by natural selection."
In other words, pan-selectionism is rubbish because much evolutionary change is neutral and random; but features of organisms that appear designed almost always are, in fact, the products of selection.
So I guess Salvador has provided another example of ParaSpinning to add to Mike's collection – or does that term only apply to anti-IDists?
Comment by Mesk — February 19, 2007 @ 6:12 pm
February 19th, 2007 at 6:15 pm
And the answer I am giving is that it's a non-issue: selection acts on the genome which includes its repair mechanisms. Again, selection operating on evolvability is not a new idea. Repair mechanisms are part of the genome. It simply doesn't make sense to separate them, except perhaps in thought experiments (and perhaps in some future real experiment).
Comment by jeff_alexander — February 19, 2007 @ 6:15 pm
February 19th, 2007 at 6:39 pm
And the answer I am giving is that it's a non-issue: selection acts on the genome which includes its repair mechanisms.
So we are told. The truth lies with testing theory.
Again, selection operating on evolvability is not a new idea. Repair mechanisms are part of the genome.
They are more than part of the genome. They are the part that maintains the integrity of the entire genome. Without this part genomes decay- rapidly. The question, that is open to all but ideologues, is whether decay outpaces any selective features that evolve.
Comment by Bradford — February 19, 2007 @ 6:39 pm
February 19th, 2007 at 6:51 pm
True. We observe selection operating with reference to fully functional genomes. The issue for me is what generates such genomes. How does this proceed from a selection paradigm? Citing selection is meaningless in this context without supporting data.
Comment by Bradford — February 19, 2007 @ 6:51 pm
February 19th, 2007 at 7:02 pm
You realize your alternative is essentially an appeal to magic right ?
Comment by thesciphishow — February 19, 2007 @ 7:02 pm
February 19th, 2007 at 7:23 pm
If appeals to very, very lucky coincidences do nothing else they indicate that the advocate for them has departed science in favor of a hope.
Comment by Bradford — February 19, 2007 @ 7:23 pm
February 19th, 2007 at 7:32 pm
Mesk argues: "Orr says no such thing in that review, nor anywhere else to the best of my knowledge. "
If selection does not trade in the currency of design, engineering design (which are designs) cannot be defined or identified in terms of reproductive fitness. I even pointed to the example of cave fish which is exactly the same example Orr references.
Orr referred to Lewontin.
Lewontin makes a devastating case in the failure of selection to be useful to describe biological properties in general:
Santa Fe 2003
Andreas Wagner writes in Robustness and Evolvability in Living Systems:
It's hard to imagine a scientific theory which cannot purport to measure it's most fundamental quantity. This is a horrible situation, on has to wonder if such a theory can be viewed as scientific.
In trying to define what error is, one must define what the basic system that is being compromised by the error.
Wagner proposes rather than using selection to characterize systems (because of the problems laid out above), to describe systems terms of function, and unwittingly applies design principles of looking for engineering analogies and irreducible complexity:
In fact, he sounds more like Behe than Darwin when trying to characterize systems so that one may characterize the meaning of "error".
Finally, I pointed out, conigency designs are designs that are empirically demonstratable to be invisible or almost invisible to selection here: Airplane magnetos, contingency designs, and reasons ID will prevail
In fact, rather than an error correction strategy, there are error toleration strategies like mutational robustness, but these are designs shown to be almost mathematically invisible to selection:
If a error happens in a contingency design it will be invisible to selection. That's another reason selection is a poor method of assess the existence of errors.
Comment by Salvador T. Cordova — February 19, 2007 @ 7:32 pm
February 19th, 2007 at 8:24 pm
Agreed. By all means, let's set up as many experiments as possible which are aimed to knock down the current theory. No holds barred. Either the theory holds up, or gets knocked down in favor of something else. That's science.
Go for it. Set up an experiment which measures the evolution rate of repair mechanisms verses the evolution rate of the rest of the genome. I don't know where you would begin, since they evolved together in a mutually dependent relationship. I am tempted to invoke the metaphor of trisecting the angle, but this is science, not mathematics, so pretend I didn't mention it.
If such an experiment does come to pass, and it demonstrates that ordinary selection is insufficient to explain the results, then a new day will dawn in the history of science. Revolutions do happen from time to time, so who knows, this could be it.
But until then, Darwinian selection is sufficient to explain the current state of evidence (to my knowledge) and does not require the additional hypothesis of a mystical front-loader.
Comment by jeff_alexander — February 19, 2007 @ 8:24 pm
February 19th, 2007 at 8:45 pm
Your assessment is inaccurate. Selection has been used to explain evolution and most biologists would agree that it does so. However it does not explain the origin of life by pointing to empirical confirmation of even the basic contention that RNA self-replicators evolve greater replicative efficiency. BTW, noone with even a small degree of familiarity with DNA repair mechanisms would doubt they are essential. On a cellular level there is no controversy. It is only at an origins level that this even becomes an issue.
Comment by Bradford — February 19, 2007 @ 8:45 pm
February 19th, 2007 at 8:56 pm
Good link Salvador. Backup systems would pose an interesting challenge particularly when the backup is rarely used. Of course METers would claim selection generated them too.
Comment by Bradford — February 19, 2007 @ 8:56 pm
February 19th, 2007 at 9:45 pm
Bradford:
Bradford, from the original post:
Bradford,
You seem to be assuming that ancestral organisms would have required all of the same repair mechanisms as their modern descendants. This is not true. As I mentioned earlier in the thread, the allowable mutation rate is much higher for smaller genomes.
Comment by keiths — February 19, 2007 @ 9:45 pm
February 19th, 2007 at 9:47 pm
No disagreement here. I know of no empirical confirmation that RNA self-replicators evolve greater replicative efficiency. However, I see no particular reason why selection would be unable to do so. Selection does explain the origin of life, but not to the detail that we would wish. That's life (pun intended).
However, I also know of no empirical evidence for front-loading, or for anything which demands an explanation beyond that of ordinary selection. Until such evidence is brought forth, you can expect ID to remain ignored by the mainstream scientific community.
I am not being derogatory. If the evidence ever appears, then believe me, you'll have your day in the sun. A valid concern might be whether anyone will listen. If that is the case, I'll give you my real name and I'll pound down the doors of the peer-reviewed journals for you. But first things first. Produce the evidence.
FWIW, I have enjoyed our conversation.
Comment by jeff_alexander — February 19, 2007 @ 9:47 pm
February 19th, 2007 at 10:07 pm
Life is characterized by an array of different biochemicals having different functions. Selection of RNA based on replication efficiency does nothing to explain why efficient replication of this one biochemical would start a pathway toward a cell. (There are many obstacles to such a theory not even touched on.) Basic to any selection paradigm centered on RNA is an answer to the question of why selection would favor the type of sequence specificity needed to form a minimal cellular gnome. I've asked the question often and never received a response.
Thanks for your contributions to the blog.
Comment by Bradford — February 19, 2007 @ 10:07 pm
February 19th, 2007 at 10:18 pm
Bradford:
Of course. As Jones wrote in his article,
But nobody thinks that gene repair mechanisms are a recent phenomenon. The question is whether they could have evolved at the time they showed up, given the size of the genome and the rate of uncorrected mutations at that time.
