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.
Ruraket cites and irrelevant paper to the point I was making.
Here is a snip from that paper:
So where is the case where the palindromic sequences evolve as well? And I wasn’t talking about TF’s that bind to locations only.
From wiki:
I was talking about binding domains on the exons, not adjacent to the genes, Dab Gummit!
This is what I was talking about:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0035202
See that which is bolded. DUAL FUNCTION baby. That’s poly constraint. Just like I said, DNA is not just about coding, it serves as road signs and parking lots for molecular machines.
John, to Rumraket:
Mung:
That doesn’t get you off the hook, Mung. Your statement is as goofy as ever:
Sal,
Are you ever going to get around to telling us why your God is so obsessed with unguided evolution and intent on mimicking it? Why the objective nested hierarchy, when trillions of other options are available to him?
Just because prokaryotes aren’t a proper clade doesn’t mean archaea and bacteria don’t nest within one. They both share a common ancestor, the last universal common ancestor.
Sal, you’re asking for details about how DNA and proteins that are constrained to bind to one another, and regulate other cellular processes, could evolve if all these mutual factors of contraint are active on them. So you got what you asked for. An example of transcription factors with such multiple levels of mutual constraint can emerge and change due to the stochastic accumulation of mutations.
So it’s as directly relevant as it is possible for it to get.
Oh by the way, what is your explanation for the nested hiearchy of life? Why is there an extremely significant level of consilience between independent phylogenies? Your “gap” digression isn’t going to get you off the hook. And your demand for ANY level of mechanistic detail, when you yourself is capable of supplying exactly none at all, is extremely hypocritical.
You have an obvious double standard.
Rumraket:
Right. And Mung’s trichotomy neglects that obvious fact:
Rumraket, to Sal:
The objective nested hierarchy is the 10^38 pound elephant in the room. It’s amusing to watch Sal pretending it isn’t there.
ETA: And colewd. And Erik.
stcordova,
It’s dead easy to generate a palindromic sequence. Take a stretch of double stranded nucleic acid (complementary sequence) where each strand reads the same in the same direction (ie sense and antisense, reading 3′ to 5′ or vice versa, are the same). At one end, ligate 3′ to 5′ in a loop. Either before or after this, get rid of all the hydrogen bonding in the original dsxNA. Bingo. You have a palindromic sequence, continuously reading 3′ to 5′ on one strand. Now synthesise its complement – eg reverse transcriptase.
Well they have these concerns. It could be all wrong, just like all of the other theories with exactly the entailments predicted that turned out to be wrong. You know, like, well, all of the other ones.
OK, I can’t think of any. What were the ones that they mentioned?
Glen Davidson
It is directly relevant. It shows how TFs can emerge and change both in sequence and their preference for DNA binding spots. Both things change, the DNA and the protein that binds it. It is so simple, they can change due to a combination of gene duplications and epistasis. Duplications yield redundancy, which allow more change, which together with other permissive substitutions allow even more change.
In the paper Sal. Both the transcription factors AND the DNA regions they bind to, change.
From the paper: “There are two phylogenetic classes of SRs in vertebrates, which have distinct specificities for both DNA and hormonal ligands; the two SR classes therefore mediate distinct regulatory modules (Figure 1B). One class, the estrogen receptors (ERs), are activated by steroid hormones with aromatized A-rings (Eick et al., 2012) and bind preferentially to estrogen response elements (ERE, a palindrome of AGGTCA) (Welboren et al., 2009). The other class contains the receptors for the nonaromatized steroid hormones, including androgens, progestogens, glucocorticoids, and mineralocorticoids (AR, PR, GR, and MR; Eick et al., 2012); this class of SR preferentially binds to steroid response elements (SREs), including palindromes of AGAACA (SRE1) or AGGACA (SRE2) (So et al., 2007; Chusacultanachai et al., 1999). The two classes’ DNA specificities are distinct—ERs bind poorly to and do not activate SREs, whereas members of the AR/PR/GR/MR group bind poorly to and do not activate ERE (Zilliacus et al., 1992). Although SRs can and do bind variants of these classic sequences (Welboren et al., 2009; So et al., 2007), the classical ERE and SRE sequences are physiologically relevant and have been the subject of extensive biochemical and structural analysis (Beato et al., 1989; Luisi et al., 1991; Zilliacus et al., 1992; Lundbäck et al., 1993; Schwabe et al., 1993).”
