Front-loading with Homeodomains
by MikeGeneFor years, I have been trying to flesh out the conceptualization of front-loading evolution at the origin of life. A working hypothesis has been that the first cells (uni-cellular life forms) were front-loaded with information that would facilitate the evolution of multi-cellular life. One possible candidate for such front-loaded "˜information' would be the homeodomain proteins. These proteins play essential roles in metazoan development and are considered part of the developmental toolkit as outlined by biologist Sean Carroll.
A few months ago, a study was published that outlines data and arguments that perfectly resonate with my front-loading views. Let's have a look.
September 25th, 2007 at 2:33 am
But Mike clearly you must be wrong because you are really just a secret fundamentalist trying to get creationism taught in public schools. Trust me Nick Matzke will back me up 100% on this.
Interesting discovery though. Given it can't be true there must be something else going on, but it sure looks like your idea may be bearing fruit, even though we know this is impossible because you are a fundamentalist.
Comment by thesciphishow — September 25, 2007 @ 2:33 am
September 25th, 2007 at 4:37 am
Mike,
You wrote:
The question is not whether the homeodomain proteins are essential to unicellular life in general, but whether they were adaptive in the (unicellular) LCA. To make a convincing case for front-loading, you would need to show that these proteins were not useful to the LCA. Lacking evidence for that, you would need to show that the homeodomain proteins could not have evolved, despite selection pressures in their favor.
No, because all the study tells us is that the homeodomain proteins were present in the LCA. It doesn't tell us whether they evolved or were front-loaded.
Comment by keiths — September 25, 2007 @ 4:37 am
September 25th, 2007 at 8:59 am
Keiths,
This objection has come up a few times now and Mike has addressed it each time. Have you been following his posts both here and at DM regarding front-loading? You probably should if you're going to raise this concern.
Are you saying these are the only two ways to establish front-loading as a viable alternative?
Comment by Doug — September 25, 2007 @ 8:59 am
September 25th, 2007 at 9:13 am
Doug wrote:
I'm not aware of anything that Mike has written that settles the issue. Do you have something in mind? If so, could you point me to it?
No. There are other things, like finding a 4-billion-year-old diagram representing the function of homeodomain proteins in multicellular organisms, that could be persuasive.
Comment by keiths — September 25, 2007 @ 9:13 am
September 25th, 2007 at 11:31 am
Keiths wrote:
and also:
It appears to be an open question with Mike having secured a pathway in one direction while you point to the opposite direction and pose the evolved vs. FL options. The question that runs through my mind is what precursor life forms lacking transcription factors would have "looked like?" Do you have an idea as to how they would have functioned?
Comment by Bradford — September 25, 2007 @ 11:31 am
September 25th, 2007 at 12:57 pm
Hi Keiths,
"To make a convincing case for front-loading, you would need to show that these proteins were not useful to the LCA."
No, as that would mean that those genes were removed by the culling hand of mutation. Remember, this was the problem many critics pointed out with Behe's supercell scenario.
In case you want a way to distinguish front-loading from traditional neo-darwinism, here's a better way:
Front-loading would lead one to expect homeobox genes to be found in the first eukaryotes. Neo-darwinism would be fine, whenever those gene turned out to have arisen.
Comment by Krauze — September 25, 2007 @ 12:57 pm
September 25th, 2007 at 1:50 pm
Krauze:
Thinking that is consistent with FL leads to a greater degree of specificity with regard to a timeline prediction.
Comment by Bradford — September 25, 2007 @ 1:50 pm
September 25th, 2007 at 2:37 pm
Keiths wrote:
The study discusses preadaptation and their possible ancestral sophistication, not just that they were present.
Comment by Guts — September 25, 2007 @ 2:37 pm
September 25th, 2007 at 6:13 pm
Hi Krauze,
That's the dilemma facing the front-loading advocate.
Genetic information that is unexpressed or unselected-for will quickly degrade, so the time between front-loading and expression/selection must be short. On the other hand, information that is expressed and selected for doesn't need front-loading as an explanation — the selective pressure is already there to account for its existence.
At best, you're back to arguing that something couldn't have evolved, and therefore that it must have been designed — the standard ID gap argument.
In terms of Mike's example, the homeodomain proteins are already there in the LCA. Why should we suppose they were front-loaded as opposed to evolving via a Darwinian process?
Comment by keiths — September 25, 2007 @ 6:13 pm
September 25th, 2007 at 6:18 pm
Keiths:
The neo-Darwinian process is that they go from a low complex/primitive state to a high complex/sophisticated state, usually via gene duplication. Front-loading states that the complexity/sophistication was already there to begin with and facilitated the evolution. There is no "ID gap" and no need to show that there was nothing of selective value.
Comment by Guts — September 25, 2007 @ 6:18 pm
September 25th, 2007 at 6:29 pm
Keiths:
Based on many previous exchanges along these lines the issue of whether something could or could not evolve is irrelevant to critics' conclusions. Assume for the sake of argument that x could not evolve. What would the critics conclude? There is a gap and as we all know gaps cannot be filled with ID solutions.
Comment by Bradford — September 25, 2007 @ 6:29 pm
September 25th, 2007 at 6:59 pm
If the HD protein is necessary for the multicellular lifestyle, can it be a surprise it was there before multicellular life evolved? Of course not. If you can prove that the protein had no function (for a long time) before the advent of multicellular life, you might have a case. But you don't. And please remind me how (by what mechanism) front-loading is supposed to occur.
