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.
That’s cute.
Here’s the context.:
keiths, replying to Zachriel’s Topiary comment:
From this context, the clear implication that any sane reader would draw is that inferring guided evolution is what either Zachriel, or John, or DNA_Jock, is accused of doing.
So I asked Why even bring it up?
[As in, “Who’s ever kissed a chipmunk?”]
Keiths replied: “Because it’s my central point”
Swoooosh.
keiths: “I told you already: I brought it up because it’s my central point. In this thread I am arguing that just as the evidence is fatal to ‘common design’ and the Rain Fairy hypothesis, it is also fatal to the hypothesis of guided evolution. It’s my central point, and you are arguing against it, so why on earth wouldn’t I bring it up? It makes perfect sense to do so.”
“fatal to”, but simultaneously “compatible with”, I guess. Okaaay.
[/snark]
Your point (which I have never misinterpreted) is that, because there are many more ways for the guider to NOT produce an ONH than to produce an ONH, an ONH is compelling evidence against guided evolution, despite it being “logically possible” or “compatible” with guided evolution.
I know this may be hard for you to accept, but I understand and I disagree.
Third time of asking, would you care to describe my argument?
Sal’s MO in this thread is: Try to just spam the thread with crap and irrelevancies until everyone gets bored. And most of what he says is just ignorant nonsense.
No. Sal, you are looking at branches, not nodes. Remember.
Yeast did not evolve from E coli, and mammals did not evolve from yeast.
Rather, the 2 and 3 domain lipoyl proteins probably evolved independently from a single-domain ancestor in LUCA. There is no reason to postulate 3 domains evolved, then 2 were lost, and 1 was re-gained.
A real phylogenetic analysis might actually help make sense of it and could potentially shed light on the relative timing of domain gains and losses.
You don’t claim a meaningful origin of the patterns of similarity and diversity, you just claim it’s designed without showing any kind of evidence of design. Real design is a causal explanation, and you don’t begin to show a causal explanation of anything in wild type life.
And since you don’t actually have an observable cause you think you can just say “design” for any sort of anomaly or whatever. That is not how anyone discovers actual design. In archaeology or what-not you have to demonstrate some sort of reasoning or ordering that is done by humans exists in an artifact, or any old fossil would be considered to be “designed.” Only IDists/creationists think they can get away with finding functional complexity and calling that design.
Yes, anyone can, because it’s not just an anomaly or pattern that hasn’t yet been explained. It’s something rationally designed, and implemented by means that humans are capable of wielding.
No, intelligence is understood “mechanistically,” in your IDist language. No real scientist considers intelligence to be magic or “non-mechanistic” (however bizarre it is to use IDist jargon).
No, that makes no sense at all. That’s like saying we don’t know the cause of ball lightning, thus it has to be “designed” or some sort of miracle.
This is the problem with ID at the current time–instead of making causal arguments based on known aspects of effective design, IDists just default to “design” or “god did it” whenever there’s something not known, or even when something is quite well understood via cause and effect, such as evolutionary processes as the cause of the nested hierarchy. You don’t explain anything, you merely assume miracles or design when questions arise in biology (or don’t, for that matter).
Glen Davidson
Rumraket,
You misconstrue the argument. Yeast evolved from some prokaryote-like creature like E. Coli.
You totally missed the more important point. Any bets on the similarity of the three lipoyl domains in EACH prokaryote? If they’re similar, do you understand what that means?
On the contrary, you’re just misreading and misinterpreting what was said.
It doesn’t matter, the point is the similarity of the 3-lipoyl domains in each prokaryotic species preserved over a buzzillion years. And if not this, then I’m relatively confident I can find some other candidate.
Before you accuse me of spewing ignorant nonsense, remember I’m the one who is setting the record straight on nylonases while the world ignorantly listens to Ohno and publishes evolutionary papers on Ohno’s theory that is now falsified.
So basically you’re making up a phenomenon that probably doesn’t actually exist and calling it a problem for common descent. Check. And you’re making up a “Sternberg-Collins paradox”, ditto. This is the classic Gish Gallop. Meanwhile, you have never managed a single sentence on the supposed subject of this thread.
Back to the drawing board, the 3 lipoyl domains might be just expressed 3 times form the same gene. But, I think I have an idea of what to look for next time.
stcordova,
After you are famous, maybe they will name an Ark after you.
