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.
It even says it in the Collins quote: “The cause of the unusual distribution patterns of SINEs, accumulating in gene-rich regions where other interspersed repeats are scarce, is apparently a conserved feature […]”
Gene-rich regions = euchromatin, to a fair approximation. Why do they accumulate there? Because it’s accessible. Heterochromatin is tightly bound, and transposons can’t get in. Or, once in, are less likely to get out and generate further copies. This generates a bias.
Also, in actively transcribed regions, there are more of the sundry molecules upon which transposons depend for transposition. If they need to make proteins or RNAs, they can’t do that without the machinery to do so, which is dilute in regions of heterochromatin.
stcordova,
So, if someone tries to use Alu sequences to do a paternity test, are they wrong?
What function is it that can only be carried out by a transposon? I mean, if I were trying to put some vital function into a piece of code, I wouldn’t give it the capacity to hop around the code like a madman on acid, corrupting it and wasting valuable bits I could actually use for function. I’d concentrate on the function.
Take the Alu’s which Ayala needs remedial training on since he is so dismissive of them. The contain collectively on the 100 million Adenosine-to-Inosine editable sites that are apparently important for brain development.
And what of the L1s? Well they may not jump much anymore in the germlines but they jump or do something in the SOMATIC cell lines, and so far they are indicated in the necessity of differentiation and wiring of the brain cell. It’s early to tell but the Salk Institute, Mayo Clinic, Howard Hughes institute are following it. You have been arguing the L1s are dead, not so! You and Larry Moran and friends are arguing from 10-year-old obsolete data that medical researchers (not evolutionary biologists) have made obsolete.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4443810/
Read it and weep.
So did those “conserved” (dare I say common-designed) banding patterns that appeared after lineage split the product of common descent? No, because they happened after the lineages split. If these transposons provide vital function to the extant organisms, then I’d say that’s a problem for the premise of random mutation, and worse, how the heck did these creatures function prior to these important transposon coming into play.
Oh yeah? Name one who has published in a prestigious journal.
What? All of them?
OMG, that’s absolutely incredible!
What banding patterns appeared after the lineages split?
A few points before we get started: First, you raise peripheral issues while ignoring the bulk of the evidence, i.e. radiometric dating, biotal succession, the sheer time-ordered extent of the geologic record, the processes that resulted in that record, etc. Second, even if the anomalies you point to actually are anomalies (which I doubt), they are at best unexplained, not reasons to reject the geological time scale. Third, your alternative, which you have yet to make clear, must explain the data — not just the anomaly — better than the standard model.
I seem to recall, in the previous discussion, a number of citations to the effect that the faint young sun model is incorrect and makes invalid assumptions about the solar luminosity curve. Anyway, even if it takes a miracle, wouldn’t that argue for divine intervention rather than young life?
Don’t know much about either. But if you want to argue the C14, wouldn’t that require life to be less than 60,000 years old? Is that your model? I know little about the unracemized amino acids; perhaps you could cite.
You are confused about erosion rates, which differ radically depending on geological setting. Erosion in mountains has a high rate, in plains much less, and in marine environments generally negative (i.e. depositional). This is why some sections of the column are missing in various places: a period of erosion rather than deposition.
You would have to flesh this one out for it to mean anything. What’s your alternative model here? Are you trying to make all sediments the result of a single worldwide flood?
Those ancient bacteria are universally ascribed to recent contamination. I don’t understand your second sentence at all, which seems to contradict everything you have said so far.
Anyway, those can’t be the reasons you became a YEC, because none of them would convince anyone who wasn’t already looking desperately for reasons to become a YEC.
Irrelevant, but it would be interesting to see the reasons you think so. All the evidence suggests that evolution is reversible; that is, for every mechanism that would produce mutation X, there is a mechanism that would produce mutation -X.
Why special creation rather than miracles plus common descent?
stcordova,
That doesn’t answer the question.
Why transposons? Why not just a tailored piece of DNA for the specific function required?
Why waste so many bits on function that supports transposition?
Why have germline transposition if the function is related to somatic development? Why risk gene breakage on such a scale?
Are transposons in dandelions involved in brain function too?
Enquiring minds and all that.
Mung,
John Harshman.
Another question: if, as seems to be being hinted, exquisite transposon positioning can only be caused by a Designer …. why are transposons self sufficient (or hitchhike upon other transposable elements, in the case of SINEs). These elements – these elements that can’t move without being guided by an angel – well, they can move without being guided by an angel.
stcordova,
No I bloody haven’t. I don’t care if they are dead or alive for the purposes of a discussion on common descent. Your perennial failure to grasp the germline/soma distinction, and even the basics of transposition, are a bit of a sticking point here.
