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.
keiths:
Alan:
That’s bad logic. “You’re unimpressed with lots of things you don’t understand” does not imply that you’re unimpressed with all things you don’t understand.
This was my answer:
The universe contains all things of which we can have knowledge. So, if I were a determinist, I could not “know” about anything. Lucky for me I’m not a determinist.
Alan,
That’s hopelessly confused.
First, the second sentence isn’t even true. Nothing about determinism implies that knowledge is impossible.
Next, since you are not a determinist, the second sentence doesn’t apply. Therefore it can’t function as a defense of your counterclaim.
Third, even if it were true and did apply, it still wouldn’t falsify my claim. The fact that you’re impressed by the universe as a whole doesn’t mean you’re impressed by everything within it.
You packed a lot of errors into that short paragraph.
Alan:
That’s not the question I was referring to, as you know.
I asked, regarding your LEM confusion:
Chains of causality! I reject that myself. But you asked me “You think that to reject Rain Fairyism in favor of modern meteorology is a matter of mere preference and opinion, and not of scientific validity?” which I answered. I’m sorry if you didn’t like the answer. If you want to persuade me otherwise you need to support your ideas with evidence from reality.
I’m sorry. I’m not defending any counter-claim. I’m just commenting in a blog.
What claim? That Rainfairyism is a stupid hypothesis? I’m agreeing it is a stupid hypothesis. But then, who holds it?
Alan,
I’m not sure whether you’re deliberately obfuscating or are genuinely confused about what you were responding to just moments ago.
Here is the actual exchange:
keiths:
Alan:
keiths:
Alan:
keiths:
As you can see, the topic of the exchange was my claim…
…and your counterclaim, which you mistakenly took to be a refutation:
In the future, if you find yourself getting confused about what you are replying to, just go back and read the relevant comments.
Now, do you see why your counterargument failed?
Alan,
Regarding your LEM confusion: Do you see your mistake now, or do I need to explain it?
Alan,
No one that I know of. It’s a stupid hypothesis, after all.
That’s the point. It’s a stupid hypothesis, and it’s stupid for the same reason that guided evolution is a stupid hypothesis.
Yet regarding guided vs unguided evolution, you wrote:
Choosing meteorology over Rain Fairyism doesn’t amount to merely “choosing the option that suits your opinion”. Neither does choosing unguided evolution over guided evolution.
Rain Fairyism and guided evolution are stupid explanations, and we can say that on the basis of the scientific evidence.
dazz to Mung, regarding dazz’s proposed descent-with-modification program:
It’s probably true that among the regular commenters, those who are bright enough to interpret the program’s results are already convinced of the point you’d be trying to illustrate.
There might still be some benefit for the lurkers, though.
keiths,
Apologies to Keiths for my comments last night, partly induced by a home-cooked supper washed down with my favourite merlot, which were a bit of a ramble through the long grass.
Looking back at comments by Allan Miller, John Harshman, DNA_Jock, Rumraket, Zachriel and yourself, I’m happy to concur with them that observing a nested hierarchy does not rule out a guided process per se.
Additionally, I broadly agree with Allan Miller and DNA_Jock regarding the the upward and downward paths of HGT sequences and that including them is not detrimental to common descent.
I don’t think further exchanges betwixt thee and me on either point will prove fruitful for either party, so I’ll leave it there.
Alan,
The merlot is not the root of the problem.
I have not been following all this in detail (life is too short) but have some thoughts about whether or not the genealogy of life shows a pattern of a single tree of common ancestry:
1. There is hybridization, there is horizontal gene transfer, there is symbiotic origin of some organelles, there are coalescent effects (incomplete lineage sorting).
2. All of these are cases where there is common ancestry but not a single common shared tree.
3. Horizontal gene transfer is much more visible in bacteria and archaea than in eukaryotes.
4. Nevertheless there is a tree of ancestry of cells, and we can, even in bacteria, see a signal of it.
5. Hybridization is largely confined to occurring between closely related species. Symbiotic origin of organelles is rare. Discrepancies between coalescent trees at different loci involve small rearrangements of the tree.
6. Horizontal gene transfer looks common in bacteria, but only if we look back hundreds of millions of years. The average reproduction of an average bacterium is simple vertical descent.
7. Once a gene arrives in a lineage as a result of HGT, its subsequent inheritance is vertical, and (as noted in this thread) it does follow the tree of descent of subsequent lineages, and in that it provides further evidence for that tree.