Comment by Raevmo — September 25, 2007 @ 6:59 pm
September 25th, 2007 at 7:16 pm
Raevmo:
Yes, because progressive complexity was expected, rather than reduction. Multicellularity was facilitated.
Comment by Guts — September 25, 2007 @ 7:16 pm
September 25th, 2007 at 7:32 pm
Guts:
Why expected? If a trait X evolves, there has to be something that "facilitates" it, does it not? How does that favor the FL explanation over any other?
Comment by Raevmo — September 25, 2007 @ 7:32 pm
September 25th, 2007 at 7:45 pm
Raevmo:
Nope. Actually it could have been very difficult (perhaps almost not even happen at all) if the complexity wasn't readily there to begin with. However, what we see here is that multicellularity was wired-up to the adaptation of the organisms in such a way that the evolution of multicellularity was made easier.
Raevmo:
What other? As explained by the author, the "other" was the traditional explanation — progressive complexity. The data favors the FL explanation, the complexity was there to begin with and eukaryotes were preadapted for multicellularity. The complexity didn't have to be there to begin with, and eukaryotes did not have to be preadapted for multicellularity, but they were.
Comment by Guts — September 25, 2007 @ 7:45 pm
September 26th, 2007 at 5:18 am
Guts wrote:
Guts,
I'm afraid I still don't see how this favors a front-loading interpretation over an explanation in terms of standard, unguided evolution.
The HD proteins were there in the LCA. Krauze acknowledges that they must have been useful to the LCA, or else they would have been mutated beyond recognition. You and Mike presumably agree.
The presence of adaptive traits in the LCA is a straightforward consequence of natural selection. You seem to be saying that what makes the HD proteins different is that they were not only useful to the LCA, but ended up being useful (and essential) to multicellularity, and that this therefore means that they were front-loaded.
But if you claim that the adaptation of existing traits to new functions means that front-loading took place, then you are also implying that such adaptation will never be seen in cases of pure, unguided evolution.
What is the evidence in support of this contention?
Comment by keiths — September 26, 2007 @ 5:18 am
September 26th, 2007 at 1:03 pm
Keiths:
No, natural selection is a consequence of adaptive traits.
Keiths:
You oddly cut off the relevant part of my post that answers your question:
This is not a case of pure unguided evolution, this is a case of facilitated evolution precisely because the proteins were there to begin with.
Comment by Guts — September 26, 2007 @ 1:03 pm
September 26th, 2007 at 2:02 pm
Hi Keiths,
"On the other hand, information that is expressed and selected for doesn't need front-loading as an explanation "” the selective pressure is already there to account for its existence."
The utility of a trait might be sufficient evidence for a selection when you're only considering non-teleological explantions. But once you add teleology to the mix, things aren't that straightforward. After all, designers also make things that serve a function.
"At best, you're back to arguing that something couldn't have evolved, and therefore that it must have been designed "” the standard ID gap argument."
No, that's the argument you want ID supporters to make. I can understand why it would be frustrating that Mike and I refuse to go down that path with you, though.
"In terms of Mike's example, the homeodomain proteins are already there in the LCA. Why should we suppose they were front-loaded as opposed to evolving via a Darwinian process?"
Because that is a prediction that flows naturally from front-loading, as I also pointed out in my previous comment. Orthodox neo-darwinism, on the other hand, offered zero guidance as to the time of origin of these proteins.
Comment by Krauze — September 26, 2007 @ 2:02 pm
September 26th, 2007 at 5:52 pm
Guts:
Hmmm. Natural selection is just differential reproductive success and/or survival (fitness). If there is phenotypic variation and phenotype is correlated to fitness, selection changes the phenotypic distribution. If phenotype is heritable, selection will cause phenotypic evolution between generations. So, no, natural selection is not a consequence of adaptive traits. If all members of a population have the same adaptive phenotpye, selection accomplishes nothing.
Something can only be selected if it was there to begin with. This is always true, so not an argument in favor of "facilitated evolution", whatever that means.
Comment by Raevmo — September 26, 2007 @ 5:52 pm
September 26th, 2007 at 6:11 pm
Raevmo:
Once an adaptive trait comes into existence , any variant that is more advantageous than other variants survives differentially, if under competition. Thats plain and pure Darwinism, but where they come from is still missing. You're just describing what happens after traits comes about, that is, after evolution has already happened. It doesn't follow that because it exists that selection caused it's existence, it first has to exist to be selected for.
Raevmo:
Duh. Thats what I said in my response to Keiths.
Hence, natural selection is a consequence of adaptive traits.
Raevmo:
Of course it is, and I repeat, the proteins didn't evolve step by step progressively as one would expect from Darwinian theory in the case of multicellularity, the set was already in place, which is why multicellularity came about multiple times independantly in the ancestor's descendants, hence facilitated. You and keiths just keep repeating yourselves without responding to this.
Comment by Guts — September 26, 2007 @ 6:11 pm
September 26th, 2007 at 6:26 pm
Raevmo wrote:
So, whatever is observed can be explained by its being adaptive. And the adaptiveness of a trait is 'proven' by its being observed. But this seems circular or tautologous. How does one test 'differential fitness' prior to selection? It seems that appeals to natural selection must always be liable to commit the post hoc ergo propter hoc fallacy.
Comment by stunney — September 26, 2007 @ 6:26 pm
September 26th, 2007 at 6:30 pm
Guts:
How do you know the first HD protein didn't evolve step by step? And why would that be expected from Darwinian theory?