So far you have been arguing that repair mechanisms could not have evolved, but must have been front-loaded. Your argument is based on the indispensability of repair mechanisms to modern organisms. My point, which is the same one I made to Salvador, is that the fact that something is indispensable now does not mean that it always was indispensable. And if it wasn't always indispensable, then you can't rule out the possibility of its evolving as you are trying to do.
It's easy to demonstrate. We know that current human genetic repair mechanisms are imperfect, but sufficient to keep the species going. Now imagine that a new repair mechanism evolves that lowers the error rate. We know we don't need it, because we got by for years without it. It's a bonus.
Now fast-forward millions of years. The improved error correction has allowed us to evolve a larger genome with more functions, many of them critical to our survival. Future Bradford argues, "This repair function couldn't have evolved. If we disable it, it kills us. How could it have evolved if it didn't have itself to protect it during evolution?"
Do you see the mistake that Future Bradford is making?
Comment by keiths — February 19, 2007 @ 10:18 pm
February 19th, 2007 at 10:45 pm
So far you have been arguing that repair mechanisms could not have evolved, but must have been front-loaded. Your argument is based on the indispensability of repair mechanisms to modern organisms. My point, which is the same one I made to Salvador, is that the fact that something is indispensable now does not mean that it always was indispensable. And if it wasn't always indispensable, then you can't rule out the possibility of its evolving as you are trying to do.
You have misstated my point which is that repair is necessary to any organism modern or not. It is not modernity that is protected but rather the integrity of DNA. Nucleic acids have fixed chemical properties that do not vary with time. Neither does radiation, chemical reactions or copying errors. The entire set of dynamics would have been present on earth at any point in natural history. The damage occasioned to DNA would have been inevitable without protective mechanisms present at the outset.
It's easy to demonstrate. We know that current human genetic repair mechanisms are imperfect, but sufficient to keep the species going. Now imagine that a new repair mechanism evolves that lowers the error rate. We know we don't need it, because we got by for years without it. It's a bonus.
Now fast-forward millions of years. The improved error correction has allowed us to evolve a larger genome with more functions, many of them critical to our survival. Future Bradford argues, "This repair function couldn't have evolved. If we disable it, it kills us. How could it have evolved if it didn't have itself to protect it during evolution?"
Existing mechanisms are extemely efficient. The base excision repair mechanism alone makes about 20,000 repairs in every cell of your body each day. Could the efficiency become greater? I suppose so but that argument is not analogous to the problem facing an initial genome. Our repair mechanisms are already sufficient enough to ensure the perpetuation of our species. Tweaking them is superfluous from the standpoint of mother nature. OTOH, a protectionless genome is at the mercy of environmental factors and its own imperfect copying capacity. This spells the type of dysfunction that leads to extinction.
Comment by Bradford — February 19, 2007 @ 10:45 pm
February 20th, 2007 at 12:18 am
Bradford,
The evolutionary difference between a bare replication mechanism, and that same mechanism augmented with repair mechanisms, is only one of degree, not of kind. Both of them produce imperfect copies, but the former makes more errors than the latter.
The relevant figure of merit is the number of uncorrected errors that make it through the system. In evolutionary terms, a replication process that makes one mistake per 10,000 codons has the same effect as one which makes 100 mistakes per 10,000 codons but repairs 99 of them.
The fact that repair is or is not happening is irrelevant. The number of uncorrected errors is what matters.
Second point: Your argument still doesn't take the size of the genome into account. The criterion that determines whether "mutational meltdown" happens is the number of mutations per offspring. If species A and species B have the same uncorrected error rate per nucleotide, but species B has a genome which is twice as big as that of species A, then species B will have twice the number of mutations per offspring. This alone may send species B into mutational meltdown while species A continues intact. Species B would require an improved error rate, but species A would not.
Thus, you cannot argue that all life, both modern and ancient, would require genetic self-repair in order to survive. It depends on the size of the genome and the error rate.
Comment by keiths — February 20, 2007 @ 12:18 am
February 20th, 2007 at 3:27 am
Salvador,
You quoted Orr:
And stated:
The first sentence doesn't even make sense – what do you mean by "engineering design (which are designs) cannot be defined or identified in terms of reproductive fitness" Who is trying to define human engineering in terms of reproductive fitness?
I'm forced to return to your initial claim to see if the quote from Orr backs it up:
In fact, even the segment of Orr's review you quoted provides clear support for the opposite view, when he says that "[a]n optic nerve with little or no eye is most assuredly not the sort of design one expects on an engineer's blueprint". In other words, there are features of the natural world can be explained perfectly well from a selection viewpoint but not from an engineering perspective.
You're not going to get very far with this line of argumentation, Salvador – anyone familiar with Orr's work will know that he is well aware of the power of selection in driving adaptive change. Try quote-mining someone else.
Speaking of sloppy quote-mining, you quote Andreas Wagner:
And go on to say:
But of course Wagner doesn't say that fitness can't be measured, but simply that it is difficult to do so, a statement with which any evolutionary biologist would agree. That doesn't stop them from actually measuring fitness, of course: this is in fact done as a matter of routine in dozens of labs, using competition assays and other techniques. And the difficulties associated with defining fitness haven't stopped theorists – like H. Allen Orr, in fact – from deriving models of adaptive evolution that have proved extremely successful in predicting patterns of evolutionary change in experimental systems.
As an aside, the fact that an advocate of ID would criticise evolutionary theory for being unable to measure "it's most fundamental quantity", when the most fundamental properties of ID (the designer, and the mechanisms used to design) are cheerily waved away as unknowable and irrelevant, brought a welcome ray of ironic sunshine into my day.
Comment by Mesk — February 20, 2007 @ 3:27 am
February 20th, 2007 at 6:58 am
The evolutionary difference between a bare replication mechanism, and that same mechanism augmented with repair mechanisms, is only one of degree, not of kind. Both of them produce imperfect copies, but the former makes more errors than the latter.
The relevant figure of merit is the number of uncorrected errors that make it through the system. In evolutionary terms, a replication process that makes one mistake per 10,000 codons has the same effect as one which makes 100 mistakes per 10,000 codons but repairs 99 of them.
The fact that repair is or is not happening is irrelevant. The number of uncorrected errors is what matters.
The number of uncorrected errors in an organism devoid of DNA repair mechanisms is equal to the number of errors. That spells disaster for the affected genome. The difference is not one of degree. It is intolerable decay. To say that both are imperfect and leave it at that reveals a total misunderstanding of the subject matter.
Second point: Your argument still doesn't take the size of the genome into account. The criterion that determines whether "mutational meltdown" happens is the number of mutations per offspring. If species A and species B have the same uncorrected error rate per nucleotide, but species B has a genome which is twice as big as that of species A, then species B will have twice the number of mutations per offspring. This alone may send species B into mutational meltdown while species A continues intact. Species B would require an improved error rate, but species A would not.