Concomitantly with the transcription factors changing their DNA binding preference(oh and btw, they can tolerate mutations to the binding spots), the steroid hormone receptor domain changes too. It’s a multi-function protein. It binds to DNA, and It has a receptor domain and is regulated by a steroid hormone molecule. There used to be only one such steroid hormone receptor TF over 450 million years ago (AncSR1), which had broad acceptance towards hormones, but preferred only a particular DNA sequence. Today there are several distinct classes all specialized towards individual types of hormones. Even more importantly, within each distinct class of steroid receptor TF (like, androgen receptors, or oestrogen receptors, or corticosteroid receptors, and so on), there is variation between species. From small to large variation. The crocodile estrogen receptor differs from the orthologous sheep estrogen receptor by 80% of amino acids. Yet they both are activated by the same estrogen hormone. Of course the human and sheep estrogen receptors are much more similar. Human and mouse even more similar. And so on and so forth.
So what? Coding sequences are fourfold degenerate at the 3rd nucleotide in the codon. So the DNA can change despite it being coding, and the protein that binds the DNA can change to accomodate the mutation in the DNA. Gene duplication and epistasis all over again.
And it still doesn’t get you to your sought conclusion. You have not somehow DEMONSTRATED that they can’t possibly change simply by waving your hands in the general direction of multi-layered constraint.
Your argument here merely amounts to an insinuation. All that does is explain why they are more conserved over time, than other regions which are less conserved. But they’re still not immutable. We still detect changes between species, and those changes become larger with increasing distance of species relationships. Exactly as you would predict if evolution by common descent was true.
Multiple levels of constraint just means change is slower, it doesn’t mean the function can’t emerge, or that it can’t change at all over time.
It. Simply. Doesn’t. Follow.
So enough with your faulty inductive generalizations (flat out contradicted by comparative genetics). Stop vaguely just hinting at “poly constraint”. To get where you want to go (immutability), you need to show immutability. Not just sorta suggest it by regurgitating examples of things that constrain.
Your kids are surely much smarter than I am if they see a way to learn about the distribution of distinguishing characters from features that are shared by every organism.
Unless you were talking about differences in proteins, DNA and enzymes (are they not proteins?) among organisms, but I didn’t get that from your statement. There are no differences in ATP by the way. It’s the same stuff in every cell.
Hint:
J-Mac,
I also note that you were greatly inspired by Sal’s habit of ignoring lengthy posts except for the itty bits where you think you can score a point. So I am going to politely ask again until I learn what I want to know from you:
Why do we need to recreate life to learn why the Designer created a nested hierarchy?
Do organisms have designed adaptations that make them fit their place in the world?
Mung accepts common descent, J-Mac. Either start crying on Sal’s and Erik’s shoulders or accept that species have split and diverged.
Thank you! That’s a relief…
Unfortunately, unless you and a couple of clever guys like you here solve the problem of the inter-dependency of those components ATP, DNA, Proteins, Enzymes etc, you can speculate all you want about whether God created nested hierarchies or not…My kids love when adults pretending to scientists make fools of themselves trying to avoid serious issues…
There is nothing wrong with lying to yourself that there is no problem with your beliefs as long as you believe it…
“…Its not a lie if you believe it…”
Congratulations! You must be very proud of yourself…
No kidding!? Then you expect me to reconsider my position instead of you providing evidence for it? Well I sort of expected that…;-)
Well, just like I wrote earlier, seems you will do anything as long as your beliefs are safe…
Unfortunately, you found the wrong guy…I’m not that naive and I will not lie to myself…
I did…. As you have observed it yourself, I disagree with many people here on many issues…
As I recall, Sal is a big fan of orphan features and systems as I am…
I will leave it up to him as to how he reconciles those with common descent…
BTW: I descended from my parents, and down the line they must’a descended from Adam and Eve… Does this make me a common descent believer? 😉
Kids???
Please just ignore him. Please.
It just makes you a believer in some massive amount of incestuous inbreeding.