It seems to me all you're saying is that you can't believe the precursor to HD came about by unguided mutation, but must have been created with multicellularity as the goal. If so, what's your evidence for this?
Comment by Raevmo — September 26, 2007 @ 6:30 pm
September 26th, 2007 at 6:38 pm
Raevmo:
Whence the first HD proteins is a seperate research question, the case being discussed in this thread supports FLE.
As an aside though, if this series of events turned out to be caused by simple Dariwnian processes (and hence just a lucky fluke) I'd still find it intriguing. Nonetheless, IMO FLE predicts that the LCA was also borrowing deeply and/or the result of facilitated evolution. All you're saying is that the hypothesis in this thread is falsifiable.
Comment by Guts — September 26, 2007 @ 6:38 pm
September 26th, 2007 at 6:42 pm
stunney:
No, my friend, I don't blame you for being ignorant in this respect, but that is not the case. There's a large body of mathematical theory that accurately predicts the outcome of phenotypic evolution given an initial distribution of phenotypes. Experimental evolution has confirmed this. See, for example, Griffin et al. (2003), Nature 430, pp 1024-1027.
Comment by Raevmo — September 26, 2007 @ 6:42 pm
September 26th, 2007 at 6:46 pm
Guts:
No I'm not. How can FL be falsifiable? How can it be distinguished from random mutation? Mutations could have been specially created, but there's no way of telling, as far as I know.
Comment by Raevmo — September 26, 2007 @ 6:46 pm
September 26th, 2007 at 6:53 pm
Raevmo:
Yes you are, thats why you accused me of believing the precursor to HD couldn't have come about by unguided mutation. That would contradict the conclusion, thus falsified.
Raevmo:
It's random mutation under control.
Comment by Guts — September 26, 2007 @ 6:53 pm
September 26th, 2007 at 7:51 pm
Raevmo wrote
Er, this seems to support what Guts was saying. He was arguing that adaptive traits cause natural selection. He said, in opposition to keiths, that:
That seems entirely consistent with "predicting an outcome of phenotypic evolution given an initial distribution".
In other words, natural selection is a post hoc rationalization of fitness qualities that were already there, rather than an independently and antecedently predictable causal factor. Which was my point—appeals to natural selection to explain adaptive traits always seem to be liable to the post hoc propter hoc fallacy. I doubt the predictive problem with respect to the role of natural selection is solvable on a large scale in the real world because there are too many unknown variables, such as asteroid trajectories, the climatic effects of industrialization, genetic mutations, etc.
Comment by stunney — September 26, 2007 @ 7:51 pm
September 26th, 2007 at 9:58 pm
Raevmo:
There are cellular mechanisms whose adjustment could lead to non-randomness. It is not difficult to conceive of how mutation rates could be adjusted based on signals induced by environmental conditions.
Comment by Bradford — September 26, 2007 @ 9:58 pm
September 27th, 2007 at 1:18 am
Stunney wrote:
The problem of distinguishing causation from accidental correlation afflicts science generally, not just evolutionary biology. There's no reason to single out natural selection unless you believe the rest of science is hamstrung as well.
Comment by keiths — September 27, 2007 @ 1:18 am
September 27th, 2007 at 2:07 am
Y'all,
Here's the issue in a nutshell:
1. Homeodomain proteins (HDPs) appear to be essential for multicellularity.
2. HDPs were present in the last common ancestor (LCA) of living eukaryotes.
3. The LCA was unicellular.
Two competing hypotheses:
A. The LCA's HDPs were front-loaded.
B. The LCA's HDPs evolved without guidance.
The question is: Given statements 1, 2, and 3, plus everything else that biology has discovered to date, which hypothesis is more likely to be true: A or B?
Raevmo and I are scratching our heads because none of you have offered any reasons why hypothesis A is more likely than hypothesis B to be true, given the facts.
Comment by keiths — September 27, 2007 @ 2:07 am
September 27th, 2007 at 2:16 am
Keiths:
The traditional explanation for the evolution of multicelluarlity (and virtually all of yourattempted responses to it , which were incredibly weak I might add) turned out to be wrong. What do you think about the evidence that eukaryotes were preadapted for multicelullarity and the evidence that the ancestor is now thought to be more complex than previously assumed (which actually played a hand in facilitating this evolution)? Do you find it objectionable? Your assumptions about the LCA are not true by default, but do speak to the fact that this hypothesis is falsifiable.
Comment by Guts — September 27, 2007 @ 2:16 am
September 27th, 2007 at 3:13 am
Guts,
This reply is to the first version of your comment. I didn't know that you had edited it in the meantime.
Guts wrote:
True, but that doesn't cast doubt on standard evolutionary theory. NDE didn't dictate the traditional explanation. Both the old and the new explanations are compatible with NDE, and NDE by itself cannot rule out either.
I think you're reading too much into the word "preadapted." Look at how the authors used it:
Nothing magical is implied here. The LCA had the HDPs. They turned out to be useful or even essential for multicellularity. That doesn't justify the leap you are making, which is to say that the LCA got the HDPs because they would eventually be useful for multicellularity.
I'm not sure what you mean by "speaks to". If you mean "is compatible with", I would agree. But it's also compatible with NDE. The question is, why should we prefer the front-loading explanation over the standard NDE explanation?
Which assumptions do you dispute, and why? The three facts I listed all came from the abstract.