8. Nevertheless … in bacteria, the HGT that we see does affect many genes. So the tree of bacteria is less than totally useful in predicting the trees at the individual loci.
9. In eukaryotes, particularly in multicellular animals, plants, and fungi there is a strong signal of a genealogical tree that is seen in almost all genes, with discrepancies due to hybridization and due to coalescent effects greatly constrained by that tree. So that tree is critically important to understanding the diversity of life.
10. I have phrased all this in terms of genealogy and trees, not classifications.
A high road less taken
I would call evolutionary convergences an example of common design. That is to say, even evolutionary biologists would say the similarity is not due to common descent of parents to children or “common descent” of genes via HGT. So clearly there are common designs that are not explicable by common descent, even according to evolutionary biologists.
One such notable common design which was reported by evolutionary biologist Richard Sternberg and was originated by the Illustrious Director of the NIH and head of the human genome project, Francis Collins. The common design is what I call the Sternberg-Collins Paradox.
I described it here:
Paul Nelson said it gave him goosebumps reading Sternberg’s account. John Sanford also found this compelling evidence of design. Sometime thereafter, I began looking into this and reporting on it as it was interesting on so many levels:
So, imho, we have evidence of non-random mutation or even common design by an act of miraculous special creation. Whatever it is, it superficially looks God-guided to me, either through non-random mutation or an instantaneous poof.
This common design of SINES can’t be willy-nilly, it must be carefully coordinated. Such SINES are often road signs and parking lots for molecular machines like the CTFC machine.
One important aspect of SINES are the CTFC binding site motifs often found in SINEs. The motifs can’t be randomly located, otherwise they would not properly create something known as a chromatin extrusion loops. Further, these CTFC binding site motifs must be coordinated to “point” in the right direction many base pairs away in order for these extrusion loops to form. See this amazing video of extrusion loops and CTFC binding sites (which are often found in SINES):
One important aspect of SINES are the CTFC binding site motifs often found in SINEs. The motifs can’t be randomly located, otherwise they would not properly create functional chromatin extrusion loops. Further, these CTFC binding site motifs must be coordinated to “point” in the right direction many base pairs away in order for these extrusion loops to form. See this amazing video of extrusion loops and CTFC binding sites (which are often found in SINES).
The video suggest to me this common design in the rat and the mouse didn’t happen by random mutation. It happened either by God-guided mutation or special creation.
newton,
Alan’s problems run far deeper than a bit of extra merlot with dinner. He isn’t dealing with the real issues.
The wine is an excuse, and it’s a poor one. If you think that pointing that out amounts to “a high road less taken”, then so be it.
This has always puzzled me, Sal — what is involved when God intervenes in the observable world. How does he do it without leaving a trace? In fact, there should be an anomaly because a supernatural input would be an undetectable action. For example if God decided to act by kicking a football, the ball would appear to be launched without any apparent cause, a violation of the laws of physics. Have you ever considered how God might intervene in the real world?
How, when, why, what, where? We’ll skip “who,” since you’ll just say “God,” like any meaningless placeholder.
Oh that’s right, you’re not providing any answers or doing any science with ID.
Glen Davidson
Yes, absolutely. If God is the designer, He has also chosen not to be so “in your face” as to make people believe. He could in principle do what he did to the Apostle Paul and give everyone a direct experience that would be as certain as the air we breathe. He has chosen not to do that.
For that reason, many people do not believe, and I respect that, but I decided if I could accept that God has chosen to be so oblique, then I could accept his existence.
FWIW, I think I have personally seen answered prayers, and others I’ve met whom I respect, like Astronaut Duke worked a miracle in the name of Jesus.
That said, I don’t believe in miracles or ESP on demand as I describe the James Randi challenge:
stcordova,
What, all of ’em? This is your ‘found-a-constraint-therefore-not-one-bit-can-vary’ nonsense again.
You need to explain, from a design perspective, why a particular SINE used in a phylogenetic study is present at a particular site in all members of a given clade and not in any outgroup, rather than just handwaving in the general direction of something functional you found on the internet applicable to some members of a molecular class.
[eta – and you need to bear in mind that SINEs are used in within-species relationship tests. If your pet function is truly universal, applicable to every single bit of every single SINE insert, it invalidates these too. Are you prepared to be so bold as to go that far out on a limb?]