But no idea of how to actually provide evidence for your design claims.
Glen Davidson
What does that even mean?
I don’t think you can
A general affliction of creationists seems to be that they spectacularly underestimate bacterial diversity. If you bothered to read Larry’s posts you linked to, you could already have learned that several bacterial species do not utilise pyruvate dehydrogenase at all, but an alternative enzyme. If there is one thing bacteria and archaea can beat us at, it is metabolic versatility.
DNA_Jock,
Your inability to admit your mistakes is approaching an Alanesque level of absurdity.
I’ve explained how you could have avoided your mistake.
I do not think that any of the four of you are arguing for an inference of guided evolution, and I do not think that any of you are IDers.
You are making a bizarre and obviously false claim.
Please learn from your mistakes, be a little more careful next time, and drop the false claim you are continuing to make.
Jock,
Regarding your counterargument, I have pointed out a major mistake you are making.
Do you see your mistake?
keiths,
Guided evolution can produce an ONH.
No-one here has suggested otherwise.
Specifically, DNA_Jock has never thought that keiths has ever claimed that guided evolution cannot produce an ONH.
So, I have not made the mistake that you ascribe to me.
DNA_Jock does, however, think that keiths views an ONH as evidence against guided evolution, because keiths reckons that there are many more ways for a guider to NOT produce an ONH than for a guider to produce an ONH, and hence his disputing of John’s statement.
For the fourth time, would you care to try to repeat my argument back to me.
Active listening, it’s a skill you lack.
DNA_Jock,
I am now, for the fifth time, pointing you to my explanation of your error. In Alan-like fashion, you keep trying to change the subject away from it. Is it really that hard for you to admit your mistake?
Please address the issue this time.
You wrote:
keiths:
DNA_Jock:
keiths:
Do you see your mistake?
If you think it isn’t a mistake, then explain to us what it is in those comments that constitutes a counterargument.
Brilliant and unanswerable. Assert there’s a mistake and put the burden on your opponent to refute the bald, evidence-free assertion. Demand a counter-argument without making one of your own. Works every time! 🙂
Alan,
Here’s a hint. Did you notice this sentence?
Now see if you can figure out where one might go to view the evidence.
keiths,
QED 🙂
Alan,
You might be having trouble, but I think DNA_Jock is bright enough to follow his own links to the comments I’m referencing.
keiths,
I’m merely making an observation regarding your usual style of participation. On any sane measure, it seems counter-productive, unless your aim really is to be last man standing.
Alan,
No, you claimed that my assertion was “evidence-free”:
I showed otherwise. Your attack backfired, as usual.
This is how you think? You do actually want to be the last man standing?
Yes, Alan, it was an attack. And a false one:
Feel free to deny the obvious.
You can characterise it how you like. I maintain it is a typical example of your commenting technique. I think it is counter-productive and results in fewer people engaging with you on any meaningful level. I think it is fixable, unless due to a pathology, in which case my sympathy, but continue as you are and more people will tend to refrain from engaging with you. I would have thought your aim was to persuade people to your point of view. It’s a reasonable aim and your point of view often has merit but your technique is something else.
Ah, now I understand what you mean. Before you triumphantly post on an example of this, look up the following word in your text book:
Concerted Evolution
Alan,
You periodically offer me your advice, but you never seem to question your competence to offer it.
I don’t aspire to your failures as a moderator, your poor reasoning, your intellectual laziness, your inability to admit mistakes, your self-admitted lying problem, or your insecure need for approval. Given all of that, you would be one of the last people I would ever consult for advice. Your judgment is terrible, as your many moderation screwups demonstrate.
TSZ is working fine for me. Not so well for you. You’re a fish out of water here. I would suggest working on yourself instead of offering advice to others.
Yep, looks like you discovered examples of concerted evolution. Look up “gene conversion” as well, while you are at it. Ribosomal RNA genes are good examples of this process.
Corneel, to Sal:
Very cool.
stcordova,
Utter tripe. If transposition coupled with common descent can cause the same sequence (flank-SINE-flank) to appear in a clade, but not in outgroups (flank-flank alone), I don’t need to explain this from first principles of physics and chemistry. After all, as I have said repeatedly, this is the basis of paternity testing, among other within-species tests accepted by even the most ridiculous of your ilk. Try going into court and insisting that they need a mechanistic explanation from first principles before you will accept the verdict, and watch them laugh.
stcordova,
Ah yes, a squirrel. Very nice. Now, about the presence of a single SINE of your choosing in any clade of your choosing vs the presence of its flanking sequence alone in outgroups. Design or descent, and why?