Comment by keiths — September 27, 2007 @ 3:13 am
September 27th, 2007 at 3:22 am
Keiths:
Then it's useless.
keiths:
Nothing magical need be implied here, I'm not making any leap. The leap is the oxymoron that this is just another example of standard unguided evolution while at the same time, it is also an example of facilitated evolution.
Keiths:
I understand how it could be made compatible with NDE with some strenuousness but it was the FLE perspective that actually was able to predict it. With NDE, progressive complexity was assumed, which, according to the evidence, turned out to be wrong.
Comment by Guts — September 27, 2007 @ 3:22 am
September 27th, 2007 at 4:49 am
By your standards, then, ID is also useless, because it also fails to rule out one or the other. Both scenarios — HDPs present in the LCA, versus HDPs developing later over time — are compatible with ID. The first scenario is the one you're arguing for. The second could be explained in ID terms as the result of discrete mutations orchestrated by an intelligent designer.
No contortions required. It's fully compatible with NDE.
Frontloading predicts that at some point in time, an ancestral organism will possess traits that in a different context will turn out to be useful to its descendants. NDE predicts the same thing. Why? Because NDE holds that the function of many adaptations will shift over time as evolution proceeds (a classic and dramatic example being the derivation of two bones in the mammalian middle ear from what were jawbones in its reptilian precursors).
That's like saying "With heliocentrism, circular orbits were assumed, which, according to the evidence, turned out to be wrong." True, but irrelevant. Heliocentrism didn't require circular orbits, even though Copernicus believed in them. The fact that he was wrong about circular orbits does not mean that heliocentrism is wrong. Exactly the same reasoning applies to NDE in this case.
Comment by keiths — September 27, 2007 @ 4:49 am
September 27th, 2007 at 5:04 am
Keiths:
Actually , I'm not sure where you're getting that second from, it's completely irrelevant to anything discussed in this thread. It may be compatible with some strained or unknown (to me at least) hypothesis of ID but not the FLE I discussed.
Keiths:
Anything is compatible with anything if you strain it enough after the fact.
Keiths:
Keiths, you can't just say that it is compatible and then go off on a tangent about another case, you have to look at what the data shows. FLE in this case, predicted deep borrowing, NDE as admitted by the author predicted progressive evolution. And this is not the only case. There was an earlier example showcased in this blog concerning WNT genes. The entire set of WNT genes is now thought to have been present in ur-bilaterians.The reason why this was unexpected is because (quoting myself) the idea was that cnidarians have one, nematodes and insects about 4-5 and vertebrates 12 (because NDE predicts progressive complexity via gene duplication). If you want to compare a similar case to the one we are discussing, this is as close as you can get.
Now, I'm not saying that this overturns neo-Darwinian theory as a whole, not sure where you got that from or why you would say that, but in these cases, FLE was able to shed light on the subject, which makes it more plausible.
Comment by Guts — September 27, 2007 @ 5:04 am
September 27th, 2007 at 5:26 am
The second scenario is the one in which the HD proteins develop gradually in the descendants of the LCA. My point is that this scenario is just as compatible with ID (via discrete directed mutations) as it is with NDE (discrete undirected mutations). Therefore your criticism of NDE as "useless" backfires.
No tangent. I showed that NDE, contrary to your assertion, makes the same prediction as FLE: the occurrence of traits in an ancestral organism that will prove to be useful, in a different context, to its descendants.
The authors did not attribute the traditional view to NDE (which makes sense because, as I noted already, NDE does not dictate the traditional view):
Guts again:
What light was shed? What do we know now, via the telic perspective, that we didn't already know from the study?
Comment by keiths — September 27, 2007 @ 5:26 am
September 27th, 2007 at 5:33 am
Keiths:
No , that HD proteins develop gradually in this case has nothing to do with FLE it has to do with the failed prediction from NDE. What do you think about this biological concept? Do you find it objectionable?
Keiths;
Through progressive evolution. NDE actually predicts that small gradual step by step evolution is the reason for adaptation, whereas FLE predicts it was the result of function following already existing form. If you can show that the mamilian bones already existed in the ancestor in such a way that actually facilitated co-option and thus evolution of ear bones that independantly evolved in different lineages, then of course, you'll be showing another example of front-loading. However, this is the direct opposite of , as you yourself admit, "standard unguided evolution", which would be the case if this was just a local example.
Uhh, the "traditional view" of course was evolution via ND processes. Do you think it is something else? Symbiosis perhaps?
Keiths:
Nice snipping there, I guess the new atheists only put reason and evidence in high regard when it suits them.
Comment by Guts — September 27, 2007 @ 5:33 am
September 27th, 2007 at 6:13 am
Guts,
ID is compatible with both scenarios, just as NDE is.
Scenario 1: HDPs in the LCA.
NDE-based explanation: HDPs evolved over time in the line leading to the LCA.
ID-based explanation: HDPs were front-loaded by the designer.
Scenario 2: HDPs developing in the LCA's descendants.
NDE-based explanation: HDPs evolved over time in the LCA's descendants.
ID-based explanation: Mutations were inserted by the designer at discrete times.
Gradual evolution is not incompatible with function following already-existing form.
Go back to my previous comment and read the heliocentrism example, and then tell us why the same logic doesn't apply to NDE in this case.
Nice try at avoiding the question. You said that FLE was able to shed light on the subject. What light did it shed? What do we know, via the telic perspective, that we didn't already know from the study?
P.S. You do know there is a preview button, right? It makes it hard to engage in dialogue with you when you when you're constantly editing your previous comments.
