I promised John Harshman for several months that I would start a discussion about common design vs. common descent, and I’d like to keep my word to him as best as possible.
Strictly the speaking common design and common descent aren’t mutually exclusive, but if one invokes the possibility of recent special creation of all life, the two being mutually exclusive would be inevitable.
If one believes in a young fossil record (YFR) and thus likely believes life is young and therefore recently created, then one is a Young Life Creationist (YLC). YEC (young earth creationists) are automatically YLCs but there are a few YLCs who believe the Earth is old. So evidence in favor of YFR is evidence in favor of common design over common descent.
One can assume for the sake of argument the mainstream geological timelines of billions of years on planet Earth. If that is the case, special creation would have to happen likely in a progressive manner. I believe Stephen Meyer and many of the original ID proponents like Walter Bradley were progressive creationists.
Since I think there is promising evidence for YFR, I don’t think too much about common design vs. common descent. If the Earth is old, but the fossil record is young, as far as I’m concerned the nested hierarchical patterns of similarity are due to common design.
That said, for the sake of this discussion I will assume the fossil record is old. But even under that assumption, I don’t see how phylogenetics solves the problem of orphan features found distributed in the nested hierarchical patterns of similarity. I should point out, there is an important distinction between taxonomic nested hierarchies and phylogenetic nested hierarchies. The nested hierarchies I refer to are taxonomic, not phylogenetic. Phylogeneticsits insist the phylogenetic trees are good explanations for the taxonomic “trees”, but it doesn’t look that way to me at all. I find it revolting to think giraffes, apes, birds and turtles are under the Sarcopterygii clade (which looks more like a coelacanth).
Phylogeny is a nice superficial explanation for the pattern of taxonomic nested hierarchy in sets of proteins, DNA, whatever so long as a feature is actually shared among the creatures. That all breaks down however when we have orphan features that are not shared by sets of creatures.
The orphan features most evident to me are those associated with Eukaryotes. Phylogeny doesn’t do a good job of accounting for those. In fact, to assume common ancestry in that case, “poof” or some unknown mechanism is indicated. If the mechanism is unknown, then why claim universal common ancestry is a fact? Wouldn’t “we don’t know for sure, but we believe” be a more accurate statement of the state of affairs rather than saying “universal common ancestry is fact.”
So whenever orphan features sort of poof into existence, that suggests to me the patterns of nested hierarchy are explained better by common design. In fact there are lots of orphan features that define major groups of creatures. Off the top of my head, eukaryotes are divided into unicellular and multicellular creatures. There are vetebrates and a variety of invertebrates. Mammals have the orphan feature of mammary glands. The list could go on and on for orphan features and the groups they define. Now I use the phrase “orphan features” because I’m not comfortable using formal terms like autapomorphy or whatever. I actually don’t know what would be a good phrase.
So whenever I see an orphan feature that isn’t readily evolvable (like say a nervous system), I presume God did it, and therefore the similarities among creatures that have different orphan features is a the result of miraculous common design not ordinary common descent.
stcordova,
After.
That is my opinion, yes. I think the origin of diploidy was simultaneous with the origin of sex (by which I mean alternation of ploidy, not recombination).
[eta – you may be interested to follow Corneel’s link. In that OP, I link to a 50 page dissertation on the topic, summarising my views, though obviously it’s a bit evolution-oriented! 😉 ].
Rumraket, to Mung:
That’s Mung. When he’s stuck, his first reponse is to Make Shit Up. He may not have an argument, but he’s got dishonesty, and that’s good enough for him.
If smart cell phones evolved from desktop computers, why are there still desktop computers?
John,
You’re right that the ONH pattern, taken in isolation, doesn’t show that evolution is unguided. But neither does it show that common descent is true.
Both inferences depend on background knowledge and assumptions.
With those in place, however, it is true that the ONH pattern is decisive in both cases.
Mung:
Neil:
Mung was joking, Neil.
Get ready for a lot of speculations Sal…All of them are going have to be right even if they are contradictory… which is expected when evolutionists have no shred of evidence to support their wild assumptions… 😉
BTW: Don’t ask them about the mechanism of this appearance because Hashman has already admitted to miraclevolution… If there is another one, there may be a dissent and riots… lol
I’m beginning to explore detection of patterns via hidden Markov, partly because I’m using them for my nylonase paper, version 2 (for OA journal submission).