Sure it can vary just like cave fish can go blind. The creature still lives, but the question is why is it in such an improbably fine-tuned state?
You may say, “selection”, but the problem is this is a complex system that is weakly selectable.
No I don’t any more than I need to explain why the statues of Mt. Rushmore exists. It suffices to point out a structure is not consistent with ordinary expectation.
The SINE patterns between mice and men are not consistent with random mutation but rather coordinated mutation (assuming no special creation).
That’s more a problem for you however because are you going to argue a bunch of mistakes created the similar distribution between Mice and Rats?
Some SINES are mistakes, the rest look really coordinated. More evidence of recent special creation, otherwise those poor rats would be dead from all the junk in their genome by now.
stcordova,
A within-species relationship test means ‘within mice’ or, separately, ‘within rats’, so I don’t get the point.
Sal, SINEs are transposons. They contain within their sequence the means to transpose, albeit ‘fossilised’ in those that have lost the ability. This is not even slightly a problem for Common Descent. Having transposed, the presence of these sequences in clades, and absence in any outgroup, are precisely predicted by common descent. What this ‘separate mistakes giving similar distribution’ thing means, I have no idea; that is not what common descent means.
3000 comments in, I’m beginning to thing you just can”t grasp common descent. Something is getting in the way of basic comprehension.
stcordova,
As far as your average SINE insert is concerned, it is not in an improbably fine-tuned state.
No, I don’t say ‘selection’. That would be silly. After all these years of arguing the Creationist corner, going to the trouble of taking courses, you still think evolution amounts to ‘RM+NS’.
The thread title is ‘common design vs common descent’. You need to explain why common design is a better explanation for the generality of SINE patterns. It is entirely consistent with ‘ordinary expectation’ on common descent, not at all on ‘common design’, so your alternative theory has work to do.
Allan:
My assessment of Sal hasn’t changed:
Sal, who made mount Rushmore? When was it made? Why? How?
This interests me. Most creationists argue that the evidence for the creator is all around for everybody to see, but some people blind themselves to that. You seem to be saying that the evidence is actually very subtle.
Have you also considered why God has chosen to be oblique?
Allan,
I think you’re not characterizing my argument correctly. It could be I didn’t state it well enough.
When I say a site is constrained, it is functionally constrained, not selectably constrained, like a cave fishes ability to see or a beetles ability to fly. These traits can be actually LOST by selection. Therefore these functionally constrained sites are selectable. Someone can develop sickle cell anemia or any number of birth defects. It doesn’t mean the sites in question weren’t functionally constrained.
Unfortunately, the “selection = function” notion vs. the medical notion of function leads to all sorts of absurdities as I pointed out here:
and
But you have the problem that if something is neutral then why is a pattern convergent? Here it is again. Read it and weep:
God wants to play hide and seek?
"It is the glory of God to CONCEAL a matter, it is the glory of kings to search out a matter." Prov 25:2
and
"11 Therefore God sends them a strong delusion, so that they may believe what is false, 12 in order that all may be condemned who did not believe the truth but had pleasure in unrighteousness."
In other words, God lets people who think they are wiser and morally superior to God condemn themselves. Example of such a person:
or we could view ourselves as deserving of God’s wrath. Obviously there is a right and wrong answer. But if there is an intelligent designer, then the designer is quite CRUEL as I pointed out here:
if he is that cruel, he will play cruel pranks on people he wants to condemn. But the design is evident enough for people wanting to see it and repent.
stcordova,
So stop handwaving and show us a SINE that has been used in a phylogenetic study which is functionally constrained. In anything – bird, bat, primate, rodent, whale, fish, whatever. Take your pick. There is a lot to go at, but I’m feeling generous. You only have to find one.
My irony meter went off hearing that come from you….
This was straight from the article:
http://www.nature.com/nature/journal/v428/n6982/full/nature02426.html
Here’s the pattern again. You can try to deal with the problem or ignore it or misunderstand it pretend it doesn’t exist, or make endless irrelevant demands of me for more explanations.
The problem is, the Sternberg-Collins pattern isn’t explained by random neutral mutation. You want to argue it appeared by natural selection and argue SINES are selectable? Well then that contradicts your notion that they are unselectable junk. Catch-22, checkmate.
I don’t need to explain the motivation of an intelligent designer to make certain patterns anymore than I need to explain the motivation of the sculptor who built Mt. rushmore. Sternberg highlighted a non-random pattern not due to common descent, therefore it is a common architecture (aka common design) by definition.
stcordova,
So you have circumnavigated the problem of evil by assuming that God is deceptive and cruel?