I care only what the pattern is for a given insert in germline DNA. Whether or not that copy itself can become copied elsewhere – ie, is ‘alive’ – is totally irrelevant on that score, be it somatic or germline activity.
C-14 is radiometric evidence. I could say the same of your views, you ignore the bulk of the evidence and focus on peripheral issues. Mountains of peer reviewed publication does not equate to mountains of facts. The Faint Young Sun Paradox is a serious problem, so is the C14 so are the chemical states of fossils, so are the smooth contact domains, so are the erosion rates, etc. etc.
stcordova,
Like I say every time this comes up, why is there C14 in the coal but not in the limestones in cyclothems – interleaved deposits of the two? Cherry picker.
You ignore the evidence that presents a coherent picture of evolution through time. Not only that, you ignore cross-correlated evidence, like the fact that birds and pterosaurs have ancient homologies, while they lack homologies (“common design”) in the more recent features, such as flight adaptations, while the geologic record also indicates long separation of the two lineages.
What we “ignore” are disparate and disconnected outliers and questions that pseudoscientists use to simply criticize science rather than to even try to find a good coherent model of creation.
The difference is the difference between science and mere denialism.
Glen Davidson
Why not? Why the peacock’s tail which made Darwin sick. It’s sufficient to demonstrate it works inside the Rube Goldberg machines of biology. Rube Goldberg machines are the result of intelligent design. I don’t have to explain why an intelligent designer would do something to assert he designed something. You apparently won’t be satisfied unless you get an explanation as to why the designer did something. This is like someone saying he won’t believe in a miracle even if he saw it with his own eyes unless he gets and explanation as to why the miracle was done!
But now you’re going down the rabbit trail. You have to explain this pattern that isn’t the result of common descent, and preliminary evidence indicates it has functional utility, therefore it is common design.
Have you come to the realization the problem the pattern poses, especially if we find out the SINES are important, like say for chromatin extrusion loops, and who knows what else? It would mean vital function evolved AFTER it was needed in two separate lineages.
Hmmm. I wonder what the distribution of SINE insertions that predate the separation of mice and rats might be. Do you suppose it might conceivably be similar to the distribution of subsequent SINE insertions? And of course you are assuming without evidence that there is a vital function here.
No I am not assuming without evidence. There is promising evidence. Remember the extrusion loops? The problem for you is that some amount of evolutionary credibility always seems to rely on lack of function in the genome.
A lot of heritable diseases, like say 90% are indicated in the non-coding regions of the human genome. That finding by the director of the NIH himself, Francis Collins.
You can claim junk all you want, but you know which side is slowly prevailing in that debate don’t you?
That Sterberg-Collins SINE signal isn’t the first time we’ve noticed common design appearing after a lineage split. Here is one example, the Placental and Marsupial forms:
stcordova,
Because it makes no sense, for reasons I have outlined. Why not just say ‘God did it’ as an answer to everything, and eliminate all curiosity?
The best explanation for the widespread existence of transposons is their ability to transpose. You are asserting that, despite the fact that transposons can transpose, and most of their sequence is made up of the means of transposition, their function isn’t transposition at all, and transposition is actually neither here nor there. The only thing they can categorically do, in every single lineage that has them, and which can definitely cause their proliferation, is nothing to do with actually causing their proliferation! No reason given for this peculiar reasoning, except to give God something to do.
Ach, you are getting repetitive. Puppy-beating and 747s.
The distribution appears to me to be entirely consistent with common descent of the coarse pattern of heterochromatin and euchromatin in rats and mice, inherited from a common ancestor with that same approximate structure. This constrains the pattern of transposition to the same broad genomic bands of euchromatin. On what grounds do you dismiss that?
So rats and mice separately developed a need for a nervous system?
stcordova,
And what persuades us that there is homoplasy? Common descent. I’ve said this before – you think your can destroy phylogenetics using something which depends upon it.
It’s ad hoc to say the insertions happened after the split, and by different SINES to boot. Why not before? 300,000 insertion correlated sites suddenly for no good reason, and different SINES in each lineage.
If the SINES have developmental significance, well, there is a problem.
But regarding transposons in general, get a load of the differential expression of this baby, the Tc10-2_Xt transposon in blue during phases of development and in the various tissue types and locations.
http://www.tandfonline.com/doi/pdf/10.4161/mge.18550
Now where is the presumption this is junk? Is it for direct experiments? Not really. Is it from evolutionary biology? Pretty much.
Do evolutionary biologist want to bet against possible function in light of the differential expression patterns shown during development (below). Be my guest. Now which side is being dismissive of mountains of evidence. Not those in favor of functional DNA and transposons.
stcordova,
I don’t see where ad hoc comes from, especially from someone whose only candidate explanation so far is ‘A Masked Designer Done It’.
