I do think this site needs a thread to discuss phylogenetics and whatever the creationist alternative might be. Let’s start with this quote from Sal Cordova:
stcordova: Insisting on the truth of naturalism in the disguise of evolutionary theory could impede scientific progress in the medical sciences if the whims of some evolutionary biologists like Dan Graur are realized. The National Science Foundation (NSF) has invested 170 million dollars in unresolvable evolutionary phylogenies of little or no utility to medical science.ii To date, no therapies based on the 170 million dollar phylogeny project have come to market. By way of contrast, with the help of research like ENCODE, epigenetic therapies are already being delivered to patients with more such therapies in the pipeline. Therefore, a gambler’s epistemology that seeks to maximize reward in the face of uncertainty would seem a superior approach versus blind insistence on impractical naturalism.
This short paragraph raises a number of questions, a few of which seem like topics for discussion.
1. Assuming for the sake of argument that investing in phylogenetics doesn’t help medical science, why should we ignore other benefits? Is basic knowledge useless unless it contributes directly to human health? Should NSF be concerned only with medical sciences, and if so, shouldn’t it be folded into NIH?
2. Phylogenetics actually does have practical applications, even in medical research. Feel free to discuss that. Me, I’m into knowledge, regardless.
3. What is “unresolvable” intended to mean here? NSF grants, the AToL program in particular, have produced great amounts of phylogenetic resolution. My project, Early Bird, for example. Is it all somehow bogus? How much phylogeny is there, anyway, and how would a creationist tell where it begins and ends?
4. And a minor point: Where does this figure of $170 million come from? Is it the total amount awarded by the NSF Assembling the Tree of Life program from beginning to end? Or does it also count various other programs that have funded systematics research? I find it hard to pull any aggregate info from the NSF web site.
John Harshman,
I am surprised you would make such a juvenile comment. Sure observation is fine but you are not observing anything and assuming common decent. What scientific integrity are these nodes built on? I should not have to tell you that testing is fundamental to the scientific method.
John Harshman,
John, I understand the inference standard and this weak standard is what common decent is built on. One of the conflicting pieces of evidence I have seen is that there is a gene inside the “telomere” of theoretically merged chromosome 2. This has been acknowledged by both sides of the argument.
Rumraket,
Yes, I have read the paper and agree there is lots of common biochemical mechanisms among living organisms but common decent implies a mechanism that through reproductive isolation that new kinds can form. Your paper argues common decent independent of a mechanism and I find that a flawed argument.
colewd,
No, he meant that you should actually read it.
You say that because, apparently, you know nothing about how phylogenetics works. Every tree built is a test of multiple hypotheses of descent. Every time the trees from different data sets match, that’s a test of that particular hypothesis of descent. Every statistical or quasi-statistical test (e.g. bootstrapping) of the fit of data to a particular tree is a test of that particular hypothesis of descent. What you are observing is the data, and beyond that a pattern in the data for which common descent is the only credible explanation. That comment was by no means juvenile.
You understand very little. All science, including experimental science, depends on inference. It’s not at all weak. Some inferences are weak, others are strong, depending on the data.
No, there is no gene inside the telomere. That’s a misinterpretation by creationists, one you will find only on creationist web sites. And suppose there was. Does that outweigh the rest of the genome as evidence? How, in fact, would it be evidence against common descent at all?
One of the very first things in that is a discussion of why knowing the mechanism is unnecessary in order to reliably infer common descent.
However, I applaud your honesty in finally coming out as a creationist after having simulated neutrality for so long. Only creationists talk about “kinds”. The evolution of reproductive isolation results in new species, not kinds (there is no such thing), and we know quite a lot about the mechanism. I suggest reading Speciation by Jerry Coyne and H. Allen Orr. It’s quite accessible and explains the mechanisms very well.
John Harshman,
John, what is a creationist? Are you an evolutionist? Are you a chance creationist? I am interested in understanding the science strengths and weaknesses. When I see you struggling to back up your claims you start to resort of ad hominem arguments. You do the same thing with Sal. If you make a reasonable case for common decent I will be right behind you. Until then you are blindly following dogma without critical review and that is not very scientific.
colewd,
Very interested your argument for why you can claim common decent without a mechanism.