At least two issues are not covered by Theolbald’s umpteen decimal cherry picked data. The most glaring is protein evolution that ignores the underlying DNA pattern as in:
When we run hidden markov on the proteins, we focus indirectly only on the X regions and ignore the problem of the introns.
The next problem of Theobald is that it doesn’t explain very well why chickens share genes with humans that no one else in the diagram provided shares. Why is that? You can apply hidden markov to proteins that are shared, it doesn’t do well for proteins that are missing!
So ad hoc apologies and excuses have to be made for these anomalies.
So I’ve established 2 problems that Theobald’s analysis just avoids. There is a 3rd problem, and I’m trying to formulate it in a way that is clearer. So far it’s not yet a clear as I’d like it to be. But here goes….
The problem is that we look at an ancient conserved protein like say those in the amimo acyl tRNA-synthase family, aaRS for short. There are about 20 or so of these for each of the amino acids.
So the story goes the prokaryotic aaRS are distinct from the eukaryotic aaRS’s. The difference reflect supposedly billions of years of evolution. So far so good. But the skunk smell in this hypothesis that no evolutionists seems to acknowledge is that why are the prokaryotic aaRS so similar to each other?
If we use the approximation of the neutral model that most residues are changeable, then why are so many prokaryotic groups so similar to each other? Shouldn’t bacteria be as different from each other as they are from eukaryotes?
Now if you say, “well natural selection keeps the proteins the same within bacterial groups for billions of years.” Ok, so you’re willing to say every residue, probably every nucleotide counts? I mean, we have codon bias in bacteria. How much of the bacterial geneome do you want to insist is under selection?
If the bacterial geneome is under strong selection like that, like say for aaRS genes, then how can an aaRS gene evolve? You end up with all these fitness peaks of acceptable aaRS forms, without a lot of explanation for how transitions formed.
Theobald’s analysis doesn’t account such for problems. Like I had intuition about the nylonase issues, I have an intuition a dead rotted corpse of a rat is lurking in the similarity of bacteria to each other.
Allan:
colewd:
Mung has already offered his rather inane take:
Mung:
keiths:
According to this discussion with John, what? Are you trying to make some kind of point? What is it?
These are questions one could answer using phylogenetic analysis, or one could look up the answers already arrived at by phylogenetic analysis, if one had actually intended the question seriously, which one probably did not. Stop stalling, Sal. Get to it.
Phylogenetic analysis gives answers, they could be the wrong answers. You’re assuming the thing you are trying to prove, that is circular reasoning. You could just admit it’s a just a faith belief on your part without direct evidence of how mechanistic gaps dealt with.
How big of a gap do you need before you’ll accept a miracle was needed?
John Harshman,
This is answering one of Allan’s questions of why I think guided evolution is a potential component of common descent.
Two? There are millions of issues not covered. Why is the sky blue? Why is the rotation of Venus retrograde? How did the bacterial flagellum evolve? Of course all those issues are irrelevant to the question Theobald was asking, but so are yours.
The origin of introns is irrelevant to Theobald’s question. Gene loss is irrelevant to Theobald’s question. I will await a clear statement of the third problem, but it does seem at present to be irrelevant to Theobald’s question. We could certainly discuss all those, but you have to start confronting the actual question eventually. (I see that “hidden Markov model” is your new impressive buzz-phrase, by the way.)
Please explain how common design explains anything we see; I’ll be willing to start with anything at all, but you really have to make an argument and be prepared to defend it. Your little cartoon snippets are not arguments. “Wow, that’s complicated” is not an argument. Further, if you may recall, the point you were supposed to explain was the nested hierarchy of life. Do you intend to get to that at any point?
I doubt he said that. I bet he was really asking why you think it’s either necessary or useful. I just said it’s logically possible, a lower bar than anyone should care about.
Hey, thanks for proving my point.
What would count for you as an explanation. Why do you accept “common descent did it” as an explanation, yet you won’t accept “God did it” as an explanation? You provide no details of some of the gaps I’ve identified. You just provide “common descent of the gaps” with no details. That’s just a statement of faith. That’s not really a mechanistic explanation.
A mechanistic explanation goes something like:
1. initial state
2. event that moves initial state to the next state
….