Thus, you cannot argue that all life, both modern and ancient, would require genetic self-repair in order to survive. It depends on the size of the genome and the error rate.
The error rates for unprotected genomes are intolerable. A mistake inducing chemical agent affecting two genomes, both stripped of repair mechanisms, and one twice the size of the other, would be expected to produce the same rate of error in both. Seriously Keiths, if you wish to make the argument that repair mechanisms make a difference of degree rather than kind then research the subject matter more thoroughly. You will find that a mutation disabling one protein, involved in a repair pathway containing many proteins, is often sufficient to cause the death of the affected organism. There are lethal diseases, with names attached to them, describing disabling afflictions resulting from semi-functional DNA repair systems. You need not shut them down; merely impair them.
Comment by Bradford — February 20, 2007 @ 6:58 am
February 20th, 2007 at 7:16 am
Mesk, what features of the natural world could not be explained by referencing natural selection. If a system functions nearly perfectly, it is attributed to selection. Imperfection is exactly what one would expect of a non-telic process and disabled functions are eliminated by natural selection. How is selection itself tested? What results are not explained by it?
Comment by Bradford — February 20, 2007 @ 7:16 am
February 20th, 2007 at 7:52 am
Bradford,
Note that I'm stating Orr's opinion there, not necessarily my own. In fact I agree that selection (like intelligent design) is all too often used in an empirical vacuum, as an all-purpose explanation without real content. "Selection did it" alone is no more informative than "the designer did it".
However, selection does provide a greater opportunity for testability than ID, because its mechanisms are transparent, the conditions required for it to operate are known, and its effects on organisms (and importantly, on DNA sequence) can be measured. For instance, we can now use quantitative models of evolution, along with data from comparative genomics and population genetics, to determine with some precision which regions of the human genome have been subject to selection, and even infer the actual types of selection (e.g. purifying, positive, balancing) and the timing of selective events. This can't currently be done for ID, nor (to the best of my knowledge) are there even any active attempts to develop similar approaches for ID.
Comment by Mesk — February 20, 2007 @ 7:52 am
February 20th, 2007 at 8:49 am
Keiths:
The number of mutations that become established at the population level is critical. Population size is one of the main determinants of that; small populations experience a lot of drift, creating noise in the selective process, allowing more deleterious mutations to slip through. Error correction isn't optional.
Comment by Guts — February 20, 2007 @ 8:49 am
February 20th, 2007 at 9:38 am
I would not agree with the last sentence. I believe there are models that could distinguish between selection and a cause that is not attributable to selection. The search for such models should center on anomalies in present theories. That is what evoked my interest in the nature of functional genomes. If you review the comments made it is evident that some think the dynamics of a selection process are primarily one of change. I view it as primarily the opposite with respect to what occurs in the genome itself. If a change in DNA occurs that benefits an organism, the change would be selected i.e. passed on to descendents and then become predominant within a population and most people understand this part of the theory. What many do not understand is an existing conflict between forces promoting genomic disorder and mechanisms maintaining order. The balance we presently observe would either have evolved according to standard paradigms or be the product of design. One thing is evident. At the outset there could have been no symmetry between the balancing forces in an OOL non-design paradigm. Selection would have had to bring it about. But that brings up the question of why that outcome had selective value? We can see the selective value of individual proteins and repair functions in existing organisms because overall function exists. We cannot discern selection from a starting point which leads me to believe the real battleground between ID and non-IDers is at a precellular point in time. It is at such a point that current modes of thinking break down.
Comment by Bradford — February 20, 2007 @ 9:38 am
February 20th, 2007 at 12:46 pm
Am I to understand that everyone in this thread believes that once error rates are optimized, then said mutations are enough to turn molecules into Mozart? Does anyone here think that maybe this whole conversation is about something tangential to the real mechanism of evolution?
Comment by chunkdz — February 20, 2007 @ 12:46 pm
February 20th, 2007 at 3:29 pm
I do, chunkdz, because I believe that mutation rates are optimized wrt ot adaptation. And adaptation and evolution are not necessarily the same thing.
"Why not proceed to the logical next step and hypothesize the front loading of the repair mechanisms needed to maintain the previously cited balance between genomic change and stability. Front loading by design not only explains balance, it explains how a natural barrier to it is overcome."–Bradford
It goes w/o saying that designers (not trying to be provocatively "designer-centric" here) are very interested in designing systems that are capable of recovering from or correcting errors.
I think its a fascinating subject and should be explored in more detail.
E.g., one commonly repeated argument against the IDers (specifically Dembski) is that evolution is not a targeted search. But how is error-correction not a "targeted search" It has already been recognized that such error-correcting systems must be a factor–whther you imagine evolution is a trageted serach or not, life forms do engage in targeted searches and these are factors in evolution–so what could you possible mena by "evolution"
Etc. Etc. Lotsa interesting related matters.
Comment by Rock — February 20, 2007 @ 3:29 pm
February 20th, 2007 at 3:39 pm
Human engineering is not defined in terms of reproductive fitness, and if one is trying to find engineering designs in biology it doesn't make sense to define engineering designs in biology through reporductive fitness either. When we describe the coding and decoding metaphors and error correction in the genome, is it best to describe the system in terms of projecting engineering metaphors to each part or is it more informative to to describe each part terms of its the selective fitness values?
The eye of a cave fish is an excellent example where a projected engineering metaphor is far better to further understanding of a system than trying to describe the eye of a cave fish in terms of natural selection. Say we had a poplulation of seeing fish and then put them in a cave. We would observe that when we disable the eyes of some fish, they might have more reproductive success. How useful is that sort of experiment to understanding fish eyes versus any other sort of analytic method using a reverse engineering approach?
Comment by Salvador T. Cordova — February 20, 2007 @ 3:39 pm
February 20th, 2007 at 3:50 pm
Sorry, Salvador, but the marketing department insists that designs be evaluated according to their "reproductive success." I sympathize with designers and engineers who think the salesman are a bunch of "Philistines" who don't understand design. But I also have a natural sympathy for the salesman–Who pay my salary.
Comment by Rock — February 20, 2007 @ 3:50 pm
February 20th, 2007 at 4:41 pm
Salvador:
Rock:
I think Sal is correct that functions, or designs, cannot be coherently defined in terms of reproductive success. In fact, if we were to literally and consistently define them only in terms of reproductive success, then the only difference between a flagellum and an eyeball that we could note would be the degree to which each one contributed to the differential reproductive success of its host organism. But of course, those aren't the only differences, or even the most notable differences, between them. They work entirely differently from each other, and what we're really interested in is how they work. That isn't to say that they don't contribute to reproductive success, because they obviously do, and they can certainly be evaluated in terms of reproductive success, but they cannot be defined that way, not without throwing most of what's interesting in biology out the window.
Sal:
Or, let's put it this way. If we were to use reproductive success as our only criteria in defining and evaluating function, then we would be compelled to say that the function of the atrophied eyes of blind cave fish was to not see, just as much as we could say that the function of the eyes of regular fish are to see. Neither statement would be more valid, and all we could really talk about was how different genome sequences affect overall reproductive success. But, of course, this is counterintuitive and simply isn't what anybody means by "function". Rather, we are inclined to say that the cave fish have lost the function of sight. We are interested in learning how regular fish eyes work, not in how dwindled cave fish eyes don't work, even though not seeing may be just as much a reproductive advantage for the cave fish as seeing is for the regular fish.