Comment by keiths — September 27, 2007 @ 6:13 am
September 27th, 2007 at 6:22 am
Keiths:
Yeah but do you understand that thats not FLE, but some bizarre ID explanation you came up with?
Keiths:
Gradual evolution is form following function.
Keiths:
I'm not saying that this falsifies Darwinism as a whole, Darwinism is still in the picture.
Keiths:
Hmm, if you hadn't snipped it, you would have easily seen it, here I'll restore it:
This case is the same, the set required for the evolution of multiceullarity didn't evolve gradually in descendants, but was already there, in a sophisticated state, in the last common ancestor. The theme of highly complex ancestors whose complexity facilitates evolution supports FLE. This is the sort of thing TT bloggers have been talking about (and predicting) for a couple of years, and here we see yet another example.
Keiths:
I offer 30 minutes of editing, maybe you should try letting the evidence seep in rather than shooting from the hip. Anyway, I'm off to bed now, more later.
Comment by Guts — September 27, 2007 @ 6:22 am
September 27th, 2007 at 6:48 am
Go tell a room full of ID supporters that no, it's simply not possible that
Godthe Designer would choose to insert mutations discretely over time and see what kind of a response you get.Let's see… I take the time to get my comments right before posting them, and you don't. That means I'm the one who is "shooting from the hip".
It probably makes sense in Gutsworld.
I asked:
You replied:
As if the research that uncovered that fact was done from a telic perspective.
Comment by keiths — September 27, 2007 @ 6:48 am
September 27th, 2007 at 7:21 am
Why would the mutations have to be "inserted?" If a genomic change occurred through an adjustment of genomic repair mechanisms allowing for greater fluctuation within a region subject to selective pressure the "insertion" would be the consequence of flexibility in a genomic regulatory mechanism indicating that mutations are not necessarily random- not very NDE like.
Comment by Bradford — September 27, 2007 @ 7:21 am
September 27th, 2007 at 8:32 am
Mutations are not absolutely random. They are random with respect to fitness. And we already know there are genetic hotspots and genetic coldspots, and that environmental stress can affect the rate of mutation and hence the rate of evolution (e.g. bacterial mutators). None of this supports a claim of Intelligent Design, but is very important in medicine.
Comment by Zachriel — September 27, 2007 @ 8:32 am
September 27th, 2007 at 10:51 am
I'm aware of this dictum but am not convinced it is necessariliy the case under all conditions. It would not be the case if environmental stress influenced the relationship between mutations and a fitness outcome. I also would not take a doctrinaire approach to whether or not non-random mutation generators would support design. They would not support NDE.
Comment by Bradford — September 27, 2007 @ 10:51 am
September 27th, 2007 at 11:46 am
What about LexA's role in the SOS response? The repression of genes that try to solve an environmental insult that is effecting the species survival. And trying to solve that problem in an orderly fashion (repair, recombination, mutation, cell suicide).
Certainly more deliberate than mutations randomly occurring and just happening to be useful in a particular environment with a particular insult.
ID would have assumed it moreso than some non-teleological process.
Comment by Doug — September 27, 2007 @ 11:46 am
September 27th, 2007 at 2:34 pm
Keiths:
Keiths where did you get that from?. I didn't say it was not possible, I simply said it was not FLE. Do you understand the difference?
Keiths:
No, what I have been saying all along was that the reseach was expected from a Telic perspective, and unexpected from a non-telic perspective. It's almost as if you're just ignoring what I'm actually saying and arguing with someone else.
Comment by Guts — September 27, 2007 @ 2:34 pm
September 27th, 2007 at 3:43 pm
Guts:
Guts,
This is getting pretty tiresome, and has obviously become more of a face-saving exercise on your part than an honest attempt at discussion, but let me give it another shot.
I explained that NDE is compatible with both the pre- and post-LCA scenarios of HDP development. That makes you unhappy, because it means that you can't blame NDE for the mistaken expectations of researchers prior to this study.
Tough. Whether you like it or not, the fact remains that NDE is compatible with both, just as heliocentrism is compatible with both circular and elliptical orbits. You can't blame NDE for this one.
Comment by keiths — September 27, 2007 @ 3:43 pm
September 27th, 2007 at 3:59 pm
Keiths:
Really? My argument has been the same since the first post, and occasionally correcting some error you make about basic evolutionary biology. What possible face could I be trying to save? Your arguments on the other hand have been a complete mess, from "heliocentrism" to "selection causes traits" to "this is unguided evolution", it's really quite hilarious. I guess judging from the way you structured your response it looks like you're not going to answer any of my questions.
Keiths:
No I guess I should blame symbiosis or neo-Lamarkism.
No I got an even better idea, lets blame ID!
Keiths:
All I have to do is quote myself, NDE is gradual evolution, usually via gene duplication, form following function. The paper however shows evidence that contradicts this expectation, it shows the opposite, function following already existing form. You can say NDE is compatible after the fact, but it played a very controlled role in this situation. Take a look back and tell me which one of us has been the most specific about the actual biology and which one of us is spaced out…literally.
Comment by Guts — September 27, 2007 @ 3:59 pm
September 27th, 2007 at 5:10 pm
Hi Zachriel,
You wrote…
.
At the risk of being too argumentative…. (may the Intelligent Designer forbid)
When we have a situation of selectively changing rates in select genetic hotspots, how can you say mutation is random with respect to fitness?
I suspect you are familiar with the game of Yahtzee. When you start rerolling the select dice based on the outcome, it is no longer random.