N. final state
When I studied physics and chemistry, I saw a lot of mechanistic details like that. “Common descent happened” or “evolution is fact” is not much of a mechanistic explanation is it?
Maybe there is no mechanistic explanation for common design that we can comprehend. To comprehend it we might have to be God.
No, you mistake what I’m trying to prove. We’re talking about when and in what order various characteristics arose. One can use a tree to determine that. The tree is not produced by the characteristics in question, so nothing is circular.Of course any answer could be wrong, but if you know of another way to answer the question, please suggest it. Of course it’s clear that your question wasn’t sincere in the first place and you aren’t at all interested in answering it. You think all the plants and animals were separately and simultaneously poofed into existence, though you will never provide evidence for that claim.
First, I don’t know what you mean by “gap”. Second, you are again confusing the issue. Even if it takes a miracle to produce a particular mutation, even if that mutation is the instant introduction of a new gene, that new gene would be part of the nested hierarchy that’s evidence for common descent. Evidence of miraculous origin of system X (assuming there were any) is not evidence against common descent of the species containing X, or of those species and other species lacking X. When do you intend to begin discussing the actual issues? Is it likely to be within my lifetime?
John Harshman,
Does logically possibly mean that it is now a candidate to be debated or do you consider it something to be dismissed up front?
And thanks for quote-mining me to score a cheap point. Very Christian of you.
You still seem to have no idea what common descent is invoked to explain. Once more: it explains the nested hierarchy of life. It doesn’t explain the origin of adaptations, though it does explain why, after those adaptations arise, they are distributed as they are observed to be. It doesn’t explain “gaps”, whatever those are, though it does explain why gaps and their absences are distributed as they are observed to be. The question we’re supposed to be discussing is the nested hierarchy of life. Can we agree that common descent is a very good explanation of nested hierarchy, since the latter is a natural expectation of the former? Now you. Please tell me how common design explains the nested hierarchy of life. And please stop bringing a banana to a gunfight.
It’s something that has no relevance to the topic at hand, which is supposedly common design vs. common descent. Had you forgotten? It’s not a “candidate” for any office that’s on topic here.
But to merely assert that it happened you just have to be arrogant and ignorant.
Glen Davidson
Thank you for your reply. A mechanistic difficulty given plausible environmental conditions.
For example, emergence of spliceosomal introns and chromatin from an organism lacking these systems is a mechnistic gap. In contrast a bacteria having one measily point mutation from one generation to another is not a gap as it is mechanistically explained. A detailed mechanistic explanation is:
So a detailed mechanistic explanation for common descent would start with a description of the ancestor in question. Then the evolutionary steps.
A phylogenetic tree can do this for a single protein or set of proteins. It utterly fails as a mechanistic explanation for orphan proteins/genes and Taxonomically restricted systems.
In other words, how novel a system or how unique a system is to a creature or group of creatures for you to be persuaded a miracle was needed to make such a creature possible? Chromatin and spliceosomal intron process is a big enough gap for me. Obviously it’s not big enough for you. So what would be a big enough mechanistic difficulty to make you disbelieve in common descent?
Hypothetically one creature could be silicon based another carbon based. I’d presume you’d reject common descent in that case.
Ok, so then what if both creatures had DNA to code proteins, like say prokaryotes and eukaryotes, how different would prokaryotes and eukaryotes have to be before you accepted prokaryotes and eukaryotes didn’t share a common ancestor? If you say, “well as long as they share DNA to code proteins, I suppose there could not be any difference so large to cause me to reject common descent as the way it happened.” I hope that clarifies what I mean by gap. How big a gap of functional differences are needed before you’d reject common descent.
stcordova,
Sal, thank you for ignoring everything in my reply except for the one sentence that lets you continue to focus exclusively on irrelevancies. Gaps are irrelevant. In order for me to accept that prokaryotes and eukaryotes didn’t share a common ancestor, it would be necessary for them not to exist within the same nested hierarchy, or you would have to propose an explanation for that hierarchy, not involving common descent, that explained the data at least as well, preferably better. To put it in your terms, the difference would have to be such that separate origin explained the data better than common origin. You know, like in Theobald 2010. When do you propose to begin discussion of the actual issue?
If keiths means UNIVERSAL common descent he should say so.
I don’t think Erik is a young earth creationist.