Rumraket,
Sorry. Yes, you are right. I hoped that at some point we might get a glimpse of an actual opinion, but it seems the smirking is really all there is.
Allan Miller,
It’s also easy to evolve complementary changes in a palindromic sequence, if that’s what Sal meant. A single base change will reduce the binding affinity of the looped structure. A change to its complement will restore it. Provided any reduction in fitness is not too detrimental, they can drift in parallel.
Oh! Look who is here…
After your last flop based on your confidence in “evolutionary truths” I don’t think there is much you can say here anymore… You can pretend everything is OK…
I guess… we have many of those here…so you fit right in… 😉
Corneel,
Harshman believes in the many miraculous gene insertions into the tree of life…
How do they fit into the nested hierarchies?
I will! Thanks, as there is no way he can or is willing to explain the fundamentals of his faith…but I guess that’s what blind faith is all about…
How do the many variation in the genetic code, 31 so far and counting, contribute to the evidence of the nested hierarchies? With 10 billion species on earth, that number will have to go up, and up… 😉
I’m not so sanguine as some of my colleagues here that there’s only one life form on this planet. We have a lot of different types of metabolism, different organisms…
One of the most profound implications of the net of life (rather than the tree of life) is that it’s consistent with several independent origins of life that preceded the rise of a modern genetic code and contributed to existing species….
Why would I believe in common descent and nested hierarchies if evidence points to more than one origins of life?
J-Mac,
It doesn’t. Venter Is Wrong.
I was also quoting Larry Moran…Is he wrong too?
“…One of the most profound implications of the net of life (rather than the tree of life) is that it’s consistent with several independent origins of life that preceded the rise of a modern genetic code and contributed to existing species….”
How many respected evolutionists actually agree with your nonsense here?
J-Mac,
Yes.
The whole problem with this argument by authority thing is that your opponent simply has to find another authority who supports the opposite case – if, that is, one is so pathetic as to be unable to argue one’s own case. I’ll cheerfully argue with Moran and Venter on this, if you’d care to bring the real thing along instead of your ridiculous glove puppets.
The Mycoplasma that Venter was referring to differs in 1 position out of 64. That’s 63/64 identical assignments. If one thinks that points to a separate origin, I’d say one was talking crap (and spare me the Dawkins quote that always follows this point).
LUCA isn’t a clade either.
The “life clade” and the “LUCA clade” are just as nonsensical as the “prokaryote clade.” All you’ve done is give a different name to an ad hoc whatsit.
You may as well believe in The Independent Birth of Organisms.
Yes. Adaptations are clearly designed. 🙂
And No.
Organisms fit their place in the world. We call this their fitness. It’s the fitness that we call adaptation. The adaptations don’t make them fit. Their fitness makes the adaptations.
But I am the worst sort of believer. 🙂
Universal common ancestry? meh.
Hyperastromical search spaces that are “just right” to allow life to evolve? meh.
I’m no fun.
Evolutionary theory in a nutshell. Incoherent. Not at all like gravity. More like flat earthers.
I’m not saying LUCA is itself a clade. No single species or organism is a clade. The common ancestor species and all of it’s descendants define the clade. In the case of LUCA, it would have to be the clade that contains all currently known cellular life on Earth. Bacteria and Archaea nest within that clade. Your argument was wrong from the beginning, regardless of my incorrect usage of prokaryotes as a clade.
What is incoherent about it?
Mung’s manglings of it.
Glen Davidson
Why should I listen to you then if the only authority you respect is the authority that suits your beliefs?
Give me one reason why I should even pay attestation to your nonsense claims?
John Harshman and I were arguing over coalescence theory. I was a bit appalled he’d try to apply it to LARGE bacterial populations spread around the globe.
After looking at Dave Carlson link:
http://www.math.ku.dk/~wiuf/journalWiuf/coal_bac_2010.pdf
My intuition about John Harshamn’s wrongness on applying coalescence theory to large globally spread populations of E coli (or whatever bacteria) was confirmed.
The diagram below, especially the fission model from Dave Carlson’s link shows some of the salient points.