Why, you are a creationist. Clearly. Only creationists commonly cite only creationist sources and refer to “kinds” as if that word meant something. Again, just about any paper on phylogenetics with a well-resolved, well-supported tree makes a good case for common descent (of the taxa included in it). If you want one particular example, try this one. I could have given you any of thousands of other examples, but I picked this one because 1) it’s mine and 2) it’s available online for free. I swear you have no real idea what science is; that’s not intended as an insult, and certainly not an ad hominem (whose definition you should look up before using it again), just a statement of my understanding of your state of knowledge.
Without a mechanism for what, exactly? The evidence for common descent relies on only three things: long-term reproduction within species, the occasional splitting of species, and the occasional fixation of genetic changes within species. Which of these do you think we have no mechanism for?
But no, you don’t actually need a mechanism. If common descent is the only thing that would explain a set of observations, those observations are evidence for common descent, even if we didn’t know how reproduction (or even inheritance) works, or how speciation happens, or how genetic changes arise or become fixed. How could it be otherwise?
Let’s suppose, for example, that god carefully guided each sperm to each egg, put up walls (for which Mexico would have to pay) to divide populations from populations, and lovingly zapped each and every mutation into place. Would the evidence for common descent suddenly change into evidence against common descent? Not that I can see. It’s the pattern of similarities and differences that matters, not how each difference arises.
John Harshman,
So what set of observations lead you to believe that chimps and man split from a common ancestor 6 million years ago?
John Harshman,
Here is the image of the gene inside chromosome 2.
Here.
Again, let me just cite one paper to stand in for thousands: This one.
colewd,
I agree that I understand very little about science from the lens of an evolutionary biologist. With all due respect I understand the practice of the scientific method and the what else could it be hypothesis is weak. Maybe these leaps are accepted in the evolutionary biologists circles but outside they get you fired.
Did you mean to cite something else? Not only is there no image on that page, it’s a debunking of the claims that there’s a gene inside the vestigial centromere.
So you suppose. How, then, was the Higgs boson discovered; or, how do we know that the Higgs boson was discovered? Isn’t that just an inference (meaning, to you apparently, a wild speculation) based on what data we think a Higgs boson — and not something else —would produce? How is anything in science different from that? No, I don’t think you have any real idea how science works. Are you a scientist? If so, then we must accept that there are scientists who don’t know how they do what they do.
John Harshman,
Thanks, I have started the paper.
John Harshman,
Via experiment with the hadron collider in Switzerland. Yes, experimental evidence of its existence as gravity (general relativity) experiments using solar deflection during eclipse. None of these are the what else could it be hypothesis. John, the world outside evolutionary biology practices real science.
colewd,
You’re embarrassing yourself pretty badly here.
Why not take a break and do some reading? Make sure to actually read Theobald — he explains just how strong the common descent inference is.
This is a common trope found only among creationists, that there is a fundamental difference between experimental and observational (or historical) science. This is not something that actual scientists think. Again, it was concluded that the Higgs boson had been detected because the data was the sort expected from a Higgs boson and not expected from anything else. The precession of Mercury’s orbit was evidence (not experimental, oddly enough for you) for general relativity because it was consistent with that theory and not with Newtonian gravitation. We accept common descent rather than separate creation because the phylogenetic data are consistent with the former but not with the latter. It’s all the same.
One of the problems with chromosome fusion theory in light of some of the discoveries of higher order chromatin structures (which include the work of ENCODE’s 5C experiments) is that chromosome structure counts in terms of gene expression. Sure the organisms can function with chromosomal re-arrangements, but that is only because there is such deep redundancy in gene regulation.
[FWIW, colewd has always struck me as trying to hear both sides of an issue. He’s asked me pointed questions as well, and I took no offense. If I felt my position was weak, I said so. I’ve told him some of my YEC ideas have problems. ]
DNA has a 3D structure, and colewd is very aware of how enhancer elements thosands of base pairs away affect protein expression. Not only will this happen on the same chromosome (cis-acting) but we also know now it happens across chromosomes (trans acting).
There are topological enhancer domains and they are optimized based on chromosome structure not being random and willy-nilly.
https://en.wikipedia.org/wiki/Topologically_Associating_Domain
Below is a diagram showing how the looping is important to creating domains. The drawings are just depicted as 2D, but in actuality the interactions 3D. DNA as scaffolding (not just providing coding sequences) are highly important to this form of regulation.
Willy-nilly breakup of chromosomes has to compromise something. We’re only beginning to understand the importance of 3D structure of chromosomes in gene regulation.