Here is Bradford's opportunity to shine (or any other ID proponent with the knowledge). Are there different genetic hotspots whose mutation rates vary dependent on the TYPE of environmental pressure?
If there are, I would suggest these dice may be loaded. Not perfectly, but biased with respect to fitness.
Comment by Thought Provoker — September 27, 2007 @ 5:10 pm
September 27th, 2007 at 7:14 pm
TP:
TP, ask and you shall receive. This is one of several articles I have encountered indicating that mutations are not necessarily random with respect to fitness. Hot and cold genomic regions can influence the course of adaptive responses and genomic maintenance. The former can induce an increase in available options for regions that yield phenotypic adaptations. The latter preserves invariance of essential genomic regions so that survival possibilities are maximized. Mutations are not truly random with respect to fitness after all.
Mutation Rates and Gene Location: Some Like It Hot
Comment by Bradford — September 27, 2007 @ 7:14 pm
September 27th, 2007 at 8:23 pm
Guts:
Please stop embarrassing yourself. All you're saying is that an earlier trait X makes it easier for trait Y to evolve, and therefore X was front-loaded since Y was part of the designer's plan. Good lord. Every trait has some evolutionary precursors. Does it follow that all those precursors were front-loaded? If not, how do you know which ones were, and how did the FL occur exactly?
Comment by Raevmo — September 27, 2007 @ 8:23 pm
September 27th, 2007 at 8:32 pm
Raevmo:
So Raevmo, you think that just by describing what I'm saying in general terms, you're actually responding? Do you really think all this shows is that a trait x had a precursor? If so, please explain why the author thinks that the traditional evolutionary explanation failed in this case.
Comment by Guts — September 27, 2007 @ 8:32 pm
September 27th, 2007 at 8:57 pm
Raevmo:
Not every trait has evolutionary precursors- at least none that are identifiable. Follow things back in time and that becomes apparent. One means of distinguishing mainstream theories from ID lies in their predictive utility. How are mainstream theories able to predict what constitutes a minimal level of genomic function based on available data? Existing genomes show indications of irreducible complexity.
Comment by Bradford — September 27, 2007 @ 8:57 pm
September 27th, 2007 at 10:28 pm
I've been too busy to participate, but let me go back to keiths' original criticism.
No, the question is not whether the homeodomain proteins were adaptive in the (unicellular) LCA, but whether they are essential to unicellular life.
Convincing to whom?
Why?
Why?
Comment by MikeGene — September 27, 2007 @ 10:28 pm
September 28th, 2007 at 8:07 am
Genetic hotspots may evolve due to inherent advantages in rapidly changing and stressful environments. Any mutations still appear to be random with respect to fitness. There have been a few results that suggest directed mutations may occur in some situations, but these results are ambiguous at best. Research continues.
Keep in mind that even if directed mutations were shown to exist, this would not falsify evolution generally, but only the Central Dogma of Molecular Biology. Furthermore, Intelligent Design, as normally construed, will be supported only if there is evidence of foresight due to an outside agency. Genomes can be very "intelligent" and still have spontaneously evolved by incremental adaptation.
Comment by Zachriel — September 28, 2007 @ 8:07 am
September 28th, 2007 at 9:28 am
Hi Zachriel,
You wrote…
And the specific Yahtzee die role may be random with respect to a player's desire but the Yahtzee's overall "mutation" process is not.
Was that a tactical withdrawal?
My compliments on being reasonable.
While some ID proponents are looking to overturn mainstream evolutionary thought, I suggest MikeGene is not. There is some middle ground between the two extremes.
I am currently engaged in some interesting discussions with what Joy calls the swamp (After the Bar Closes forum). Yes, that started up again.
It seems that the existence of the Vernanimalcula guizhouena in pre-cambrian runs counter to a mind set that presumes early organisms were simple. Also, I think you know how difficult it is to make presumptions about Quantum Mechanics' impact (or lack thereof) to the microscopic workings of a cell.
Comment by Thought Provoker — September 28, 2007 @ 9:28 am
September 28th, 2007 at 10:02 am
The player's desire is equivalent to fitness. When we say "mutations are random" we mean "mutations are random (uncorrelated) with respect to fitness". This has been repeatedly clarified on this forum.
I have no interest in tactical games in such discussions. I have previously commented on the possibility of directed mutations.
Comment by Zachriel — September 28, 2007 @ 10:02 am
September 28th, 2007 at 10:28 am
Hi Zachriel,
Excuse my bluntness. How long before you lighten up?
I suggest you aren't going to convince any more lurkers with a take-all-give-nothing-back attitude.
Even MikeGene offered that he may have overreacted (due to lack of sleep).
But back to the point at hand…
The concept I am trying to illuminate is the possible distinction between the narrow focus and the larger one.
While this is something that you probably already know, it might help others…
Imagine two cards, one is blank on both sides the other is blank on one side and has an "X" on the other.
The cards are randomly mixed up and randomly placed on a table. By random happenstance a blank side is showing.
What is the probability that the card on the table is the one with an "X"
Zachriel, please tell the listening audience the answer and explain why I offered it as a thought-provoking puzzle.
Thanks
Comment by Thought Provoker — September 28, 2007 @ 10:28 am
September 28th, 2007 at 11:56 am
Even if mutations are random, variation really isn't because it's borrowing from what already exists.
Comment by Guts — September 28, 2007 @ 11:56 am
September 28th, 2007 at 2:18 pm
I'm light as a feather. Rest assured, I still don't use rhetorical tactics in order to score points.