If euchromatin ‘attracts’ SINEs (it does), and euchromatin maps to the same axis, then that explains the pattern. I don’t know if it does or it doesn’t, but you haven’t exactly supported your contention either. You’ve rejected mine because you’re keen to find somewhere to squeeze God in, no other reason.
Why should it be before? There has to be a reason for a particular expectation. Are you saying that lineages should never change once diverged? That would be dumb.
No good reason? Transposons transpose, and prefer euchromatin. I may have mentioned this. If rats and mice have similar patterning of euchromatin, I have a very compelling explanation for that up my sleeve …
The approximately equal numbers of post-split inserts is hardly at odds with a mechanistic process, is it, assuming both lineages spent the same amount of time on the planet … ? What should the differential be, on a mechanistic model? Anything as long as it’s not about equal?
No, there really isn’t. What developmental pattern do mice and rats share that requires an approximately parallel pattern of insertion of different SINEs, viewed on a very coarse scale, but which was not shared by their common ancestor? How different from rats and mice do you think it actually was?
Yes, another squirrel. Again, very nice, and again just another irrelevant bit of Gish Galloping.
Can we just take it as read that there are numerous different kinds of transposon, and some copies definitely have function? Do we really need a frantic flurry round Google between every post to squeeze every last drop out of this class of elements, pretty picture and all?
Now … croak! … back to the very common, taxonomically informative pattern flank-SINE-flank shared by clades but by no outgroup.
Wow, that’s a strange circumlocution: “indicated in the non-coding regions of the human genome”; did you mean that “say 90% of disease-associated SNPs are in non-coding DNA”, perhaps?
If so, then that result doesn’t mean what you think it means. How about a citation so that we can figure this out?
And note that, once again, he’s equating “non-coding” with “claimed to be junk”. He can’t help himself.
DNA_Jock,
Indeed. You wasted a lot of our time trying to cover up your mistakes. If you had just owned up to them, we could have gotten to this point a lot sooner.
keiths:
Jock:
And restrictions on the nature and rate of mutations, and restrictions on the nature and rate of horizontal transfers.
keiths:
Jock:
We aren’t talking about “four generations of a homothallic yeast”. We’re talking about the objective nested hierarchy of life on Earth!
You’re repeating your mistake: looking at one instance and taking it to be representative of an entire class.
Yes, there would be a “lot of signal” in the case you described. But that “lot of signal” is there because of the low rate of anomalies and their restricted nature in that particular case. Jack up the rate of anomalies, or change their nature, and “a lot of signal” becomes “less signal”. Eventually you get to a point where you can no longer infer the ONH.
Remember, we aren’t just talking about unguided evolution here. We are also considering guided evolution, which doesn’t suffer from the same restrictions as unguided evolution.
keiths:
Jock:
You’re equivocating on the word ‘support’, just as I predicted you would.
keiths:
Jock:
Silly Jock. Humans can and do evolve their designs, and ONH-destroying modifications of the kind available to humans are also possible in guided evolution via common descent.
keiths:
Jock:
Oh, please. As if the discussion I had been having with John — which you joined — had been a purely academic exercise, with no relation to biological reality.
In any case, my argument does not depend on the qualifier: “of the kind we see in nature.”
As I said above:
Jock:
No, the existence of the ONH allows us to dismiss guided evolution. There are many more ways for a guider to wreck an ONH than to maintain it, and as I emphasized above, you have no special insight into the guider’s nature. That gives you no basis for assuming that he would operate in such a way as to maintain an accurate and recoverable ONH.
Yes, and your earlier mistake, which you tried to cover up, was to think that the possibility of such “minimalist” guiders constituted a counterargument against mine.
keiths:
Jock:
That’s not enough, as I’ve already explained.
John:
Jock:
No one has been talking about “the precise nested hierarchy that we observe”. Were you thinking instead of “an ONH of the kind we see in nature”?
No. As I said, my argument does not depend on the qualifier, even though the qualifier is obviously relevant to the real and important issue, which is whether the actual ONH allows us to dismiss guided evolution. It does.
Jock,
You’ve made a lot of mistakes in this discussion, but by far the worst was your decision to dishonestly try to cover up your mistakes.
This CYA move, in particular, was pathetic. It was on a par with Alan’s pitiful attempt to argue that “Well, no” didn’t mean “no”.
If you can’t be honest for the right reasons, I’ll hope you’ll at least realize that being dishonest backfired badly on you here, and that it isn’t worth risking it in the future.
keiths:
I was entertained by which bits of my comment you chose to not quote…
Well, if the “real and important issue” is whether the actual ONH allows us to dismiss guided evolution, I have always viewed the actual ONH as being compelling evidence against guided evolution. So we really haven’t ever disagreed on that issue.
But John’s original statement, which you disputed, was correct, and you have been behaving as if the “real and important issue” is who’s wrong. You are, and I hold out no hope whatsoever of your ever conceding this.