Here is the paper where the diagram is from:
http://www.cell.com/cell/fulltext/S0092-8674(14)01577-3
Here is a another paper to that shows the importance of chromosome architecture:
http://www.sciencedirect.com/science/article/pii/S0092867415003773
Wow, just like I said, the non-coding regions have structural significance! Medical researcher are finding this to be the case and ENCODE with it’s 5C topological experiments along with other topological experiments like High-C is paving the way for understanding this stuff.
The group of naysayers like evolutionary biologist Dan Graur are the ones calling such researchers “crooks” and “ignoramuses”. Apparently they don’t like the suggestion of extensive interdependent complexity in biology. It threatens evolutionary theory that claims ordinary and typical and non-thinking processes can lead to such large scale coordination across millions of base pairs and across chromosomes.
Before and shortly after going to ENCODE and NIH meeting I thought Graur and Moran might have a case, but after pondering and studying the issues, there claims are looking desperate and fringe.
One thing that has come out of the camp of evolutionary biologists is the argument that the C-value paradox is evidence DNA is mostly junk. The problem is that not only does the genome create length requirements for the DNA but moreso does the chromatin-epigenome create length requirements for DNA. And definitely this can be seen in terms of gene regulation that is involves 3D topology of DNA.
The importance of the information processing of the ROM genome is now being rivaled by the information processing of the RAM chromatin-developmental-epigenome. Epigenetics is more than the few examples of lamarkist looking transgenerational cases, it is about development and management of 100 trillion cells in a human.
The differing genome sizes suggest strong non-homology of the epigenomes of creatures. DNA isn’t just about genomes but the chromatin-epigenome. But these considerations don’t figure into much of phylogenetics does it? They aren’t welcome complications for evolutionary biologists, hence it’s no surprise medical researchers are far more motivated to investigate the complexity of biology, whereas evolutionary biologists like Graur want to pretend such large scale complexity and interdependence doesn’t even exist.
colewd,
This is relevant to the question of whether chromosomes can be rearranged willy nilly.
The video is powerfully enlightening:
But here is a text version:
http://news.rice.edu/2014/12/11/3-d-maps-reveal-the-genomes-origami-code/
The High-C experiments were extension of the 5C type experiments of ENCODE and were featured at the ENCODE 2015 meeting.
This seems odd to me. The Higgs boson was not and perhaps IS not an actual thing, it was a prediction of a model. The observation was LABELED a Higgs boson, which was never actually observed, because decay byproducts were consistent with the model. But some models predict a much more massive Higgs, while other versions of the model predict several Higgs bosons at varying masses.
In short, the answer to “what else could it be” is, in reality, several things – some new particle, some misreading of the decay data, something incomplete in the standard model. So we have “observed” the Higgs boson because while there are multiple “else” alternatives, their probability seems low at present.
John is exactly right – science builds models from available data, from which predictions are made, leading to further observations with better focus, and the models become gradually more predictive. Nothing is qualitatively different between branches of science.
How is any of that a problem for “chromosome fusion theory”? Chromosome rearrangements by the thousand are documented within many species, including a great many Robertsonian fusions. And the “TADs” you refer to are much smaller than chromosomes.
There you go again, equating non-coding regions with junk DNA. Nobody has ever claimed that.
While these few bits were marginally on-topic for this thread, the rest of your post was not. I hope you don’t intend to hijack the thread.
“Before and shortly after going to ENCODE and NIH meeting I thought Graur and Moran might have a case, but after pondering and studying the issues, there (sic) claims are looking desperate and fringe.”
Please permit me to DOUBT this statement. You have been both adamant and consistent in your position that those whose analysis and understanding conflicts with your religious requirements have NEVER had a case. All you’ve done is illustrate, once again, that for the creationist, doctrine trumps evidence without the need for “pondering and studying”.
stcordova,
It wasn’t an assertion, it was a conditional: an understanding of phylogenetics (which you claim to possess) ought to lead you to the realisation that there should be a detectable discontinuity in trees if the Orchard Model were the case. It’s a testable hypothesis. Tree building is hypothesis testing.
All of this is just smokescreen. One does not need to know anything about the ancestor at a node to determine that there is a node – or a discontinuity.
Yes, I’d second (or third) the encouragement of colewd to actually get to grips with the issues rather than commencing from a position of dismissal because ‘the inference is weak’. This is a gobsmackingly dismissive position on an enormous mass of mathematical, statistical, computational, genomic and morphological work.
I realise I am not really a disinterested observer, having swallowed all the evolution hooey years ago, but protests to the contrary notwithstanding colewd really does not come across as open minded on the matter. At all.