That is .. an interesting viewpoint. I feel that I either must have misunderstood what you are saying or that you are pulling my leg. Is that really what you want your God to be?
Actually, my question wasn’t so subtle. I was wondering what the method of intervention might be. How does the “intelligent designer” or God act to bring about whatever is supposed to be brought about. Presumably, at the interface between reality and wherever God is intervening, there’ll be a local
disturbance in the forceviolation of the laws of physics. We could look for examples presumably. I don’t think anyone has reliably observed any such event. It does seem God is hiding his power exceedingly well.And yet you fail consistently to give us this evidence. You’d rather attack evolution, as if design were the default. I don’t think any IDist does otherwise, but it’s not a legitimate means of argumentation.
The evidence against any kind of design we know is good, of course. The simple fact that “innovations” in vertebrates are limited to lineages (thus homologies between birds and mammals exist, but only old ones) and not used to provide function for needs is clearly evidence against empirically-known design processes (and other design processes are not known).
Glen Davidson
Figured that
So? What do you think that means and why?
I would like an explanation of what you think the pattern is and what it means. Why isn’t it explained by random neutral mutation? Surely you don’t think that “random” requires a uniform distribution.
Who says it’s non-random? What does “random” mean to you? And how have you managed to suppose that everything non-random must be designed by definition? You need to explain your hypothesis, what the evidence is, and how the evidence fits that hypothesis but no other, and you need to explain it clearly and completely.
I find your lack of faith disturbing
Alan,
Corneel was replying to Sal, not to you.
Corneel,
🙂
stcordova,
And then you proceed to handwave some more. Priceless.
I am hardly handwaving in talking of something quite specific – the presence of a given SINE at a given position (you get to pick which one), and the competing explanations for that: design vs descent. I’m not the one bafflegabbling about SINEs in general, or some broad pattern such as distribution between euchromatin and heterochromatin. A SINE can be located down to the precise bit on either side. That is what is used in phylogenetic analysis.
You have not given a functional explanation of a given SINE sequence at a given position – a site that can be detected either as flanking sequence alone, or flanking sequence including SINE, allowing distinction between the haves and the have-nots. I don’t need 300,000 SINEs; just one, with a functional explanation of the role that SINE plays in the clade that has it. Not SINEs of the same class, nor even SINE instances with the same sequence, but that SINE – that instance of the SINE, at that location.
stcordova,
I don’t have a universal rule. Some loci containing SINE sequence are under selection, some (I’d say most) are not. Why the insistence on a dichotomy? It doesn’t matter hugely anyway – a SINE used in phylogenetic analysis could be under selection or not – it’s subject to common descent either way. Only Common Designers need to care about function – and they have to find a function for every single one, at whatever taxonomic level they think Common Descent ceases.
I note that Sal is being coy on this point too, since he has only supposed “for the sake of argument” that mice (Mus musculus?) and rats (Rattus norvegicus?) might be related. I’m wondering if Sal is one of the few YECs who think that every species is a unique fiat creation. Bet he won’t say. A clearly expressed hypothesis is a target for refutation, but a moving, diffuse target is hard to hit.
DNA_Jock,
Let’s review the exchange.
You wrote:
I responded:
Despite being corrected, you are still bizarrely asserting that I accused you of arguing that we should infer guided evolution from the available data.
Let’s talk about your mistakes and how a more careful and thoughtful reader might have avoided them.
You saw the following…
…and assumed it was about you. That was a mistake of reading comprehension, one that you could have recognized if you had simply thought about it. I obviously do not think that you (or the other three) are IDers. Yet we all know that to infer guided evolution makes one an IDer. Therefore I was obviously not accusing you of making that inference.
If you had figured that out, you could have gone back and double-checked your reading comprehension. Had you done so, you would have seen that I did not attribute that inference to you, and that you had jumped to an erroneous conclusion.
You were a little too eager to find something to disagree with me about, and it caused you to make a couple of dumb mistakes, leading to a bizarre and false conclusion.
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.
Please learn from your mistakes, be a little more careful next time, and drop the obviously false claim you are continuing to make.
Jock,
Here’s an earlier comment of mine:
Do you see your mistake?
Allan, to Sal:
They’re decorative flourishes in the various genomes, and the Designer just happens to think that the most beautiful cross-species pattern is one that reinforces the appearance of common descent.
