Thanks for the clarification.
The evidence I see against a single tree claim is not in phylogenetic analysis but in the different gene and chromosome arrangements in vertebrates. I don’t see any good way to convince someone that mice, humans and chickens come from a single origin and their gene and chromosome patterns were the result of reproduction and natural variation. This is why I think multiple trees is the better model given the large differences in gene and chromosome arrangements.
Please show your math suggesting there is any problem at all with these patterns being the product of reproduction and natural variation.
What did you use to compare the two models? Do you even know how to compare two models?
Here is my hypothesis again about the nested hierarchy of species…
Analogous phenotypic traits were designed separately in unrelated families and orders in response to similar needs.
If this is true, then we should observe similar patterns of positive selection in HOXA3 genes or convergent amino acid changes in DYNC2H1, PCNT and HOXC10 genes across those families and orders.
Are you telling me these are just retrodictions or assertions instead of predictions?
Not true, I gave you those primary studies that support quantum mind theory. Or are you referring to something else?
My day job right now is serving the lord by developing this theory with all of you until it is ready for publication or reaches its full potential. Whatever that is, of course.
Yes, I agree now, but this mainly just happens when I input a question. I usually try to paraphrase and cut down on its responses when it is too large.
Nevertheless, I have decided to stop doing this since I have noticed it is not as helpful or useful as I thought it was.
Yes, I agree. If it is any consolation, I was testing for the first time how useful ChatGPT can be and what are its limits. It is definitely not something I normally did in the past on this forum nor do I see myself doing much in the future.
What refutations did I ignore exactly?
We don’t see those discontinuties because HGT can mimic or create the same patterns:
“Organisms that frequently exchange genes become more similar, and transfers between these groups may then be categorized as HGTs with a bias reflecting overall relatedness, even though the initial transfers may have been biased by other factors. We have previously shown that biased gene transfer CAN CREATE and maintain phylogenetic patterns that resemble the signal created through vertical inheritance .” [emphasis added]
Biased gene transfer and its implications for the concept of lineage (nih.gov)
Now, I am WELL AWARE that this particular study emphasized that this mainly happened below the family level because greater genetic and phenotypic differences between taxa make it more difficult for BGT to create nested patterns.
But, this does not mean it can’t or does not happen at or above the family level as other studies could suggest:
A phylogenetic tree built from BovB sequences from species in all of these groups does not conform to expected evolutionary relationships of the species, and our analysis indicates that at least nine HT events are required to explain the observed topology. Our results provide compelling evidence for HT of genetic material that has transformed vertebrate genomes.
" we statistically tested for incongruence between the topology of the promoter sequences against the species tree. The null hypothesis of this test is vertical inheritance (as defined by the species tree); therefore, rejection of the null hypothesis is a strong indication of HRT. We found that 51% of all core gene promoters are incongruent with the species phylogeny, indicating that regulatory regions, similar to coding genes, are frequently transferred. " Transfer of noncoding DNA drives regulatory rewiring in bacteria | PNAS
“Because of the critical tasks of translation elongation factors, it is widely believed that EF-1α/EF-Tu genes have been vertically inherited from the last universal common ancestor (3–5), and the gene products are ubiquitous in all extant cells. However, large-scale sequence data from phylogenetically diverged organisms started unveiling cases that clearly violate the above preconception about EF-1α/EF-Tu evolution.”
Direct phylogenetic evidence for lateral transfer of elongation factor-like gene - PMC (nih.gov)
The Common archetype theory suggests that independent phylogenies emerged from archetypical blueprints in the mind of God, which contain nested hierarchies within them.
This means that these nested patterns don’t exist above and at the level of Order from the supposed universal of tree life. But, no one is saying they don’t exist at all because both common archetype and common descent suggests that created kinds of invertebrates emerged from stem metazoans during the Cambrian explosion. The only difference is that common design claims that created kinds from other animal groups continued to emerge from stem metazoans.
More importantly, observations do NOT show a universal nested tree of life. As described by Eugene Koonin, it looks like a bush or star tree of life at the base of the tree:
“A Bush of Life: a typical tree with unresolved deep branches. The tree was generated from simulated data using the TreeView program [114].”