Chromosome 2. The genes on it map very well onto the proposed separate chromosomes from other lineages (and not just chimp), oriented exactly as one might expect if it were a fusion. There are telomeric sequences within it, and a second centromere. There are 22 other chromosomes. Do they map? What about indels?
And we can just throw this data away because there might be a gene at the fusion site. So what? Can’t genes move or something? How do people think translocatory differences arise between species? Genes are not pinned in place by an imaginary ‘3D code’. They are regulated by molecules, and molecules find ’em by binding energies, not by some kind of Genome GPS.
Well you are of course correct, even if there was a gene of some sort spanning the site, it doesn’t invalidate the inference of common descent. After all, there are in fact a central telomere, which, if the chromosomes hadn’t fused, there simply shouldn’t be.
Regardless, there isn’t a gene spanning the telomeric fusion site. It’s a creationist lie. One that colewd blindly believed because it came from someone from his “camp”.
Rumraket,
Yes, granted, it appears to be untrue. Either way, it’s hardly a problem for evolution (damn that pesky theory that can accommodate all data!).
@ colewd
There’s a commenter at Uncommon Descent who posts under the name Bill Cole. He seems less diffident about his doubts about common descent than you are here.
We must allow thé possibility that colewd believes what he posts.
Of course. I am guilty of not reading Sal’s posts closely. I didn’t realise he wanted a candidate basal vertebrate rather than a chordate.
On thé other hand, what I suspect Sal would like to find is not Cambrian chordates but Cambrian rabbits. Evolutionary theory may be hard to prove but there should be anomalies that would make it possible to disprove, if it was incorrect.
Chromosome 2 has a special place in my heart, ’cause it pushes the creationists’ “I ain’t no damned monkey” button.
Well thank you for answering my question. Apologies again for thinking you said it was Lampreys.
I was the one who put coelacanths and lungfish on the table. Despite this you said:
And you’re the one complaining I said evolutionary theory asserted birds descended from fish, and there you just said it.
Absolutely not, because pathogen evolution involves mechanically feasible changes that are observable and testable and relatively small, and in fact sometimes the common ancestor can be verified since a sample of it is sitting in some lab refrigerator, and in the case of Lenski it definitely is. Furthermore sister relationships are respected which is more than I can say for the supposed fish-to-bird scenario.
What you have just said affirms what I said, evolutionary biologists assert the ancestral form of all birds and many extant fish is a fish! Whereas the molecular data show at best birds and fish descended from a common ancestor that was neither a bird nor a fish since they look more like sister groups rather than the fish group looking like the mother of the bird group.
You just suggested something close to a lungfish or coelacanth was the ancestor of birds. Coelecanths and lungfish are practically living fossils, with lungfish presumed as far back as the Devonian (Devonian is 412 million years ago, but I don’t have the supposed exact date of the oldest fossil) and Coelacanth 360 million years ago.
Assuming accepted paleontological ages for the sake of argument, what the physical fossil evidence suggests is that lungfish give birth to lungfish, coelacanths give birth to coelacanths, and after N generations spanning 300-400 some million years, at the end one still gets lungfish and coelecanths!
So despite this physical evidence of the resistance to evolution of some extant lines, why do you jump to the conclusion something split off from the fish group and became a bird? For all you know the birds and fish had already split off from a common ancestor that looked nothing like a fish! Why do you rule out that possibility? Answer: circular reasoning toward a predetermined conclusion.
How much sequence divergence do you expect between the genes or proteins of lungfish and coelcanths? If you have the accession numbers of some genes or proteins used for phylogeny of lungfish, coelacanths and chickens then let’s pump them through an NIH NCBI BLAST search comparison. If the lungfish and coelacanth molecules look similar to each other more than they do to birds, that means your rates of supposed evolution are all wrong. Proof by contradiction.
If your molecular clock hypothesis is right, there should be intraspecific variation going on the coelecanths and lungfish, unless of course the extant creature respectively had a recent MRCA, but then if coelecanths and lungfish have similar molecules (compared to their distance to birds) then the coelacanth and lungfish share a recent MRCA which conflicts with paleontological evidence which says they were already diverged 300-400 million years ago.
Do I have to dig up the accession numbers and go to the gene banks myself or are you willing to get some data for all of us to examine? At the very least you could suggest what shared genes or DNA we can examine between lungfish, coelecanths and chickens (or some bird) we can all look at and build molecular taxonomies on. This should be that difficult to do once we have names of proteins or genes that are accessible in public databases like Uniprot, Genbank, Ensemble or whatever.