Comment by Deuce — February 20, 2007 @ 4:41 pm
February 20th, 2007 at 5:22 pm
I agree with you, Deuce, there are different ways to evaluate the "success" of a design. Evolutionary theory does (or should) take that into account. A design is to be properly evaluated in a (possibly quite complex) context. Reproductive success is important to the salesmen. But it may be of zero importance to me, the designer of the system. I have other criteria for evaluating the "success." Salvador?
The immediate object of my (the designer's) purpose is to reproduce exactly one unit of the design. The salesman wants as many as he can sell. That's why I design for reproducibility. Reproducibility is a constraint upon design that is too little appreciated. It is physically impossible to reproduce a van Gogh. It's quite possible to reproduce a Buick.
But there is a bit of the van Gogh in the Buick"”especially those late 50's models.
LOL Did I just say we are more Buick than van Gogh? (I did!)
(What that has to do with error-correction I don't know.)
Comment by Rock — February 20, 2007 @ 5:22 pm
February 20th, 2007 at 6:34 pm
"Is evolution possible without a means to limit damage to genomic sequences having selective value?"
Yes. Look at retroviruses and RNA viruses. They evolve very rapidly.
Viruses replication is host dependent. Hosts are dependent in turn on genomic fidelity made possible by DNA repair mechanisms. Without such mechanisms viruses replication would last only as long as their hosts survive- not very long.
Comment by Bradford — February 20, 2007 @ 6:34 pm
February 20th, 2007 at 6:38 pm
Agreed
Good question.
Comment by Bradford — February 20, 2007 @ 6:38 pm
February 20th, 2007 at 6:45 pm
What do you have in mind as the indicator of a norm? For example, would the norm for human eyesight be 20/20 vision? In general how is this determined?
Comment by Bradford — February 20, 2007 @ 6:45 pm
February 20th, 2007 at 6:59 pm
Yet Orr says in your own quote of his review:
Can we now agree that this claim of yours was completely false:
All I want is a frank admission of error, Salvador. I don't care about your opinion on whether engineering is a better metaphor for a cave fish's eyes than selection – I just want you to admit that you were wrong to claim that Orr's review supported this opinion.
Comment by Mesk — February 20, 2007 @ 6:59 pm
February 20th, 2007 at 7:17 pm
Bradford:
I agree. Consider the rabies virus:
It's not going to replicate and exist without proteins. And these proteins are not going to exist without ribosomes (just one part of host). Thus, the virus is completely dependent on the ribosome for its existence, yet it's up to the cell to maintain and propagate the ribosome independently across deep time. All of this leads to a simple question "“ why is it that viruses don't bring their own viral ribosomes along with them?
Comment by MikeGene — February 20, 2007 @ 7:17 pm
February 20th, 2007 at 7:19 pm
1. Can you point me to active research into the development of explicit, testable models that will allow the identification of design events from DNA sequence data?
2. The idea that models of ID should focus on anomalies in existing theories is a terrible idea. Anomalies in existing theories could easily represent natural processes as yet unexplained. Models of ID need to take the example of models of selection, and look for specific, objective, measurable signatures of design.
In fact the theoretical basis of purifying or stabilising selection (the force that maintains essential regions of genomes against the buffeting winds of mutation) is very well-characterised and is the basis of existing algorithms to detect conserved functional regions using comparative genomics – the area of theory that still needs most work is the adaptation process (the bit you say "most people understand"). H. Allen Orr, who Salvador quote-mined above, is one of those leading the charge in developing these models.
I agree that IDists need to focus on OOL, because it's becoming increasingly difficult to find room for the designer at any point in the following 3.8 billion years (with the possible exception of the Cambrian explosion).
That said, I think you are making the traditional IDist mistake of assuming that the first error correction mechanisms must have been similar to the existing, rather elaborate mechanisms. In fact the first error correction mechanisms must have been exceedingly simple – small changes to polymerases that increased replicative fidelity, cellular mechanisms that excluded contaminants and increased the concentration of the appropriate nucleotides, and so on. Small genomes can handle surprisingly high error rates, as testified by the HIV genome (your point above about host error correction is irrelevant – the fact that the HIV genome itself can survive in a hostile environment with a huge mutation rate indicates that small RNA genomes could have done the same in a non-host environment close to the OOL). Of course, any small mechanism that increased fidelity would have been immediately favoured, because it boosted its own probability of viable replication.
I'm not saying these questions have been answered definitively – as I've said before, I see ID as a live (if not likely) possibility for the OOL – but they're not the killer blow for a naturalistic scenario that you imagine.
Comment by Mesk — February 20, 2007 @ 7:19 pm
February 20th, 2007 at 7:21 pm
Did you soak that in Smokey.
Comment by Bradford — February 20, 2007 @ 7:21 pm
February 20th, 2007 at 7:26 pm
No. You failed to quote the relavant portion of the Gammarus minus paragraph.
"the kind of Design we associate with engineering" How do you associate a design with engineering except by projecting an engineering metaphor upon it and seeing how it stacks up? Therefore you can hardly boast that this claim by me was completely false in interpreting Orr:
Selection is a waster and destroyer of engineering design. The Orr cited the optic never of Gammarus minus an example of an engineering design destroyed by natural selection.
The fact that as Orr says the artifact deviates from "an engineer's blueprint" is exatly pointing out that it is in reference to enineering blueprints we identify operational design. And with reference to engineering blueprints we define failed or dysfunctional designs.
Orr is showing the Gammarus minus optic nerve are the remnants of a failed or broken design. Exactly the way we conceive of the concept of "error".
Furthermore, regarding selection, we have the "adaptation" of sickle cell anemia. By most accounts this is broken function, but just because we can find malaria rich geographical regions where this "adaptation" is selectively favored, does that make sickle cell anemia a non-error but rather a feature. As programmers like to say, "it's not a bug, it's a feature".
So, I don't agree with your interpretation of Orr. "Selection does not trade in the currency of design". It is via reverse engineering methods that functional designs are measured and failed designs or relics are identified. Orr seems to see that rather well, he even uses the right words: "engineering" "blueprint" "design"
I think you have a weak case to say my claims are completely false. You may just not like my interpretation.
Comment by Salvador T. Cordova — February 20, 2007 @ 7:26 pm
February 20th, 2007 at 7:29 pm
With a simple answer – because they don't need to. Viruses are subject to exceptionally strong selection for genomic streamlining due to the need for rapid replication, so any gene that isn't completely required for viral survival or reproduction will be shed. If a virus (or any other parasite) can rely on the host to perform any of its functions for it, it will. This is a trend seen in all parasitic organisms, including bacteria and eukaryotes. And I guess the classic example of gene loss in an intracellular parasite is mitochondria, which have shed genes like crazy as they adapted to their host cell environment until they have only a handful of absolutely essential genes on a tiny chromosome.
