Out of interest, what is your purpose in discussing this paper? By that I mean, is there a theory that is supported by this work, or is it to compare simulations with CD and seek to replace CD with something else, such a dependency (something)? Do you have a theory of dependency and if so, what is it?
Perhaps I misspoke, or perhaps you misunderstood? I don’t even understand where you’re coming from with this comment, and I say this not with an exasperated tone but an honestly bewildered, brotherly tone. Similar in what way? And how did I imply that? How is my comment different from a thousand other discussions of miracles and resurrections and naturalism on the Forum?
I was merely trying to understand Cornelius’s mental image of an “evolutionist.” He was painting what seemed to me to be a straw man of “everybody who believes in evolution must of necessity be of Richard Dawkins’ ilk.” I was reassured to find, upon further prodding, that I was wrong, and that he does allow that there are people who accept evolution who also believe in miracles such as the resurrection of Jesus. This is a (small) win for gracious Christian dialogue, even if my approach (using the term “denialist” in particular) was less than 100% gracious.
haha Well I should hope so!
I admit that the use of “denialist” was a bit of a barb, and if our dear moderators (particular @BradKramer) had been watching more carefully, it might have been removed just like my other snarky comment at the outset of this thread.
It’s kind of you to ask, but I don’t feel I could add anything worth reading beyond the thoughtful (and not unkind) critiques that have been offered by several on this Forum and over at Peaceful Science.
I think overall what I see is that Dr. Ewert has offered the tentative beginnings of a research program, and he has admirably entered the ring to test it, and you have lifted up his arm and declared him the undisputed winner by KO before the fight has even really begun.
It seems that I misunderstood and for that I am sorry: .
Why Aren't the Twin Locations of >100k+ ERV's (human vs. chimp) Discussed More?
The null hypothesis is randomly distributed characters. The null hypothesis would also be able to capture Ewert’s model because there would be massive discordance between modules of genes. I’m not talking about small incongruencies like the deep nodes shared between yeast species, but massive discordances like jellyfish and a rodent group being placed in the same group with other rodent species in the outgroup.
Occam’s razor is also being misused in the paper. The razor slices away extra assumptions, not complexity. It isn’t the simplest answer that is preferred, but the one with the fewest assumptions. A complex explanation with fewer assumptions is preferred over a simple explanation with more assumptions.
I think that sums it up. He is being suitably cautious, but he needs to be given space to explore and respond to the questions people are asking. I’m not convinced yet, but I like Dr Ewert’s attitude.
What I find interesting about this approach is that it is very macro - scale. In this way, it doesn’t have to deal with the nitty-gritty one encounters when comparing two closely-related genomes (say for example, the human and chimpanzee genomes). It’s almost as if the anti-evolution ID group has realized they just can’t win when doing close comparisons.
I too commend Ewert for putting his ideas out there. But the skeptic in me wants to know how he deals with more the pressing problems for his idea that closely-related genomes generate. The way forward for a research program is not to try find a niche where your favourite ideas are protected from the data…
If I am reading Ewert’s thesis correctly, there shouldn’t be any closely related organisms. What we should see is a collection of species which are a mish mash of different modules thrown together. We should see one species with modules from fish, birds, and whales and another species with modules from lizards, bats, and jellyfish.
For example, we can look at Fig. 3 and this quote:
“All marine species depend on a marine module, and the echolocating species depend on the echolocation module. The dependency graph is essentially a tree with extra flexibility; the modules can explain genes shared between species thought to be only distantly related by common descent. A module is not restricted to reusing code from a single source, but can freely reuse from multiple sources. Compare this to common descent where each species must almost exclusively draw from a single source: its ancestral species.”
I am going to go out on a limb and say that Ewert is probably talking about the Prestin gene. With that caveat, I will assume that this is what he is talking about and show how this creates problem for his hypothesis.
First off, humans have a Prestin gene. We have the supposed echolocating module. I believe that almost all mammals have this gene, regardless of their ability to use echolocation or live in a marine environment. In fact, a search for “Prestin” at Homologene shows that all eukaryotes have this gene, down to C. elegans. I guess Ewert thinks little nematodes are echolocators because they have this module?
I suspect that Ewert is misinterpreting the pseudo-controversy over convergent synonymous mutations in the bat and cetacean Prestin genes, and making a few leaps of logic from that misunderstanding. If Ewert is not talking about the Prestin gene, then I would really like to know what genes bats and dolphins share that are not shared by other mammals.