Oh boy, you are really twisting in the wind there, mate.
You are correct that three of the linked comments describe situations in which guided evolution will produce an ONH. But I linked to four comments, not three, and the fourth linked comment is a doozy:
It provides the counter-argument (for which the other links are merely supporting data), which counter-argument you have steadfastly failed to address; it makes it abundantly clear that I am not making the mistake that you repeatedly attribute to me (i.e. assuming keiths thinks “GE cannot produce an ONH”), and it includes a quotation of you accusing me of “supporting guided evolution”, something you claim to have never done.
It’s the George Costanza Trifecta!
I love it!
If I am feeling charitable later today, I may explain to you where you made your mistakes, and how you might, in the future, avoid them. I guess that’s a thing now.
Your honor, we move to have the case against my client dismissed, given that we have not heard from the prosecution, an account from the fundamental principles of quantum electrodynamics, describing the complete world-histories of the total set of quarks and leptons constituting the arm of my client at the moment he is purported to have swung the knife at the deceased.
Rumraket,
Physicists don’t claim tornadoes passing through junkyards create 747s.
In contrast evolutionists claim mutation plus or minus selection results in systems capable of making 747s ( systems such as humans). Look at a bacterium, heck look at a protist. Given the sample size of direct observation, any mechanistic predictions of what it will be a buzzillion years from now? Maybe at best another protist, not something with a complex brain capable of making airplanes.
But you missed the fact the Sternberg-Collins pattern in mice and rats is not due to common descent since the SINES involved are not the same. The utter tripe is your own making. Here is the pattern again:
Sternberg is an evolutionary biologist, he appreciates the significance of this finding, apparently you don’t.
The point I was making had nothing to do with whether all bacteria had pyruvate dehydrogenases.
On a side note, Larry argues chemotrophs were examples of early life. To the best of my knowledge, chmotrophs need to live in an environment that has some kinds product of nitrogen fixing bacteria, and nitrogen fixing bacteria are more advanced life forms. So he should stop referencing chemotrophs as solving part of the abiogenesis problem. Something I wanted to mention at some point.
Regarding the phylogenetic methods. There are:
Distance based methods.
Parsimony.
Maximum Likelihood.
But unfortunately, maximum likelihood assumes common descent to begin with and it selects a tree with the maximum likely hood of being true, but that is all moot if there is no common descent to begin with!!!!!
Soooo, again there is a conflict with taxonomic nested hierarchies which are demonstrable with simple distance comparisons — eh like say Orphan Systems. The distance between a creature with given orphan systems and a creature without is, eh, pretty big. No need for maximum likelihood to build a taxonomy. We can build nested hierarchical systems without phylogenetic methods such as maximum likelihood, in fact do it more accurately if indeed there is no universal common descent. Thank you very much.
BTW, maximum likely hood on gene trees doesn’t work at all on missing genes, as would be the case with orphan systems. Ergo, taxonomic nested hierarchies are the much more accurate way to do classification if there is no Universal Common Descent.
The phylogenetic math is beautiful, it is worth studying as an art form, but if there is no Universal Common Descent, then for it to be practical it has to find a home in some other application.
Joe Felsenstein’s math is beautiful, the work of a beautiful mind, right up there with Nash who won the Nobel Prize in Economics and had a movie called a “beautiful mind” made in his honor.
stcordova,
You are just dodging Sal – everyone can see. The sole connection between SINE loci used in phylogenetic analysis and your supposed ‘Sternberg-Collins paradox’ is the word ‘SINE’. You hear a word and scuttle off to find something else with that word in. You might as well say ‘DNA? Here’s something with DNA in it’.
Focus: ‘flank-SINE-flank’ vs ‘flank-flank’. The former is shared by a clade, the latter the pattern in outgroups (if detectable at all). This has been used in many, many taxonomic analyses to supplement the pattern given by more conventional, non-transposon genes. If there’s doubt over one site, you can easily cross-check using another.