Comment by Mesk — February 20, 2007 @ 7:29 pm
February 20th, 2007 at 7:44 pm
Salvador,
I agree that biological structures can be analogised (sometimes usefully) to human engineering designs; biologists do it all the time. The question is whether this analogy provides useful information about the origins of these structures, or whether selection is the better explanation. Orr clearly believes the latter. While he agrees that some biological features look designed, again and again he states that a closer look reveals that these engineering metaphors break down in the face of biological reality, where selection reigns.
Meanwhile, you seem to be unable to prevent yourself from exaggerating the message of literally every statement you quote. Earlier you turned "fitness is difficult to measure" into "fitness is difficult to measure". Now you magically convert "Selection [...] is just as happy to lay waste to the kind of Design we associate with engineering as to build it" into "Selection is a waster and destroyer of engineering design." Orr clearly argues that selection can explain the origins of engineering-style design in biology as well as its destruction (as would be expected, since selection simply does what is required for generation-to-generation survival). You ignore the former and pretend the latter is all that counts.
I guess I've been spoiled here at TT for the last year or so – people here tend not to employ the dirty tricks of quote-mining and empty rhetoric that characterises the creationist camp. I'd almost forgotten that these tactics existed. It's a real shame you've decided to ruin my happy illusion, Salvador.
Comment by Mesk — February 20, 2007 @ 7:44 pm
February 20th, 2007 at 7:46 pm
Hi Mesk,
You replied to Bradford as follows:
I hear ya, but I don't think it is that clear such genomes are relevant as such. These viral genomes survive, across time, because they are deeply embedded in a sophisticated protein-world. Consider what is involved to keep the largest RNA genome going. http://www.onderzoekinformatie...
I agree with you about the "killer blow" point, but I also think Bradford may have his finger on something.
Yes, but this is basically a philosophical answer that might mask a more interesting problem. It would seem to me that a virus that has its own stream-lined ribosome would out-compete a virus that was relying on the slow eukaryotic ribosome (or for that matter, they could bring a tinkered bacterial ribosome along with them, as they are about 5-10 times faster that eukaryl ribosomes). Or, the virus, over time, could capture ribosomal genes and incrementally redesign the host's ribosome for speed. Viruses are exquisite evolution labs (heck, they are a mechanism of evolution), and this evolution, however unlikely, only had to happen once in the few billion years.
Yet the mitos keep their ribosomes and stream-line them.
Comment by MikeGene — February 20, 2007 @ 7:46 pm
February 20th, 2007 at 7:50 pm
Or anomalies could represent a yet unexplained design process. That's the point of the focus. Why settle for the default answer?
I'm not assuming anything other than that error inducing factors were present on earth at the outset. Refutation by imagination is poor strategy. Exclude contaminants? How do cells exclude radiation, deamination or by-products of cellular respiration. I know the response chiding me for assuming that… The trouble is my estimates are based on what we know and hypothetical counterpoints may or may not exist anywhere but in the human mind. Increase the concentration of appropriate nucleotides? What good does that do when the ones composing a genome are damaged. Got to have some way of making repairs; recognition; excision; synthesis; repairing strands…
Replication is not only relevant; it is the central theme. How do your putative RNA genomes evolve without a means of replication?
Comment by Bradford — February 20, 2007 @ 7:50 pm
February 20th, 2007 at 7:51 pm
Bradford,
One thing to consider with error correction is that for a small organism, this imposes an enormous metabolic load relative to an organism with no error correction.
We have a catch-22 situation. Here are two scenarios:
1. The genome is highly tolerant of errors, and viable organisms still result. The result is that flawed organisms replicate faster than unflawed organism because of the metabolic load associated with error correction. This is especially pronounced for small primitive replicating environments. The net result is error correction doesn't have sufficient selective advantage to overcome selective disadvantage from metabolic load.
2. If the organism is highly intolerant to errors, then it dies without error correction.
#1 might be solvable, but as a general principle for small genomes, what do we see when organism compete for better metabolic efficiency? A tendency toward a smaller genome, and no error correction. But even with large genomes, like the cave fish, we see the metabolic cost of error correction indirectly. The cave fish that allowed the error of an atrophied eye to propogate was favored by natural selection. One cannot make the general case that selection and reproductive success favors error correction, except in cases where the absence of error correction is lethal. But if such errors are lethal, how did the organism survive to evolve??
Comment by Salvador T. Cordova — February 20, 2007 @ 7:51 pm
February 20th, 2007 at 8:11 pm
Salvador: as a general principle for small genomes, what do we see when organism compete for better metabolic efficiency? A tendency toward a smaller genome, and no error correction.
Ah hah. So selection favors downsizing. But that is counter to what we observe on planet earth. So how did these large complex genomes come about?
Comment by Bradford — February 20, 2007 @ 8:11 pm
February 20th, 2007 at 9:10 pm
Building a functioning ribosome (even a bacterial one) takes a lot of genes – so the cost of carrying that excess baggage will almost certainly outweigh the replicative benefits. (From my point of view, the fact that viruses haven't yet come up with a better solution suggests that either there isn't one, or if there is it's hidden behind a huge fitness valley.)
Perhaps a more interesting question from an OOL perspective is why viruses haven't come up with an extremely stream-lined (non-ribosomal) system for translating RNA into protein that required only a few components, as must have been the case for the earliest life. My guess is that there is a major efficiency cost to stream-lining the translation machinery, such that the virus is always better off hijacking the host machinery (however cumbersome) than relying on a simpler but slower autonomous system. For the earliest life, a simple but inefficient translation system was acceptable, but such a solution simply wouldn't cut it in the fast-paced world of viral replication.
No they don't – mitochondrial ribosomes contain at least 55 proteins, most of which are encoded by the nuclear genome. A couple of rRNA genes does not a ribosome make, Mike. Mitochondria are just as reliant on their host cells for translation as they are for anything else.
Comment by Mesk — February 20, 2007 @ 9:10 pm
February 20th, 2007 at 9:12 pm
Mike,
I've got a comment in the moderation queue for some reason – can you please approve it?
While I'm on the topic, can Guts or someone else let us know exactly what it is that triggers the moderation trap? I try to avoid cussing, pornographic images and advertising erectile dysfunction treatments, but that doesn't seem to be enough.
Comment by Mesk — February 20, 2007 @ 9:12 pm
February 20th, 2007 at 9:16 pm
Mesk:
That might be the problem, Mesk.
But seriously, what is a "moderation queue" And shouldn't I know about it? I mean, I have power, now. How am I supposed to use it?
Comment by Bilbo — February 20, 2007 @ 9:16 pm
February 20th, 2007 at 9:22 pm
Because selection only favours stream-lining under conditions where stream-lining is possible. Parasites and RNA molecules evolving in the lab exist in extremely stable environments, packed with molecules that can be hijacked to aid their replication. Most organisms don't have these luxuries; they live in hostile, nutrient-poor, changeable environments. Such environments favour the development of complex, robust, flexible systems for coping with a variety of conditions. Stream-lined genomes simply don't survive in most real-world environments; they're specialists, completely (and usually irreversibly) adapted to a single, simple environment.