Here is part of the abstract:
"The relationships between major groups within an emergent new class of biological entities are hard to decipher and do not seem to fit the tree pattern that, following Darwin’s original proposal, remains the dominant description of biological evolution… In each of these pivotal nexuses in life’s history, the principal “types” seem to appear rapidly and fully equipped with the signature features of the respective new level of biological organization. No intermediate “grades” or intermediate forms between different types are detectable. [emphasis added]The Biological Big Bang model for the major transitions in evolution | Biology Direct | Full Text (biomedcentral.com)
According to the study, it includes other plants and Cambrian fish:
"The bushes in the tree of life (TOL) recently have been examined in some detail, and their appearance has been attributed, primarily, to cladogenesis compressed in time that appears to be characteristic of transitional epochs in evolution. Also, the erosion of the phylogenetic signal inevitably results in poor resolution of phylogenetic trees for ancient divergence events like all those listed above. Nevertheless, it is generally assumed that, in principle, the TOL exists and is resolvable although, in practice, full resolution might never be attained and, furthermore, might not even be particularly important for understanding the actual events that transpired during the respective transitional stages .
Here, I argue for a fundamentally different solution, i.e., that a single, uninterrupted TOL does not exist , although the evolution of large divisions of life for extended time intervals can be adequately described by trees. I suggest that evolutionary transitions follow a general principle that is distinct from the regular cladogenesis." [Emphasis added]
As further pointed out by Stuart Newman, Yes we do…
“Considering the shared and specific interaction toolkits of the various clades in relation to the physical forces and effects they mobilize helps explain how phyletically different organisms use genetically homologous components to construct phenotypically dissimilar but functionally similar (analogous) structures often without common ancestors exhibiting the character”.
The origins of multicellular organisms (uevora.pt)
Primary source:
Tetraspanin genes in plants - ScienceDirect
Algal Genes in the Closest Relatives of Animals | Molecular Biology and Evolution | Oxford Academic (oup.com)
This is false. Before I show why, here is the definition of random unguided processes……
In evolution, there is no entity or person who is selecting adaptive combinations. These combinations select themselves because the organisms possessing them reproduce more effectively than those with less adaptive variations. Therefore, natural selection does not strive to produce predetermined kinds of organisms but only organisms that are adapted to their present environments. As pointed out, which characteristics will be selected depends on which variations happen to be present at a given time in a given place. This, in turn, depends on the random process of mutation as well as on the previous history of the organisms (that is, on the genetic makeup they have as a consequence of their previous evolution). Natural selection is an opportunistic process. The variables determining the direction in which natural selection will proceed are the environment, the preexisting constitution of the organisms, and the randomly arising mutations. pnas.org/doi/10.1073/pnas.0701072104#sec-8
AND
"> (i) they are rare exceptions to the fidelity of the process of DNA replication and because (ii) there is no way of knowing which gene will mutate in a particular cell or in a particular individual.
However, the meaning of “random” that is most significant for understanding the evolutionary process is (iii) that mutations are unoriented with respect to adaptation; they occur independently of whether or not they are beneficial or harmful to the organisms. Some are beneficial, most are not, and only the beneficial ones become incorporated in the organisms" through natural selection."
Mutations are oriented to maintain the survival, reproductive, or adaptive capabilities of the organisms or population. Here are the confirmed predictions:
Most of the Junk DNA in the non-coding regions of the genome is functional
Expanded encyclopaedias of DNA elements in the human and mouse genomes | Nature
The regions encode for proteins reduce the risk of deleterious mutations.
[28] Mutation bias reflects natural selection in Arabidopsis thaliana | Nature
[4] Evidence of non-random mutation rates suggests an evolutionary risk management strategy | Nature
Saltation theory
A sudden and large mutational change from one generation to the next, potentially causing single-step speciation.
Confirmed predictions
Sudden appearances and stasis in the fossil record.
[47] The million-year wait for macroevolutionary bursts | PNAS 1
Family trees based on anatomical features contradict family trees based on molecular similarities,
Phylogenomic conflict coincides with rapid morphological innovation | PNAS
This frequently happens at the family level as well:
Understanding phylogenetic incongruence: lessons from phyllostomid bats - PMC (nih.gov)
Yeah, this reinforces my point because the study does not take into account HGT or HRT and BGT.
Relax, it was just a tongue-in-cheek response to get him to continue our discussion on the matter. Of course, I don’t think he conceded my point. Obviously, no one believes or would believe such nonsense.
No, there is no victory here. Just a tongue-in-cheek response. If you have any further objections, I would like to hear them so I can potentially make more improvements.
I am not sure I would go that far. Instead, the way I would describe it is…
John is a reasonable and respectable guy who is trying to defend a model he has studied all his professional life that is most likely only true in his imagination.
This is because the only true testable predictions common descent yields have been disconfirmed. Moreover, we still have to assume common descent is true in order to make these predictions in the first place.