Yeah, we’ll see about that after we have some gene or protein names and accession numbers, won’t we. 🙂
Good grief!
stcordova,
The mechanical feasibility of pathogen evolution doesn’t come into the analysis of relationship. It uses all the tree-building techniques of molecular phylogeny – maximum likelihood, minimum parsimony, Bayesian, multiple alignment etc. So it is hopelessly inconsistent to accept these techniques – which were not developed for this purpose – yet reject them in the area they were developed for.
If such techniques applied to a broader clade allow investigation of relationship, how can you say trees DO NOT indicate relationship simply because you have a blind spot when it comes to mechanism? If they indicate relationship, you cannot wish that away. These are, after all, objective tests of the relationship hypothesis.
Like it or not, the trees are supportive of relationship. If you decide they are therefore supportive of something impossible, you are welcome to think that. But the very fact that relationship is indicated is a data point in favour of possibility, don’t you think? I certainly see no reason to suppose that Design would produce trees of relationship that extend below the assumed (and still rather ill-defined) ground of your ‘orchard’, which is what is observed.
Why, in any case, are you looking at bird/fish, or eukaryote/prokaryote? Surely the discontinuities between Created Kinds are much higher up the scale? Dog/Cat, say, maybe Galliformes/Anseriformes, or within the Agaricales fungi? If phylogenetics works, it should be possible to use it to identify this discontinuity. If it doesn’t, you should reject it at all scales, not just those you consider, without support, to be mechanically infeasible.
I could supply blind datasets, and a program would blindly indicate the relationships (if they existed). No knowledge of feasibility or mechanism is required to test the hypothesis of relationship in this manner. Although, all that said, accumulated small change is enough at all scales, as a very coarse description of ‘mechanism’. There’s just more of it in millennia than in decades.
Alan Fox,
How come there are still monkeys?
And then there’s the situation when a significant morphological transition took place over approximately 25 million years. Leading to a prediction of a fossil supposed to exist in 375 million year old sedimentary strata corresponding to an ancient beach or flood-delta.
If your creationist views are correct, it should simply not have been possible to predict that this fossil with these particular features would be found in this particular rock strata. Yet it happened.
Moved a post to guano.
stcordova,
I don’t know if you really mean intraspecific variation – that would be indicative of something other than a recent MRCA for the 2 clades.
Still, AFAIK, coelacanths, lungfish and tetrapods diverged too close together to allow further resolution of this trichotomy. If the data actually indicated a recent MRCA, I suspect that conclusion could not possibly have been reached, and a tree with that node published instead. You seem to be hoping that phylogenetics is still in its infancy, and no-one has looked at anything yet.
Allan Miller,
What Sal means is that “if coelacanths are ancient, then there should be as much sequence variation within coelacanths as there is between coelacanths and birds.”, viz:
Which logic I find rather, err, impressive.
Allan Miller,
D’oh!
DNA_Jock,
Well, that would look like he did mean interspecific after all.
The inability to ‘think tree’, or take any real account of the dimension of time, is a real sticking point.
Ahh…my bad. Guess I don’t understand his complaint/issue.
For keiths:
Read your paper when it came out, but didn’t notice the authorship at the time. Nice work.
You stated, “The possibility that multiple, unique developmental genetic pathways underlie the ratite form should be tested in light of this new phylogenetic hypothesis.” Do you know if this has ever been tested? Other observations show that the same pathways may sometimes be followed, so it is an interesting question.
That was very well put.
keiths,
You are embarrassing yourself again keiths, by using your same tired line of ” you are embarrassing yourself again…” .
Why not just make your own emoji that shows you sticking your fingers in your ears and saying ssshhhh?
That is a very interesting paper you linked to. Here is what I find most interesting.
To which Kenneth Miller so oddly replies:
What makes it so very interesting is Miller totally ignores the point Luskin made, and instead denies that he admitted that Tompkins interpretation was correct. That’s interesting because Luskin NEVER claimed Miller admitted the interpretation was correct or incorrect.
What Luskin said was that QUOTE!!: ” Dr. Miller conceded that the fusion point was only far away from the gene when one excludes results from a genomic database called “refseq.”
Which Miller doesn’t deny at all in his reply!
Is Kenneth Miller an idiot or just a deceptive douche? Which do you think it is?
Talk about a non-denial denial…