You knew exactly that is what he meant. Your response amounts to trolling.
His notes are incoherent.
So what makes them share the same nested hierarchy? They share some proteins in common, a few other features in common. The proteins they do share follow an nested hierachical pattern. So no matter how mechanistically difficult a new set of proteins might be able to be evolved, like say some of the proteins unique to eukaryotes, even if hypothetically someone could give reasons why it’s mechanistically infeasible, you will assume common descent. Is that right?
Reminds of Allan Miller. Even if he saw God create something with his own eyes, he’d still assume common descent, despite the fact Allan doesn’t have plausible mechanistic details for bridging the gaps required for common descent to be true.
No they’re not irrelevant. Gaps that are big enough suggest the need for miracles. Phylogenies based on shared traits don’t explain unshared traits. If unshared traits require miracles for the trait to emerge, then common descent needs miracles to make it work. Denying the need of miracles to make common descent work is just plain denial, it’s not a real defense of the theory. If a theory, like common descent, needs miracles, it’s not that different from creationism, except that it pretends it doesn’t need miracles.
Saying that eukaryotes and prokaryotes have proteins that can be hierarchically arranged isn’t a mechanistic explanation of evolution of unshared traits. I already said what a mechanistic explanation actually looks like. Such mechanistic explanations work OK for shared traits, they don’t for unshared traits. That’s a problem for common descent.
Finally, I alluded to a problem with the nested hiearchy even for proteins. The intra-species and intra-group divergence between bacteria is too small and not consistent with billions of years of evolution and neutral mutation or high purifying selection. If one invokes netural mutation, then why aren’t bacteria of the same species or group far more divergent? If one says the lack of intra-species variation or intra-group variation is due to natural selection, then that says a bacteria is not evolvable, but then that’s not much good either because on is saying something isn’t evolvable!
And do you plan on sharing?
John Harshman,
This is appearing to be borrowing from the common design hypothesis in order to strengthen its position. If you want this to be a legitimate part of the common descent debate then you must agree that it is relevant.
If not you must fall back to the claim that common descent is a claim about reproduction and unguided variation and then you need to honestly deal with the problems with supporting this claim.
The existence of miraculous changes in DNA over the history of life needs to be explained.
If you say it is irrelevant to common descent then it can be claimed as a strength to the common design argument.
If you claim that it is part of common descent then your position merges what Behe’s as accepting common descent but acknowledging the possibility of intelligent design.
I honestly don’t know how Sal responds to you until you take a coherent position.
What does the objective nested hierarchy look like for just single celled organisms?
http://www.tolweb.org/Life_on_Earth/1
But I don’t want it to be a legitimate part of the common descent debate. It’s irrelevant to the common descent debate. Was that not clear?
I agree that if there were such changes the would need to be explained. But that explanation would be irrelevant to common descent, unless of course the explanation was that species were poofed into existence with all their miraculous features. And that explanation is untenable, given the data.
You will have to reveal the logic behind that claim. If any.
Agreed. Intelligent design and “common design” as used here are not the same thing. If you recall (and I suspect that you don’t, no matter how many times I explain it) the argument here is about whether common descent or common design makes a better explanation of the nested hierarchy of life. (Note: not a better explanation of every feature of life, just the existence of a nested hierarchy.) Behe’s acceptance of common descent puts him against common design as an explanation of the nested hierarchy, though he proposes design as an explanation for the appearance of some of the features making up that hierarchy.
You mistake your and Sal’s failure to understand what the argument is even about for my incoherence.
I’m deleting most of your misunderstandings, because they were already dealt with in the comment you were responding to. But this one is new:
So much wrong, so little time. You neglect coalescence, which has been my response every time you have raised this non-issue. Coalescence is for the most part a phenomenon of neutral evolution. You also neglect selective sweeps, which are not neutral. Neutral evolution results in an equilibrium genetic diversity in any population of constant size. Selective sweeps just periodically eliminate variation, and so reduces variation to lower than the equilibrium value. These are things you could look up if you cared. The remainder of the paragraph appears to be gibberish.
Take E. Coli. Here is an open question that is probably within reach. How much variation in codon bias is there between strains on essential genes (like aaRS genes).
Take another bacteria that doesn’t have the same codon bias as E. Coli. How did the codon biases evolve? Are there active selection pressures maintaining that bias today? If the answer is “no” then, how did it emerge? If the answer is “yes” then how did it evolve in the first place from a creature without that bias? And how long ago did the bias happen?