I am confident most readers, if they keep an open mind, will be convinced by the weight of argument.
Somehow you placed two cards on the table randomly, but only one face is showing. Is that correct? Let's assume they are stacked, or you are holding the second card.
There are eight equiprobability ways the cards can be shuffled and flipped. Let's number the sides and consider "1" to be the marked card.
We can disregard the first two as the "1" is showing. That leaves six alternatives, with two of them winners.
This is *not* the Monty Hall Problem, by the way. That's where you pick one, are shown a loser in one of the two other doors, then have to decide if you want to switch choices. Assume we choose the first door, and the winner is again "1". There are six choices.
Switching yields a 2/3 chance of winning.
Comment by Zachriel — September 28, 2007 @ 2:18 pm
September 28th, 2007 at 6:26 pm
Zachriel,
The answer to Thought Provoker's question,
is one third. That assumes a distribution where all eight of the outcomes in your sample space are equally likely.
(I think that's the way you were going, but what you did was kind of like a student taking a math test, showing all the calculations, but leaving out the result.)
The point I would draw is that a single blank side of a card on the table is evidence that the card is blank on both sides. By seeing that blank side, that probability goes from one half to two thirds. This piece of information confirms the hypothesis of the double-blank card, i.e., makes it more likely.
By the way, I'm not sure why you identified the side with the 'X' as a "winning" card. It's not part of the original statement of the problem.
My interpretation: Let's say that an 'X' means that no intelligent life comes into existence. A blank side means that intelligent life does come into existence. The blank-on-both-sides card represents a universe with an Intelligent Designer who sets out to design life. All such universes will have life. The card with an 'X' on one side and blank on the other represents a universe governed by random chance. Sometimes life will emerge and sometimes it will not.
If these assumptions are correct, then we can conclude that, just as looking at the blank side of the card confirmed the hypothesis that both sides were blank, the existence of life confirms the hypothesis that there is an Intelligent Designer, i.e., increases the probability that such a Designer exists.
Let's define two events, L (life exists somewhere in the universe), and D (there exists a Designer who set out to create life).
P(L) = the probability of life arising in some arbitrary universe,
P(~L) - the probability that no life arises in some universe
P(D) = the probability that a Designer exists in some universe
and P(~D) = the probability that no Designer exists in some universe
And the conditional probabilities:
P(L/D) = the probability that life exists in a universe, once we know that such a universe has a Designer that has set out to design life, and
P(L/~D) = the probability that life exists in a universe, once we know that there is no Designer.
If P(L/D) > P(L/~D), then it follows that
P(D/L) > P(D).
In other words, a universe with life is more likely to have a Designer than a universe without life. An observation that life exists in some universe increases the likelihood that there is a Designer. Put another way, the observation of life confirms the hypothesis that a Designer exists. Or, another way, life itself provides evidence of a Designer.
QED
Comment by rachelrachel — September 28, 2007 @ 6:26 pm
September 28th, 2007 at 6:32 pm
rachelrachel:
I agree with Rachel. Somebody explain to me what QED means.
Comment by Bradford — September 28, 2007 @ 6:32 pm
September 28th, 2007 at 6:37 pm
QED means "in yo face!"
Comment by Guts — September 28, 2007 @ 6:37 pm
September 28th, 2007 at 7:01 pm
Seriously? Sounds like fightin words.
Comment by Bradford — September 28, 2007 @ 7:01 pm
September 28th, 2007 at 7:11 pm
QED stands for quod erat demonstrandum. That's Latin for 'which was the thing that needed to be demonstrated'.
Meaning in effect, 'I've now proved the conclusion I set out to prove'.
Comment by stunney — September 28, 2007 @ 7:11 pm
September 28th, 2007 at 9:47 pm
Zachriel: That leaves six alternatives, with two of them winners.
Hence, the answer was explicitly provided as 2 in 6.
Thought Provoker: What is the probability that the card on the table is the one with an "X"
The bet is whether turning the card over results in the marked card.
The argument is equivalent to 'a universe with amorphous rocks is more likely to have a Designer than a universe without amorphous rocks.'
Comment by Zachriel — September 28, 2007 @ 9:47 pm
September 29th, 2007 at 9:09 am
Hi rachelrachel and Zachriel,
The answer I was looking for was 1/3 (or 2 out of 6).
I agree, this isn't the Monty Hall Problem.
While rachelrachel took a path I didn't intend and don't agree with, she (assuming "rachel" is feminine) got the basic implication.
I was discussing with Zachriel the idea that random mutation probably wasn't "random with respect to fitness" in the face of genetic hotspots that have mutation rates dependent on the type of evolutionary pressure.
Say the card with the "X" on it represents mutations that are negative with respect to fitness and the "X" side is a genetic coldspot. The card with two blanks sides would be positive with respect to fitness.
When the game is rigged so that things that would definitely be negative with respect to fitness are intentionally left out of a "random" selection between what would otherwise be an equal distribution, it biases the distribution.
The point I was trying to make is that the mutation process is clearly biased with respect to fitness if genetic hotspots and coldspots are based on the type of environmental pressure.
Another example would be if a Las Vegas casino instituted a change in Black Jack rules such that whenever the dealer has a face card or an ace showing the deal is voided. Would that be random with respect to the casino going broke?