So again – why would a clade have a specific SINE at a specific location, on a ‘design’ paradigm? I can easily say on Descent – they all inherited it from their common ancestor. That logic is accepted by the courts, for forensic and relationship analysis. What is the explanation on Design? Why on earth would a transposon follow such a pattern?
No it is not. You saying this is evidence you are mischaracterizing what the paradox is, namely the convergent 300,000 insertion points.
I’m not dodging, but if you want to see dodging taken to a level of art, look at this. Watch Tyson bob and weave with the Peakaboo style of Ali:
https://youtu.be/LSNrVew7Lb4
I apologise for misunderstanding, but you are not making your points very clear. It seems you are running out of ammo for your Gish Gallop and are now launching premature ideas.
Do I understand correctly that you are currently looking for paralogous genes or protein domains that display high similarity within species but are divergent between them, as you perceive this to be evidence of design?
I seriously doubt that Larry proposes extant chemoautotrophs to be examples of primordial cells. Don’t you think that he simply mentioned them as proof of principle that organisms need not be dependent on products of photosynthesis as a source of energy and organic compounds?
That’s a fair and accurate criticism. I’ll try to do better.
Regarding the lipoyl domain, I was hoping to get a protein with very high internal repeats in it. We see repeat sin non-coding regions, but not really in genes.
The best I could find was a frog (xenopus) that had 9 internal repeats of a zinc-finger domain, but even then the repeats were not anywhere near exact. Here it is anyway:
http://www.cell.com/cell/pdf/0092-8674(92)90601-8.pdf
Unfortunately the “tandem” repeats are not really all that similar. I tried to find such idealized repeats in bacterial genes. I thought they would be the lipoyl domains. My bad, my hasty assumption, my apologies.
stcordova,
A single flank-SINE-flank locus is still evidence for common descent, where it is shared by a clade but not by outgroups. This is the point you keep dodging.
If you are arguing that all – or even any – of the 300,000 insertion points is convergent down to its last bit, I’d say you are going beyond what that coarse genome map permits.
If it were the case that a particular flank-[]-flank locus had flank-SINE1-flank in one species, and flank-SINE2-flank in the other, that would not be evidence for the common descent of the full pattern with insert – though one would still consider the commonality of the flank+flank sequence to be evidence for the common descent of the flanking sequence.
It would depend upon the proportion of sites that had such a precise insert pattern, and how this translates up across all taxa. A few, and it could simply be stochastic noise, with the coarser pattern arising from a common distribution of euchromatin and heterochromatin (a distribution which itself supports common origin). Transposons are not randomly distributed – they tend to cluster near sites of active transcription, for mechanistic reasons, hence avoiding heterochromatin. It would be very surprising if all SINE site used in all phylogenetic analyses were homoplasic. You’d need more than that graphic to unseat their widespread use in the field.
I can’t find a paper on this BTW. I find Sternberg’s ENV article, which links to a paywalled Nature paper – with Collins as the last of dozens of authors! Sternberg seems keen to pick him out.
It sure takes a long time for some people to get bored.
You mean if you assume that apparently copied material actually comes from observed processes of copying, then one can make sense of the patterns of copying that are observed?
What a leap of faith! Who would make such an assumption, other than linguists, philologists, copyright attorneys, and judges? How is that legitimate, when poofs could do it, so long as one assumes that poofs could do it?
Glen Davidson
The Sternberg-Collins paradox doesn’t not argue against common descent! It argues against random mutation, therefore it argues in favor of common design.
This is the one case where one might assume common design in a framework of common descent. I’ve argued in light of the common design, which points to a designer, one can dispense with the assumption of common descent if there is a designer so capable of re-engineering the genomes in this way.
I am all for bacterial diversity. I even started a bacteria and diversity website. For some reason other sites keep blocking it.
You seem to have missed my previous comments, so I will warn you again: repetitive sequences within lineages tend to evolve in a concerted fashion. Several explanations have been proposed, but design is not among them.
You can tell he’s been debating creationists for a long time.
Are you talking non-coding or coding regions, I was specifically talking about repeats within coding regions. Alus, transposons are well known repeats in lineages, but those aren’t generally in coding regions (some claim some genes are converted transposon parts).
Just say it’s inherent in the Schrodinger Wave Equation.
You don’t say. The same happened to my pathogen diversity website where you could freely download viruses.