I don’t think this is the actual issue with Stuart Hameroff’s quantum origin of species model I used for mine. Instead, the real issue is how testable his speculative model is. It does not seem to be even testable in principle. However, the testable predictions I incorporated in the model should alleviate this problem.
I agree. There is no alternative SCIENTIFIC model that can even compete with the Common design/archetype model.
As I told @colewd, I don’t think this is the actual issue with Stuart Hameroff’s quantum origin of species model I used for mine. Instead, the real issue is how testable his speculative model is. It does not seem to be even testable in principle. However, the testable predictions I incorporated in the model should alleviate this problem.
There is a fundamental error that you are making here. There is no evidence of common descent in living or fossil organisms. There is nothing to infer from nature that would compel anybody to make this conclusion. The simulation of common descent is just in your mind and you are imposing it onto the data just like Darwin did in his day.
All he did was modify Owen’s theory from common archetype to common ancestor and then assumed (like you guys do) that living organisms evolved from these ancestors.
And this would mainly just be based on secular dogma and personal bias rather than scientific merit.
This does not predict the data that we see. It predicts data that we do not see.
This is not a scientific, empirical prediction. “Similar” and “convergent” are subjective and designed to allow you to pretend to be scientific. There’s also no reason for you to focus on specific genes. “Or” is a pure weasel word in this context.
Citing studies the way you do is purely rhetorical. Cite the data in those studies as a real scientist would.
You’re doing a very poor job of it.
Speaking of day jobs, I’m still waiting for an explanation of the reasoning and evidence that led to your claim that I’m not a neuroscientist after I provided a list of my publications and stated very clearly that I studied LTP.
Do you not see that this case clearly demonstrates that you will blatantly fabricate even the most simple, factual information, showing that your ability to understand more complex information is nonexistent?
No. It is based upon (i) a basic understanding of science (something that you, along with your two sole supporters on this forum – Bill ‘The Performing Sealion’ Coll and Sam Foerster, provide every evidence of lacking), and 18 years of observation of creationist misuse, misrepresentation and misunderstanding of science.
Your claims of a vast “secular” conspiracy, including the Catholic Church, working to protect Evolution from scrutiny is patently ludicrous – and is simply a psychological defense mechanism against acknowledging how little credibility your claims have.
Your harping on about “scientific merit” when every single scientist on this forum who has commented on your blather has been scathing of it is equally ludicrous.
I would note that you have carefully avoided the most commented-on part of my post:
But really, I’m rather tired of you making excuses to yourself (nobody else here takes them seriously) as to why your vacuous blather does not earn the reception you think it deserves. These excuses are …
You need to elaborate on your responses Mercer.
If two unrelated lineages evolve similar traits, then it logically follows that the underlying genetic mechanisms that govern the development and function of these traits will also be similar.
So if we compare the genomes of these lineages, we would expect to find convergent changes in the genes that are involved in the development or function of these traits.
No, it is definitely not subjective because the hypothesis, the predictions, and the methods are based on a combination of previous studies done on the red and giant panda family- level taxa, which should allow us to obtain reliable and objective results.
There are several steps and methods to be taken in order to distinguish homologous from analogous phenotypic traits…
1. Identify morpho-molecular dissimilarities and/or lack of fossil intermediates among order- and family-level taxa.
In the case of pandas, the k-mer signature analysis was used to identify the differences between the two pandas [30]. However, this method did not show discontinuity between the pandas and certain outgroup taxa, which would indicate that they may not share a common ancestor with those taxa.
A tail of two pandas— whole genome k-mer signature analysis of the red panda (Ailurus fulgens) and the Giant panda (Ailuropoda melanoleuca) | BMC Genomics | Full Text (biomedcentral.com)
2. Identifying functional differences among order- and family-level taxa in relation to their environment.
In the case of the pandas, the comparative anatomical analysis was used to identify the structural and functional differences between the two pandas in relation to their ecology.
This allowed them to conclude that their analgous traits evolved separately based on similar needs:
Evidence of a false thumb in a fossil carnivore clarifies the evolution of pandas | PNAS
3. Test the predictions related to the functional differences among order- and family-level taxa
In the case of pandas, they predicted and confirmed the 3D structures of HOXA3 and HOXC10 and assessment of mutation effects.
Ok, tell me which study do you want me to do this for. I will let you pick.
Well, I don’t know what you count as being an expert in a field. Simply studying it online or in school does not seem to count to you guys because I studied quantum physics online from various sources in order to develop the common design theory…
Do you have a degree in quantum biology? If so, are you a practicing scientist in that field as well?