Look at it this way: boiled down, selection is just a mechanism for transferring information from an organism's environment into the organism itself. A simple environment results in a simple organism; a complex environment results in a complex organism. And of course once you have a few organisms in the same area, they each add to the environmental complexity of the others. Over time, you get a positive feedback loop that tends to favour the generation of ever greater complexity. But give an organism a chance to live in a simple, comfortable environment, and the first thing selection will do is throw away anything that isn't required.
Comment by Mesk — February 20, 2007 @ 9:22 pm
February 20th, 2007 at 9:24 pm
Aargh, now I have a second post in the queue! C'mon, guys, how can I stop this from happening in the future? It's hard to have a real-time conversation when half your posts get delayed.
Comment by Mesk — February 20, 2007 @ 9:24 pm
February 20th, 2007 at 9:26 pm
Blame me, I'm still using the old way of keeping spam out of the threads, leaving smart moderation on (which sucks) instead of using a proper spam pluggin. I will try to fix this asap.
Comment by Guts — February 20, 2007 @ 9:26 pm
February 20th, 2007 at 9:53 pm
Thanks Guts, that would be much appreciated.
Comment by Mesk — February 20, 2007 @ 9:53 pm
February 21st, 2007 at 1:14 am
Bradford,
Sure, they could represent a yet unexplained design process – but unless you have a positive assay for the signature of design how will you ever know?
Again, the utility of selective explanations is that they can often actually be tested, because selection leaves a clear, quantitative imprint in an organism's genome. But your strategy for detecting ID would be to simply point to anomalies and say, "Look! That could have been design!" That's not useful; it tells us nothing about the actual probability of design as an explanation, or its characteristics (e.g. timing, mechanisms). What you need is a model of design that would result in specific, measurable effects on the properties of organisms – until you have that, all you're doing is guessing that design might explain some features of living organisms.
Comment by Mesk — February 21, 2007 @ 1:14 am
February 21st, 2007 at 1:44 am
No he does not clearly argue that natural selection can explain the origin of engineering style design. He merely asserts Natural Seleciton can design without justifying it. He however justifies via empirical evidence Natural Selection can destroy. I only ignored Orr's vaccuous assertion and kept the good part.
Comment by Salvador T. Cordova — February 21, 2007 @ 1:44 am
February 21st, 2007 at 1:49 am
Bradford,
Keiths last post was totally off topic. I'm happy to defend myself from his flimsy charges, but this is not the place. TT is welcome to dump Keiths post to the memory hole and we can take it up there or somewhere else.
Sal
PS to Keiths
What's the matter, Keiths, running out of counter arguments to the topic at hand? Time to resort to red herrings and misrepresentations?
Comment by Salvador T. Cordova — February 21, 2007 @ 1:49 am
February 21st, 2007 at 2:34 am
Orr's work (and that of thousands of other competent evolutionary biologists) provides plenty of evidence for the utility of natural selection in driving adaptive change – your unwillingness to deal with that evidence is irrelevant. Fortunately, most of the pro-ID posters here at TT don't share your selective blindness.
But I'm not going to be drawn into a slanging match (especially not on the same day that Vivid kindly said "Mesk does not attack the person but the science" and "you and others could learn from Mesk"!). I've demonstrated that your interpretation of Orr's review was misleading, although I guess it's unreasonable to expect you to publicly admit it. I've also pointed out that your quotations from Wagner were also interpreted in a similarly misleading fashion. I'm happy to let the discussion stand at that.
Comment by Mesk — February 21, 2007 @ 2:34 am
February 21st, 2007 at 2:35 am
I have always found Sal to be very polite in his discourse and certainly not dishonest. The same thing can be said about Mesk. They see things differently and on this one I sort of side with Mesk. However we sometime might go overboard to make our points that does not mean we are intentionally dishonest. I think you are way over the line here Keith.
As for your other citations your joking right.. Other than TT what would you expect from those sites that Sal is a good guy? As for TT here is how Sal responded.
I would think he followed up on his promise.
Comment by Vividbleau — February 21, 2007 @ 2:35 am
February 21st, 2007 at 3:17 am
But your strategy for detecting ID would be to simply point to anomalies and say, "Look! That could have been design
No Mesk, that is your depiction, not my strategy. Within the context of this specific blog topic, a strategy for detecting ID would involve assessing information flow. A natural selection paradigm would indicate a positive flow over time i.e. a net increase. If in place genomic repair mechanisms are a prerequisite to a positive flow of information, then OOL is DOA and a stagnant increase in information among RNA replicators should so indicate this to be the case.
Comment by Bradford — February 21, 2007 @ 3:17 am
February 21st, 2007 at 3:48 am
Mesk: Because selection only favours stream-lining under conditions where stream-lining is possible. Parasites and RNA molecules evolving in the lab exist in extremely stable environments, packed with molecules that can be hijacked to aid their replication. Most organisms don't have these luxuries; they live in hostile, nutrient-poor, changeable environments. Such environments favour the development of complex, robust, flexible systems for coping with a variety of conditions. Stream-lined genomes simply don't survive in most real-world environments; they're specialists, completely (and usually irreversibly) adapted to a single, simple environment.
You write: "selection only favours stream-lining under conditions where stream-lining is possible." When you look at an initial condition where zero genomes exist what makes streamlining possible and what is it that is streamlined?
Comment by Bradford — February 21, 2007 @ 3:48 am
February 21st, 2007 at 4:24 am
So far we are on the same page. We have common ground in thinking that an existing, functional genome allows for change and adaptation. That selection would weed out lethal changes and favor advantagous ones is not in dispute. Where we part company is your belief that biological structures reveal a selection paradigm is favored as an explanation for the origin of life. If I recall correctly I believe Orr indicated that asking what is the purpose of something within an engineered system made sense and then using the example of male nipples as a biological feature he inferred a lack of purpose (function) from a non-telic viewpoint. Is that your understanding too? If so I think this illustrates an example that could equally satisfy two conflicting versions of origins.
A biological feature, affording no benefit, can be argued as the likely result of a selection process that is not 100% efficient and not teleological. OTOH, it is consistent with a design paradigm that would invoke qualities other than functional utility as a causal source; namely, an appearence that is more asthetically pleasing to a designer.
I have a more basic objection to imputing selection at point of origins. It is not suggested by biological properties of life's organisms. A genome replete with mechanisms allowing for its expression fulfills a theoretical prerequisite for replication and the perpetuation of life. I believe von Neumann was on the right track in believing that a distinct transcript makes possible the replication of a cellular automaton. Other than a faith in the necessity of a non-telic process, what is it about cellular biological entities like nucleic acids, proteins and an encoding convention that correlates sequence specificity to function in these biochemicals, which suggests selection as an initial causal factor?
Comment by Bradford — February 21, 2007 @ 4:24 am
February 21st, 2007 at 6:36 am
Hi Mesk,
I agree. And this is where Bradford's point may come into play "“ the cost of carrying the genes needed to make a ribosome.