One of the many problems with Theobald’s hypothesis is that it is confronted with the possibility of immutability of form even for individual genes. There may not be just codon bias on a gene, but whatever kind of bias that is maintained for whatever reason. If that bias is maintained for a billion years, then why should it be expected to evolve in the first place!!!!
What causes things like codon bias? If one says natural selection, that’s not much of a mechanistic explanation. If one says, “the structure dna binding sites of proteins or RNAs that bind to these sites”, now you’re talking. If that is the case that then the codon bias (or whatever bias) is not subject to random variation, it requires multiple changes to change the bias. Such polyconstrained changes aren’t very evolvable, thus falsifying Theobald’s thesis of mostly a random walk on nucleotide of mostly no consequence. The nested hierarchy could not therefore proceed via common descent without miracles (yet again).
Does it work in unstirred populations where individuals are geopgraphically isolated? 🙂 Nope. I pointed out your error earlier, you just repeated it. It doesn’t work so well for strains of E. Coli around the world and in animal guts of animals geographically separated.
Only in the twisted ID world where “design” claims don’t need to be supported, because it’s believed to be the default.
Who doesn’t acknowledge the “possibility” of intelligent design, no matter how unlikely the evidence suggests that it is?
We’re still waiting for the first meaningful evidence for design, rather than illegitimate assumptions that design is the default. It is that flatly unsound reasoning that keeps you from even beginning to think empirically about these matters.
Glen Davidson
John Harshman,
What is giving your argument life is the claim that ID falls within the common descent claim. It is not irrelevant. It is the cornerstone in challenging common design. So in order to challenge common design you must accept ID as a valid mechanism of common descent.
If you reject ID then it becomes part of the common design claim and you probably lose the debate.
There are no such “unstirred” populations. Animal guts exchange bacteria with other animal guts in many ways. If you could be specific about which species, strains, hosts, and divergences you are actually talking about, that might aid communication a bit. Anyway, this is just another distraction from the issue at hand with which this thread is supposedly concerned. Please, can we have some kind of argument for the ability of common design to account for the hierarchy of life?
stcordova,
Do you agree with this?
I was debating whether common descent or common design is a better explanation of the diversity of life. Was your op restricted to a nested hierarchy debate?
I can’t really help you with this. You just spout gibberish as if under the impression that you have made some kind of argument. But here goes anyway:
No. ID is not the cornerstone of challenging common design. ID is irrelevant to challenging or supporting common design which, I hope (in vain) I don’t need to remind you, is a claim about separate creation of species, not of features within those species. ID is irrelevant to challenging or supporting common descent. ID does not distinguish between common descent and common design. ID is not a mechanism of common descent; if it’s anything (and I doubt that it is) it’s a mechanism of mutation and/or adaptation. Mechanisms of mutation and/or adaptation are also irrelevant to common descent and common design. If I reject ID nothing happens to it, and nothing happens to my argument. ID is irrelevant to my argument. (I may have mentioned that before.)
Now, why is all this irrelevant? Because what we’re arguing about is the cause of the nested hierarchy in which life is arranged. We are not arguing about the characters that are arranged in that hierarchy, at least not in this thread we aren’t. ID doesn’t explain the nested hierarchy; mutation and fixation don’t explain the nested hierarchy. They’re just mechanisms that are proposed to result in the events that are distributed in that hierarchy.
In order to explain a baseball game, I don’t have to know what process made the balls, bats, bases, uniforms, etc. I may need to know something of their characteristics, but not who made them or how they got to the field. Whether all that stuff was magically poofed into existence or made in factories doesn’t matter to the progress of the game. That’s the simplest analogy I can come up with on short notice.
I don’t think you have a clear idea of what you mean by “the diversity of life”, so it’s hard to argue about explanations.
colewd,
Yes and no. One cannot address the merits of each without addressing larger issues. If common descent fails as a mechanistic explanation for orphan features, except via miracles, it should be removed as an explanation for the nested hierarchy because it fails to account for how one creature could descend from another in the first place!
Focusing only on the nested hierarchy is a way of avoiding problems with natural unguided common descent.