Note that the fission diagram start off with 10 creatures at the top and then end up with 10 creatures at the bottom. Howmsoever, only two ancestors have their children represented in the final generation in the fission model. That is, in the fission model on the extreme right, the 7th guy from the left on the first row ends up having 7 great great great…grand kids, and the 4th guy from the left on the first row ends up having 3 great great great… grand kids. The rest of the guys on the first row have their lineage cut off forever.
Now what we can glean from this is that if all we saw was a population of 10 bacteria with 7 of the bacteria looking the same, we can guestimate they share an common ancestor 8 generations back. Look at the diagram to see this.
But I should point out, the larger the population (in the diagram only a population of 10), the farther back in time the most recent common ancestor (MRCA) can be estimated to exist. That is, the estimate of how far back in time the MRCA existed is dependent on the population size under the coalescent model, and the simplistic approach of the model when applied to the real world can lead to absurdities.
A special case of estimating how far back MRCA was is when a trait is fixed into an entire population. The MRCA in the special case where the descendants of one individual overtakes the entire population, can be estimated this formula:
https://en.wikipedia.org/wiki/Fixation_(population_genetics)#Time_to_fixation
I read that to mean the MRCA in the case of fixation is about 4 Ne generations back, where Ne is the effective population size.
But before one starts using the formula blindly, consider that it has limited application only to modest size stable (not growing) populations. Using simple coalescence theory to compute MRCA times become absurd if we are dealing with large growing populations and blindly applying the formula.
For example the current population of the plane is about 8 billion people. A rough guess at Ne is about 1 billion people for the effective population size. 4 Ne = 4 billion, that is for billion generations back to the MRCA for any gene fixed by random drift.
Uh, given the generation time for humans is about 20 years, 4 billion generations times 20 years = 80 billion years (20 times older than the mainstream age of the Earth!!!!). So there goes and example of what happens when one blindly uses coalescence theory when it shouldn’t be used!
Given a single teaspoon of soil contains a billion bacteria, it’s well within believability that there are qaudrillions of E. coli bacteria spread across the globe. Given that the MRCA increases linearly with respect to the effective population size, we’d get equally absurd conclusions about how far back MRCA of E. Coli genes went (like say trillions of years) if we use coalescence theory to compute the MRCA.
Not to mention, I pointed out stirring of the population is important, otherwise what you see in the diagrams below won’t happen since for it to work, the kids of one guy have to effectively bump off the kids of another. That won’t happen in unstirred populations like they will in stirred populations.
Sequence divergence is a better clock to estimate MRCA in such cases.
Bottom line, John Harsman was wrong to invoke coalescence theory, he was wrong to invoke drift as an explanation for the lack of sequence divergence in the aaRS genes of E. Coli.
Diagram I was referencing from Dave Carlson:
J-Mac,
The number of codons held in common between Mycoplasma and vertebrates is a matter of public record. If you think 1 difference out of 64 indicates separate origin, that’s up to you; I can’t tell you how to interpret this fact.
I can’t. But equally I don’t know why you pay attention to Moran and Venter, since you disagree with them on almost everything.
This habit of Creationists of relying on quote-mining authorities is laughable.
You mean like:
Yeah, I get a good laugh too when I see that quote.
So, would it or would it not the code mycoplasma use work in human cells?
Yes or No?
J-Mac,
Probably not, no. There are many genes one could take from many organisms that would not work in many others. This fact does not prove separate origin.
stcordova,
When you whip it out time and time again, I actually feel quite concerned that someone could be so obsessive about a single sentence.
[eta context:
What a bastard!]
So…1 difference out of 64 indicates what exactly? What does it prove?
Sal whipped your ass with that sentence didn’t he 😉
J-Mac,
Hardly. Do they have sarcasm in your country?
My country is called sarcasm… I’m all sarcasm…;-)
You’re Monday morning quarterbacking.
J-Mac,
I’m not trying to prove anything with it, you are (with your hand up the backside of your Venter glove puppet). You are saying that that one difference indicates separate origin. But I don’t see how that follows.
Still, to try and stay focussed on the OP, perhaps one of the Design-jockeys could indicate why Common Design is a better explanation of 31 (marginally) different codes. I don’t think any 2 species differs by more than a handful of positions – still upwards of 60 out of 64 held in common for any species pair. Our nuclei even differ from our mitochondria at 3.