Good points. Yet some think that viruses best reflect those earliest life forms. In that case, the question is not simply why they have not come up with a simpler protein synthesis strategy (which is a good one), but why did they lose all traces of it.
As for the mitochondria, yes I'm aware of the facts you pointed out. I was just pointing out that mitochondria have kept their ribosomes.
Comment by MikeGene — February 21, 2007 @ 6:36 am
February 21st, 2007 at 6:49 am
How could this be measured in practice?
I don't believe stream-lining would have been favoured under the conditions experienced by the first cellular organisms. Replicative efficiency would not have been a major selective pressure as competition for resources would have been minimal.
Actually, I'm agnostic about the OOL, since there's insufficient information to make any firm judgement about that distant period in time. I favour a naturalistic origin because it fits with my general world view and I think it's plausible, but I freely admit that's not an evidence-based viewpoint.
Other than the circumstantial observation that naturalistic evolution accounts well for the rest of biological history, very little, IMO. Our information about the OOL is simply too limited to draw any solid conclusions.
Comment by Mesk — February 21, 2007 @ 6:49 am
February 21st, 2007 at 6:57 am
Well, I provide at least one possible answer for that in the statement you quoted: the simple translation systems used by early life simply weren't as efficient (or accurate) as the more complex, unwieldy modern ribosomes. As soon as the efficiency of the host machinery outweighed the fitness cost of carrying autonomous ribosomes, viruses would have shed their protein synthesis machinery in a couple of generations.
By the way, I think viruses are generally a pretty poor analogy for the first life – you can use them to make some broad points, but the metaphor breaks down fairly rapidly when you get into the details.
Comment by Mesk — February 21, 2007 @ 6:57 am
February 21st, 2007 at 1:47 pm
Keiths-
Do not make comments about others on this blog including your view of their honesty or integrity. Stick to dealing with the arguments or comments they make. If you cannot do that then stay away.
I'm going to respond to the on topic part of your post which was sent to the hole. You wrote:
Bradford,
You ask whether it is our "faith" in the necessity of a non-telic process that leads us to believe that selection, rather than design, was the operative force in the origin of life.
My answer is that it is not faith but Occam's Razor, and a desire to maintain scientific progress, that keeps us from invoking a designer unnecessarily. We have explained why a repair mechanism is not necessary for small genomes. Why then insist that a repair mechanism is needed at the origin of life, and furthermore invoke a designer to explain this unnecesary feature?
Occam's Razor applies when you have a choice between different answers. In the matter we were discussing (the origin of life) there have been no plausible answers and a reason for that, in my view, is the exclusionary and artificial nature of the rules of evidence that some adhere to. Intelligent inferences are made in other areas. It's a matter of whether the evidence fits the conclusion drawn.
Comment by Bradford — February 21, 2007 @ 1:47 pm
February 21st, 2007 at 1:53 pm
Comment by Doug — February 21, 2007 @ 1:53 pm
February 21st, 2007 at 1:58 pm
Mesk: How could this be measured in practice?
It might not be easily done with regard to replicating RNA but there are patterns that correspond to specific functions. It might be the secondary sequence of a functional polypeptide, the location of a a stop codon, DNA sequences associated with promotors etc. Disabling mutations disrupt genomic patterns. DNA damage would be expected to disrupt acquired patterns about as quickly as they form. IOW, in the absence of repair mechanisms one would expect to find a tendency toward randomness from a starting point of specified patterns.
Comment by Bradford — February 21, 2007 @ 1:58 pm
February 21st, 2007 at 2:00 pm
Hi Doug. I'll send the requested information.
Comment by Bradford — February 21, 2007 @ 2:00 pm
February 21st, 2007 at 4:55 pm
In small RNA genomes (as seems likely to have been the case for the first cells) what is the error rate that results in error catastrophe? Is this known?
It may well be that for small genomes the unrepaired error rate can simply be taken care of by selection weeding out deleterious variants, but I don't know for sure – do you?
Comment by Mesk — February 21, 2007 @ 4:55 pm
February 21st, 2007 at 5:15 pm
I don't know that their are available answers. Any weeding out process needs to be balanced by a level of replacement that avoids extinction. Since cells have repair mechanisms and precursor cells are theoretical constructs testing requires no small degree of resourcefullness. However, the idea that competing and opposite forces should be measured against one another appears sound.
Comment by Bradford — February 21, 2007 @ 5:15 pm
February 21st, 2007 at 8:53 pm
Bradford writes:
We do have a choice. We can choose the design hypothesis, and shut down all of the origin-of-life labs, or we can continue looking for a naturalistic explanation.
Where Occam's Razor comes into play is that you've invoked a hugely complicated designer solely to explain where error-correcting mechanisms came from in life's early history. Talk about "multiplying entities beyond necessity"!
Mesk:
RNA viruses maintain a genome of up to around 30,000 base pairs with no error correction at all. This may be close to the maximum for uncorrected RNA — some of the best antiviral drugs work by increasing the mutation rate and pushing the virus into error catastrophe.
Comment by keiths — February 21, 2007 @ 8:53 pm
February 21st, 2007 at 9:24 pm
We do have a choice. We can choose the design hypothesis, and shut down all of the origin-of-life labs, or we can continue looking for a naturalistic explanation.
Why would we want to shut down labs? That silly canard resurfacing again? Exploring the nature of design is where the real fun begins.
Where Occam's Razor comes into play is that you've invoked a hugely complicated designer solely to explain where error-correcting mechanisms came from in life's early history. Talk about "multiplying entities beyond necessity"!
I have not invoked anything other than the suggestion that a hypothesis be tested. If the results coinfirm my suspicion then we would have to adjust our view of the natural world. If not then it's back to the drawing board. No big deal. That happens when our curiosity is not shut off by our fears.
RNA viruses maintain a genome of up to around 30,000 base pairs with no error correction at all.
That genome comes replete with protein encoding genes (in an RNA world?) and its host allows for its expression. IOW, the viral evolution spoken of is cell dependent. Not a good scenario for prebiotic testing.
Comment by Bradford — February 21, 2007 @ 9:24 pm
February 21st, 2007 at 9:58 pm
Bradford:
If the designer simply made something because he wanted it that way, and if speculations about motives or optimality are off-limits, then what is there to explore?
And your hypothesis invokes a hugely complicated designer, who might even be God, when you haven't even shown that a designer is necessary — only that we don't yet have an explanation for the OOL. That's the classic "designer-of-the-gaps" fallacy.
What results would confirm your suspicion? You haven't presented a testable model of design. The only thing that would confirm your view would be the failure of naturalistic theories of the origin of life. Again, it's the designer-of-the-gaps fallacy.
Of course, because we have no non-viral examples of RNA-based life. The point is not that RNA viruses are a good model of primordial life, but rather that a 30 kb genome can be maintained with no error correction.
For you to argue that error correction would have been required at the origin of life, as you have been throughout this thread, you'll need to demonstrate that a 30 kb genome is insufficient to maintain non-viral life under primordial conditions.