Reading further, Ewert seems to be arguing for convergent sequence evolution with respect to echolocating and marine mammals, but then abandons that whole argument for gene families. Why? I suspect that even with a few convergent nonsynonymous mutations, the overall evolution of these genes at the DNA level produces the trees predicted by common descent, so it doesn’t fit into the story that Ewert wants to tell.
After reading the paper, I suspect you’re correct.
Yep. It’s in the original Prestin dolphin / bat paper. The Prestin tree fits the prediction of common ancestry once you remove the influence of the (very few) amino acids that were under convergent selection.
If this is what Ewert is basing his thinking on for the “echolocation module” - and I agree, it seems pretty likely that this is the case - then he’s not dealing with evidence that does not support his ideas.
Or, put another way, it’s going to be hard for him to argue that the Prestin gene isn’t part of his proposed “echolocation module.”
So, one of the key genes in one of his modules has all the signs of common ancestry with convergent evolution layered over top. How does that square with his hypothesis that modules are designed apart from common ancestry?
It’s these sorts of things that skeptical, appropriately critical, peer review would address.
Population genetics and phylogenetics isn’t my strong suit, so what I say isn’t gospel (pun intended) . . .
There are also assumptions that are used in these models. For example, it is assumed that a difference at a specific base is due to one mutation. It is also assumed that if two species have the same base at the same position then no mutations have happened. This is called parsimony. It is entirely possible that the same mutation happened independently in two lineages resulting in the same base at the same position. It is also possible that two mutations have happened at the same base in one lineage instead of just one mutation. As evolutionary distance increases the chances of these occurrences increases as well. I believe some models take these possibilities into account, but I could be wrong. A search for “DNA homoplasy” returns 27,000+ papers, so this is a well known source of noise in phylogenies.
You also have incomplete lineage sorting, which is analogous to your sports betting scenario. When heterozygosity (i.e. a mix of alleles for a given gene) is inherited by two lineages after a speciation event there will be winners and losers as those alleles compete with one another. Sometimes the game goes on for a long time and the heterozygosity is kept. Sometimes the same allele wins in both lineages. Sometimes different alleles win in each lineage. This can cause two more distantly related species to share an allele not shared by the more closely related species. It is a known source of noise, and from what I have read it can be modeled if you know something about the populations and the approximate time for each speciation event.
In the end, there are known sources of noise that will accompany the phylogenetic signal. It is expected. It is no different than any other scientific pursuit. I don’t know of any scientific endeavour where there is a r^2 of 1.0000000 for every single data set, and if there were perfect correlations it would make me very skeptical of the reported results. It is strange that Cornelius Hunter cites noise as a reason to doubt the results because most scientists, in my opinion, cast much more doubt on data that has no noise.
No, this is a bizarre assertion. Ewert’s model is not randomly distributed characters. Either you really don’t understand the math, or something.
Dr Hunter, I admire your stamina in yhis thread.
I have read Ewart’s paper. A thought has just occurred to me; could the dependency model be the equivalent of adding epicycles to phylogenetic trees to get a better fit. I know from the paper that the scoring system penalises complexity but perhaps the improved fit just outweighs the added complexity.
My physics brain can only imagine Ptolemy’s epicycles… can you elaborate on what putting epicycles on a phylogenetic tree looks like and even means?
Interesting question. I think this whole area is quite complicated, and difficult to know where the epicycles lie.
Ewert’s model would result in very different trees for different groups of genes. That would be easily detectable with current methods. If all humans were wiped out and our GMO species escaped into the wild, any subsequent aliens that landed on Earth would easily detect the organisms we designed. They would stick out like a sore thumb, such as a population of fluorescent mice that carry an exact copy of a jellyfish gene.
It’s OK, Cornelius Hunter knows what I mean.
The main point to take away from this conversation is that Ewert’s model fails to address the data that phylogenies are based on. Namely, Ewert’s model does not compare the base sequences of DNA like modern phylogenetic analyses do.
“Genes within families do undergo splitting, sequence changes, and functional changes. However, such events are below the resolution of the model. This model is only concerned with the presence or absence of the gene family in a particular species.”
You don’t inherit gene familes. You inherit DNA sequences. The phylogenetic signal that evidences common descent is based on differences in DNA sequences. Ewert’s model doesn’t even look at DNA sequence. It’s a bit like someone claiming they have replaced heliocentrism with a new model, but the new model doesn’t even include planets.
In order for Ewert’s design model to be superior to the current model it has to address the same data. It doesn’t. That’s the problem.