He’s really obsessed with faux common descent, this Designer.
Wrong. I don’t claim a mechanistic origin of the patterns of similarity and diversity, you do. As I’ve pointed out several times, if you claim a mechanistic origin, you need to explain the mechanics from first principles of physics and chemistry and initial conditions, etc.
I can accept that Mt. Rushmore is created by intelligence. Intelligence may or may not be definable mechanistically — the classic argument over Artificial vs. Natural Intelligence. It doesn’t matter. It suffices to show something isn’t in agreement with random expectation to suspect something out of the ordinary is in play.
The problem for your model is that you are asserting ordinary mechanisms create things like the Sternberg-Collins paradox, but that’s reminds me of the proverbial story of someone believing 747’s can be assembled by tornadoes passing through a junk yard. How does random mutation create the Sternberg-Collins pattern paralleled in mice and rats? The problem for your model is that it is like trying to explain how wind and rain will create Mt. Rushmore — that is to say parallel patterns found in photographs and in the sculptures of Mt. Rushmore. There is a parallel pattern found in mice and rats that is not explainable by common descent, even by admission of evolutionists!
So here is a clear cut case of common architecture, dare I say common design, not explainable by common descent!
What makes you think I’m not learning it. Joe’s methods are a staple of phylogenetic methods. His name is frequently mentioned in the lectures at the NIH on phylogeny — right up there with Jukes and Cantor and Kimura.
Joe’s work into Maximum Likelihood trees is some of the most stratospherically sublime math I’ve seen, right up there with General Relativity. Beautiful math worth studying simply for it’s beauty.
But unfortunately, I have to point out a few things in subsequent comments….
If the designer chooses to fake the signature of common descent as you have claimed she does, then it is in perfect agreement with “random expectation” . And if the designer plays hide and seek, and chooses to conceal her design, nothing out of the ordinary is apparent.
So what is it? Are we looking at the biological equivalent of Mount Rushmore or are we looking at the Mars stone face?
Here is a diagram presented at a lecture on phylogeny at the NIH celebrating some of the work of Kimura, Juke-Cantor, Joe Felsenstein and others.
This represents one of the many incredible intellectual tools to create models of phylogenetic relationships. It helps model how things may change over the supposed course of common descent. But that’s all moot if there was no common descent.
Problematic are things like the Lipoyl Domain:
https://www.ncbi.nlm.nih.gov/Structure/cdd/cddsrv.cgi?uid=133458
You can see the supposed phylogenetic relationships in the above link.
Now Larry Moran criticized Ann Gauger over this protein here, but it’s not as simple as he says!
http://sandwalk.blogspot.com/2017/01/pyruvate-dehydrogenase-astonishes-ann.html
Ahem Larry!
The problem is Lipoyl Domain appears as part of the protein called Pyruvate Dehydrogenase.
There are 3 repeated Lipoyl Domains in E. Coli’s Pyruvate Dehydrogenase, 2 in Mammalian Pyruvate Dehydrogenases, and 1 in Yeast’s Pyruvate Dehodrogenases.
Get that? The prokaryote E. Coli version of Pyruvate Dehydrogenase has MORE lipoyl domains than the eukaryotic Yeast Pyruvate Dehydrogenase, not less!!!!
This repeated motif of a lipoyl domain isn’t easily captured in primitive sequence comparisons between proteins, the substitution model sort of doesn’t like such big chunks of proteins.
So the supposed ancestor of Mammalian Pyruvate Dehydrogenases starts off with the prokaryotes having 3 lipoyl domains, then it loses 2 lipoyl domains for stuff like yeast, then re-acquires 1 for a total of 2 in mammals.
But, you see, there is something a coalescence model won’t easily explain. I presume, and it’s worth checking, the 3 lipoyl domains in E. Coli are identical. Any bets on how long this can be conserved under a neutral model? 🙂 What if we have 3 lipoyl domains in every prokaryote? Perfect copies of 3 in each. So why did the copies not evolve and diverge from one another in the same organism, but they did diverge between organisms?!!!! Does that freaking make sense under a model of random mutation? Heck no. It is evidence of coordinated mutation if not special creation.
This again echoes the Sternberg-Collins paradox.
[Click here for a larger image]
http://theskepticalzone.com/wp/wp-content/uploads/2017/10/jukes_cantor-1024×819.png