Comment by keiths — February 21, 2007 @ 9:58 pm
February 21st, 2007 at 10:19 pm
Nature. What else? We have to figure out how it works and we have a long way to go.
A complicated designer who might be God? Have you been reading your Bible again?
Replicating organisms without DNA repair mechanisms would lose their genomic integrity. If genetic information is lost faster than it can be created then you have some serious thinking to do.
Even that asssumption is problematic. Over geologic time frames DNA decays. One of the reasons it does not decay faster is that mutagens resulting from cellular processes and replication error are minimized in that the host assumes these functions. This does not bode well for the arising of cellular organisms.
I gather you've located such an RNA genome in cells.
Comment by Bradford — February 21, 2007 @ 10:19 pm
February 22nd, 2007 at 1:26 am
Bradford,
I get the feeling you're neglecting the role of selection in this process. Self-replicating DNA (or RNA) will only "decay" (i.e. lose function) over time if the rate of deleterious mutations outweighs the ability of purifying selection to remove them from a population.
As keiths points out, the existence of large RNA genomes in the absence of proof-reading suggests that selection is sufficient to outweigh deleterious mutations, even in the absence of proof-reading.
If I were you I'd be focusing on the argument that the first polymerases were likely extremely low-fidelity, rather than the fact that no error correction mechanisms existed. Existing RNA viruses suggest that the latter is dispensable, but provide no evidence for the ability of genomes to persist if the actual replication process has poor accuracy.
Comment by Mesk — February 22, 2007 @ 1:26 am
February 22nd, 2007 at 12:07 pm
"As keiths points out, the existence of large RNA genomes in the absence of proof-reading suggests that selection is sufficient to outweigh deleterious mutations, even in the absence of proof-reading."–Mesk
Except that the replication of viral genomes is subject to the same error-proofing operations that work inside cells. Which illustrates a very important principle to understand: A genome, or a cell, or the insides of any living thing, or a community of life forms is also a selective environment. ((That's important to understand because it explains some of the "streamlining.")
Natural selection is not a principle that is correctly (certainly not completely) described as a set of conditions that exist outside of or independently of a life form.
(We can do that, e.g., I can determine the rate/frequency with which nucleotides "denature" under a range of conditions that are not biologically relevant. But what would the point?–since I think (presumptively) it isn't just the nucleotides themselves, but the rate-frequency with which they denature or mutate under biologically relevant conditions that was selected.)
And what, after all, is the process of natural selection? It's an error-correcting process.
Natural selection is just the basic principle that there exists a set of conditions (constraints or requirements) upon the existence (reproduction) of anything. It makes no difference if you believe it (whatever "it" is) was created or designed or evolved. At the most basic level natural selection is just the trivial observation that anything that exists (or continues to exist, persists) must conform to a set of conditions necessary for its existence. (Snowballs don't exist in hell.)
Creationists and other IDers, I believe, object to natural selection because we often attribute to natural selection "creative" powers and abilities that we have not demonstrated. Instead mostly what we observe is natural selection acting as "engineer-as-tinkerer." This is just the continual, "experimental" design process of refining a set of existing solutions (a genome) to bring it ever into closer conformity (fit as in fitness) with its own (intrinsic) and independently given conditions (constraints) that effect its vital structures and processes.
Of course, demonstrating the ability of natural selection involves a bit of a dilemma, because the experimental demonstration is a design recipe, a plan, a blueprint, a pattern that a designer can use to reproduce the object or process in question. (Per the usual requirements of scientific reproducibility.) IOW an experimental demonstration of the power of natural selection is also a demonstration of the power of design. (IDers and other creationists often just do get this.) That's why evolutionists think of natural selection as a "virtual designer." All we show is that artificial selection can do what natural selection can do! (Obviously the converse is not demonstrated, not necessarily true.)
Creationist and other IDer arguments against natural selection are subversive of their hero's, William Dembski's, argument! Remedial ID 101: Go back and look at CSI, Dembski's "explanatory filter"! You've a overlooked something very important. It includes both "chance and necessity" as prior conditions or requirements. Anything and everything (material that we know of) is subject to those conditions"”which, of course, are identifiable with natural selection. Nothing that hasn't been naturally selected passes through Dembski's filter.
Comment by Rock — February 22, 2007 @ 12:07 pm
February 22nd, 2007 at 2:01 pm
As Rock correctly points out selection is an error correcting mechanism but it is the one of last resort and it is meaningless in the absence of a means of replication.
Think about what you wrote. Existing RNA viruses provide no evidence for the ability of genomes to persist if the actual replication process has poor accuracy. You could have added if the actual replication process is non-existent for that occurs when host organisms are bereft of repair mechanisms.
If you wish to pursue your point that RNA genomes are viable and contend this is meaningful in an evolutionary context, you need a cell that is functional without DNA, able to replicate and able to outsource its metabolic activity. Your point is not unlike that of average Joe who contends he can beat the heavyweight champion of the world. When you approach ringside to see the actual fight you find the champ with both his hands tied behind his back.
Viral genomes are protected from mutagenic effects brought about by essential cellular functions. These functions, which indirectly enable the replication (and evolution) of viruses, are safely compartmentalized in the host cell. The existence of the host cell itself is made possible by DNA which is heavily repair dependent. Host DNA indirectly ensures the integrity of required RNA viral functions. So sure, make your case that evolution is possible withour repair mechanisms. But also ensure that the champ's hands are tied and that no damage is possible because an irrelevant phenomenon has been cited in an effort to circumvent obstacles to cellular evolution.
Comment by Bradford — February 22, 2007 @ 2:01 pm
February 22nd, 2007 at 11:05 pm
The high error rate of RNA places an upper limit to its size, because low fidelity replication makes it difficult for a long stretch of genetic material to preserve function. Therefore, it's not that small genomes can handle surprisingly high error rates; rather, it's that large genomes must evolve lower error rates.
Comment by Guts — February 22, 2007 @ 11:05 pm
February 22nd, 2007 at 11:16 pm
Hi Guts. My reaction to this is what selective pressure would be pushing in the direction of larger RNA genomes? Salvador cited experimental results indicating that smaller RNA has selective value. We have yet to see experimental results indicating that RNA alone is suitable for cellular function.
Comment by Bradford — February 22, 2007 @ 11:16 pm
December 9th, 2007 at 7:52 am
Hi,
Love this blog, been a lurker for a while, thought I'd try and contribute something. This might be the most appropriate place to post this.
):
An ID-friendly research proposal. (Thanks to Mike Genes' insightful thought about the Biotic reality
Epigenetic control of transversion and transition mutations and their effect on protein geometry and functionality.
Any thoughts?
Thank you
Comment by Telicmeme — December 9, 2007 @ 7:52 am
December 9th, 2007 at 11:41 am
Hi Telicmeme. (What a great moniker.)
From the link:
As one who believes that mutations in unicellular organisms are not random this proposal is particularly intriguing. This was my first visit to your blog and I'll revisit it and study it carefully. The work put into it deserves the attention. Thanks for the comment.
Comment by Bradford — December 9, 2007 @ 11:41 am