So far it wouldn’t seem so. As I myself tried to explain to you, and as @Mercer put in much more concise words I shall here hearken back to, it is not the person who makes the predictions for a model to be scientific, but the model itself. It is not enough for you to list a series of long-known facts and slap a stamp spelling “prediction” on them. The statements need to be logically entailed by the model, such that some or all aspects of the model are rendered incorrect, if the prediction had turned out so. If your auxiliary claims are not logically linked to the model, then they are not predictions of the model; so until you are willing and able to demonstrate that link, we do not get to call them so.
If I may make a suggestion, I actually have, and you even quoted me with it:
Perchance in studying the model you may find ways to actually render predictions. Considering Hameroff himself didn’t I’m not optimistic, but perhaps it is yet worth considering attempting to do something that has even the slighest chance of advancing your cause over wasting your day job hours on rhetorical games.
Excellent. How about a test on the very basics of it, then? Same conditions as before, seven days completion time, no controls against cheating, content chosen strictly from introductory materials. I’ll even weigh the score in favour of questions from the beginning, so getting tougher things from the twentieth hour or so wrong won’t cost you as much. Think of it not as a challenge, think of it as an opportunity to prove to this board that you are not completely lying about this one thing and that you actually made as much as any attempt whatsoever to educate yourself on at least one subject you say is relevant for your case.
There are thousands of them. Pick any of your long posts and there’ll be some refutation you omitted to quote and/or didn’t address.
But since you’ve asked for specific examples:
Example 1
You have ignored the evidence of common descent in Theobald’s article, especially sections 2-5, which you show no sign of having even looked at.
Example 2
Your misquote of Coyne, which you have not only never corrected, but continued to use after it was shown to be a misquote.
I fully expect this to be yet another refutation you ignore.
This is an excellent example of a refutation that @Meerkat_SK5 has ignored.
With skill, diligence, and knowledge. Why are you pretending that this work has not already been been done, Bill?
No, I do not. Moreover, addressing someone by last name only is extremely disrespectful.
No, it does not. The data that you ignore demonstrate that.
Then you have a lot of work to do. Cherry-picking 4 genes from 2 species is laughable.
You haven’t obtained any results. Science is not merely rhetorical as you pretend it is.
How is your repeated bearing of false witness doing the Lord’s work, exactly?
[quote=“Meerkat_SK5, post:878, topic:15561”]
Publications in the primary literature, already provided and ignored by you for obviously egotistical reasons.
What does that have to do with your claim that nobody here is a neuroscientist, exactly?
Please, explain. Specifically, which data is it that in your opinion favours reconstructing the history of vertebrates via multiple trees over a single tree? How does the volume of that data compare to the volume of data favouring the currently accepted mainstream inference?
Well, the problem with that is that if we pick a sufficiently large data set to construct such trees out of, we end up with trees that do in fact have a common root for, say, all vertebrates. Like things get bushy and messy at the level of unicellular organisms, but once we start classifying the “birds and bees”, so to speak, all of a sudden it’s a very unambiguous single tree, always almost exactly the same one, no matter which genes specifically we look at. An argument can be had about the very root, and how to even define things at that point, but for the sort of examples you point to in objection, like mice, humans, and chickens, the data is rather quite unambiguous. The supposition that this tree of classification based on genetic evidence corresponds to a tree of familial relations, of course, only holds insofar as we accept that genetics, inheritance, and familial relations correlate, but I don’t think that matter is under dispute here.
You haven’t looked at the evidence and you know it. It supports the nested hierarchy as well. There are none of the discontinuities predicted by your hypothesis.
The evidence is very convincing. You should consider examining it. Here’s a compilation of the mouse-human evidence:
https://syntenybrowser.jax.org/
This is yet another edition of Bill articulating a testable empirical prediction of his ID hypothesis, deliberately and falsely presented as fact.
I think that you are underestimating Bill’s impressive willingness to deny obvious reality.
At the protein level I do not see a consistent tree. One of the causes maybe functional constraint varies between proteins or some have different starting points.
I question how significant the phylogenetic tree pattern is in determining whether a single origin is real. The chromosome and gene data needs to be understood and currently there is no population genetic model that can make sense of it. I believe that there is no yet identified reproductive mechanism that can explain the origin of new functional sequences.
You don’t see it because you aren’t looking at the evidence.
Because you’re incompetent.
It isn’t even clear what he means by “at the protein level”. Is he comparing protein sequences? Presence/absence data? What do functional constraints have to do with it? Responding to Bill’s word salad as if it means anything only leads to more confusion.