Happy to know that we agree on the important stuff, though.
🙂
ROFL
I was trolling you. And, because I knew that if I tried to subsequently explain to you that I was trolling you, you’d claim that that was a pathetic CYA move, so I even went so far as to tell you that I was trolling you, right down to the winky face.
I didn’t make a mistake, either.
🙂
But surely the errors were far greater in number and HGT was far more common way back when. And yet evolution was presumably still taking place.
So the claim turns out to be nothing more than if conditions are right for an ONH then we’ll start getting an ONH. Unguided evolution produces an ONH. Except when it doesn’t. Brilliant.
That’s false. I have.
LoL. How many times have you tried this one on me and how is that working out for you?
DNA_Jock,
Yeah, right. You were just trolling me.
Your mistake got caught, so you tried to cover it up; your coverup attempt got caught, so you tried to provide cover for it; and then your coverup of your coverup got caught, so you are now trying to pretend that it was just “trolling”.
When in hole, stop digging, Jock.
And all of this to avoid admitting your confusion about my argument — a confusion which was there from the beginning:
Jock:
keiths:
keiths:
Mung:
You’re right. I forgot about the one dumb person who actually thought that was relevant. Mea culpa.
Mung,
The better question is, how is it working out for you? Take a look at your reputation, Mung.
Jock:
No, for reasons I just explained to you.
The real and important issue is that the actual, real-life ONH allows us to dismiss guided evolution, and the dispute has been over why that’s the case.
From science daily
Guess like all science these trees are tentative. TNH or tentative nested hierarchy.
colewd:
We’ve explained this to you again and again, Bill. You never learn.
Read this section of Theobald.
If you don’t understand it, refer us to the part that is baffling you, and ask questions.
keiths,
Oops.
What makes you think they are the same developmental pattern and same use. They are alu-like. And speaking Alu’s SINES, it is becoming abundantly clear the Alu that Chimps and Humans use is used differently as evidenced by the differing A-to-I editing patterns. But one thing we do know, knock out the ADAR enzymes that make A-to-I happen, and bad juju results.
But, as always, you are rushing to conclusions about biological functionality based on presumptions from evolutionary theory rather than direct observation and experiment. Not a good policy. Need I remind you of the HOTAIR lnc/lincRNA. Thankfully John Rinn, the discoverer, didn’t follow you policy of dismissal of function before all the facts were in.
The diagram of development I showed which you so quickly dismissed is analogous to the kind of patterns that Rinn was seeing with HOTAIR (an RNA, not a SINE). HOTAIR was in cells below the waist, but not above it. So if history of discovery is a guide, then differential expression of SINEs such as Tc1 which you dismissed so quickly might be an important clue. But you’d rather rush to judgement, because you’re so sure the SINES don’t have developmental significance. Suit yourself. Time will tell. The junkDNA advocates like you have everything to lose and nothing to gain as far as scientific accuracy.
Poor Bill is hopeless
colewd,
“Oops”, meaning you are baffled by the statistics? Yes, that’s the problem. It’s why I referred you to that section of Theobald. Please read it.
YUP! Everyone here agrees if we are talking PHYLOGENETIC trees.
The same is not true of TAXONOMIC molecular trees because molecules are discrete entities. You have proteins sensitive to Red, proteins sensitive to green, there is not much ambiguity. TAXONOMIC trees do not need assumption of common descent. You can classify them like you classify transportation vehicles: trains, motor vehicles, airplanes, ships, a few oddball exceptions.
For motor vehicles you can classify them as : 2-wheel, 3-wheel, 4-wheel….18-wheel. It creates a nice taxonomic nested hierarchy based on structure.
We see that with protein classification taxonomically (below). Contrast with the rather worthless phylogenetic classification that adds ZERO operational insight, and can’t even make a conflict-free phylogeny:
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0123533
Yeah oops, did you somehow think that the dinosaur data involve molecular sequences?
Basic failure to understand what’s going on.
Glen Davidson
keiths,
Oops, Theobald assumes a single function of cytochrome c which is no longer correct. Do you have a paper that is more current?
There are an infinite number of universes that the designers could have created.
Therefore, there’s no reason to believe they created this one.
How many different nested hierarchies does unguided evolution predict? Oh, wait. Unguided evolution doesn’t predict any nested hierarchy. In particular, it doesn’t predict the actual nested hierarchy.
Except when they don’t.
Do you have an example of trees from the literature that don’t match with a high degree of statistical significance? From what data are those trees drawn, and is that a problem with the inference of common descent? If so, why?
Please substantively answer all three questions. And with something more than just some deliberately misleading cherry-picked quotes from the literature you found by word-searching for something you ignorantly think means something it doesn’t. Like you did and I had to explain to you back here and here.