Going back to the “flower” diagram, one can build nested hierarchies without accounting for the anomalies and problems that diagram poses for common descent.
One might argue for common design with common descent. But that would be common descent with miraculous or intelligently designed emergence of orphan systems. The brutal example of course is:
prokaryote
XXXXXXXX
vs eukaryote
iiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiiiiiiiiXiiiii
Theobald and others build the nested hierarchy on the X’s for their protein phylogenies. It looks tidy on paper, mainly because the data is cherry picked. The other cherry picking going on is for unshared traits. Highly unique traits, like a central nervous system, or specialized cell types, etc. don’t fit the model of random variation on a pre-existing genes very well does it? They sort of just poof onto the scene.
Common design is a better explanation because mechanistic barriers preclude common descent.
The only complaint might be that special creation is a bigger miracle than a pre-existing form miraculously evolving to another form. But this is like saying 500 fair coins 100% heads happened by chance and not by design because 1,000,000 fair coins 100% heads would be miraculous.
John Harshman is trying to set the rules of the debate one way, and he complains I’m introducing irrelevancies. Nothing is more relevant than whether one form can have a line of descendants that leads to another form with radically different sets of (orphan) genes and systems. I’ve shown some of the some of the barriers to ordinary transformation.
How then are their so many strains of e-coli with only 20% conservation between strains? That’s doesn’t look like evidence a lot of coalescence is going on.
colewd: Was your op restricted to a nested hierarchy debate?
Salvador: Yes and no
Mung: *bangs head on desk*
The diagram below should be familiar to colewd regarding the vitamin D receptor and vitamin D receptor binding site. What is true of this feature is likely true for so many others, namely DNA is not just for coding proteins, but serves as parking lots and road signs. The sequence is constrained not to change too much without compromising another system.
If the genes are constrained in such ways in general, then genes can’t evolve randomly as a matter of principle without compromising something else. Yet another problem common descent must overcome via a miracle to create the nested hierarchy.
mRNAs which go on to code for proteins are constrained by the micro-RNA binding sequences on the mRNAs, thus the protein sequences aren’t as free to evolve as Theobald postualtes! Protein sequence, and the underlying DNA sequences, can’t be changed without changing the optimized regulatory schemes that are sequence dependent!
Here is a relatively trivial microRNA regulatory network that relies on DNA sequences being a certain way. Such DNA sequence aren’t free to mutate without compromising regulatory function.
Ergo, Theobald’s ideas are obsolete in light of new data.
One of the problems with the idea of “the possibility of immutability of form even for individual genes” is that all evidence ever from the entire field of biology says there is no single entity for which this is even a thing. There isn’t any single polymer of life, or gene, that doesn’t show divergence over the total history of life. If it’s “immutable”, why is it probably demonstrably different between two arbitrarily picked species? Shouldn’t “immutability” entail an exact identical copy in all species?
See, this is one of the points we’ve all been trying to get you to deal with. The demonstrable non-immutibility of even the most well-conserved and apparently fundamental genes of life.
Back to the now endlessly invoked example: cytochrome c.
Why is it different (in nucleotides) between human and chimp? Why is it even more different between human and gorilla? Why is it even more different still between human and orangutan? Even more so between humans and domesticated pigs? (Why are the most divergent “pig” cytochrome c sequences more similar to each other?)
Why are bacterial cytochrome c’s so extremely divergent? Why not just re-use the exact same one every time?
Why can we take out cytochrome c in yeast, and put in the human one, and it still functions?
From Theobald again again again again:
Ah. Sal resorts to the Gish Gallop.
You’re presuming a change to a binding spot results in either a move to complete nonfunction, or a change that is significantly visible to selection.
In actual fact, what we know about such binding spots is that many sites are neutral, and due to epistatic interactions between multiple mutations allows changes to sites that in isolation look strongly deleterious.
So there are some sites in binding spots that are strongly deleterious at any given time, so they can’t mutate without incurring a significant fitness cost (if not death) to the host organism. But, mutations in neutral sites accumulate over generations, which in turn allow the previously “immutable” site to mutate due to epistatic interactions with the neutral ones.
This is an observed fact. There are no truly immutable things known anywhere in biology. Your imagined problem here is just that, imagined.
http://www.ucmp.berkeley.edu/archaea/archaeasy.html
Just what you want when you go about creating an objective nested hierarchy!