Just in case rachelrachel wants to celebrate too readily. There is a catch to all of this. It is the assumption that things were unbiased to begin with. Like a lot of pro-ID arguments the trick rachelrachel appears to be employing is the presumption of an equal likelihood of the existence of an Intelligent Designer as not. Nice trick if you can get away with it.
BTW, this is what Dembski does in his calculations for specified complexity. He hides it behind comparing the negative log base-2 to 1.
Saying "the negative log base-2 is greater than 1" is the same as saying "it has less than a 50% chance of being true". It just sounds more profound and is less understandable in PhD speak.
Comment by Thought Provoker — September 29, 2007 @ 9:09 am
September 29th, 2007 at 9:16 am
I have a comment "awaiting moderation", please help. Thanks
Comment by Thought Provoker — September 29, 2007 @ 9:16 am
September 29th, 2007 at 11:37 am
Genetic hotspots have not been shown to have mutation rates dependent on the *type* of evolutionary pressure. People have looked, but the evidence is ambiguous at best. The most anyone has found is that mutations increase under circumstances when rapid evolution might be beneficial. Or areas of the genome of particular importance to adapting to a highly variable environment might evolve more rapidly.
An organism might have a hotspot on immunoglobulin genes having to do with immune response. This will result in a highly variable population with regards to this trait. This then allows rapid evolution when confronted with varying pathogens. But the mutations are still random with respect to fitness.
You're confused on this point. Mutations are not randomly distributed across the genome. That is not what "random mutation" means. Mutations are biased in any number of ways. The most highly conserved genes tend to have efficient and accurate repair mechanisms. Genes for which variation is adaptive will replicate with more errors. But the errors remain random with respect to fitness.
Directed mutations are certainly possible. John Cairns presented the original evidence, and many have attempted to find such a link. It wouldn't overthrow the Theory of Evolution, but it would put a serious dent into the Central Dogma of Molecular Biology.
Comment by Zachriel — September 29, 2007 @ 11:37 am
September 29th, 2007 at 12:51 pm
There is a directed component to this randomness. It is like a soldier, who knowing that the enemy is in front of him, fires in the direction of an enemy he cannot see. He might get lucky and hit some but most bullets will miss their target. If he fires a rifle, with one shot at a time, his chances of shooting an enemy soldier are less than if he fires a machine gun. The random nature of the shooting remains the same for single action and automatic weapons but the strategy differs. DNA repair mechanisms can be the means by which the rate of "shooting" is adjusted. There you go TP. You've been asking for a mechanism. You have one.
Comment by Bradford — September 29, 2007 @ 12:51 pm
September 29th, 2007 at 1:09 pm
The varying rates of mutation in different areas of the genome can be correlated with selection.
Yes, it's natural selection.
Comment by Zachriel — September 29, 2007 @ 1:09 pm
September 29th, 2007 at 1:18 pm
Hi Bradford,
You wrote…
Well knock me over with a feather.
For your information. On September 14, 2006, I wrote the following to you three days after my first post to Telic Thoughts…
What is the ID position? More importantly, what is your position?
I wouldn't be surprised that people are tiring of my pressing this point but, seriously, arguing is just a waste of bandwidth without at least some understanding of each other's reference frame.
For example, I understand Behe's reference frame includes Common Descent. So, is arguing for Common Descent still an "anti-ID position"
It is easy to nit-pick a comprehensive set of assumptions that needs to accommodate all observed phenomenon. It is also practically meaningless unless you have a counter proposal. Even a "I agree with everything but this"¦" is a counter proposal.
So, I am asking you to think about what you do and don't accept about the current position I am restating here. Of the parts you don't accept, what are your alternatives?
So, after over a year of "pressing this point", I get an answer!
Hmmm, I better think carefully about my next request. At this rate, I won't get an answer until Christmas…. of 2008!
Comment by Thought Provoker — September 29, 2007 @ 1:18 pm
September 29th, 2007 at 1:21 pm
Bradford: There is a directed component to this randomness.
That's an open question that remains to be determined. Selection lacks foresight. It selects based on available options and current conditions. DNA repair mechanisms are many and varied and taken as a whole are quite intricate in nature. Add a "thermostat" to this capable of revving up and toning down responses to not yet existing environmental challenges and you have the makings of a paradigm comparison.
Bradford: You've been asking for a mechanism. You have one.
No, it is the repair mechanisms that can adjust the rate of mutations and thereby affect the number of options available to select.
Comment by Bradford — September 29, 2007 @ 1:21 pm
September 29th, 2007 at 1:22 pm
TP:
LOL!
Comment by Bradford — September 29, 2007 @ 1:22 pm
September 29th, 2007 at 3:30 pm
Bradford:
Mutation itself is actually quite fascinating , it's not just the "zap" that people used to think it was. Translesion synthesis is surprisingly quite complex and has exquisitely precise regulation.
Comment by Guts — September 29, 2007 @ 3:30 pm
September 29th, 2007 at 5:04 pm
Zachriel:
Actually thats not entirely correct. There is also evidence that mutation to particular microsatellite alleles are associated with fungal infection, that is not observed in non-infected plants, which suggests a very highly specific stress-response mechanism.
Comment by Guts — September 29, 2007 @ 5:04 pm
September 29th, 2007 at 6:14 pm
Interesting. Do you have a cite?
Comment by Zachriel — September 29, 2007 @ 6:14 pm
September 29th, 2007 at 6:53 pm
This one The figure labels confuse the hell out of me, I think they're misplaced, but still a good read.
Comment by Guts — September 29, 2007 @ 6:53 pm