The Current Status of Ewert's Dependency Graph of Life

Hi Chris
I will when I have a chance over the next few days.
Best
Bill

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That isn’t at all what new models do. You can’t make up your own definitions if you want anyone to know what you’re talking about, especially if you don’t actually define your terms. Common descent has a meaning. Guided evolution has a meaning. Separate creation has a meaning. The only two that are compatible are common descent and guided evolution. Common descent assumes neither unguided evolution nor natural selection.

Convergence has a meaning too, and it doesn’t mean functional constraints. And in fact Ewert is contrasting convergence due to functional constrant with similarity due to re-use of components.

From the article (not primary literature, even) that you cite: “Different organisms often independently evolve similar observable traits such as anatomical or functional features, but the genetic changes underpinning such ‘convergent evolution’ are usually different.” Note that these are a couple of hundred genes out of around 20,000, i.e. 1%. I’d call that rare. And even this is an unusually high number.

Since that’s paywalled, I can’t tell what it actually says. What percentage of pseudogenes did the authors find to have function?

HGT does not produce a consistent nested hierarchy. That’s why basal relationships within Eubacteria are hard to discover.

You have to explain it until it makes any sort of sense. You haven’t answered the question either. What basic types are there? Try again.

My point is that you claimed that pseudogenes and ERVs result from horizontal transfer, but they don’t.

How is that evidence for your claims?

But it doesn’t. HGT is expected to destroy nested hierarchy, not produce it.

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This is technically true. LOL. I am simply taking the work that has been done from other experts and putting the pieces together to provide a robust theory, such as the Orch-OR theory, common design model and Winston’s model (OEC version. The only thing that could be considered my idea is the merging of all three origin of viruses models into one.

Again, that’s not what the studies suggest:

“Although observed rates of acquisition of horizontally transferred genes in eukaryotes are generally lower than in prokaryotes, it appears that, far from being a rare occurrence, HGT has contributed to the evolution of many, perhaps all, animals and that the process is ongoing in most lineages . Between tens and hundreds of foreign genes are expressed in all the animals we surveyed, including humans. The majority of these genes are concerned with metabolism, suggesting that HGT contributes to biochemical diversification during animal evolution.”

From the second study:

“We have shown three lines of evidence for preferential gene transfer having the potential to create phylogenetic patterns comparable with those generated by shared ancestry. These transfers are characterized by the preference of taxa to exchange genes with partners more similar to themselves rather than rare HGTs that may occur randomly and indiscriminately.”

Universal common descent does NOT explain the state of the fossil record or origin of life/viruses

Nope, Universal common design and common descent are mutually exclusive because Universal common descent does not explain the fossil record and the origin of life/viruses.

Well, its supposed to be evidence specifically favoring common design NOT guided evolution.

Tens and hundreds out of how many, total? Have you considered that?

As I’ve told you before, this is talking about horizontal transfer being most likely between close relatives, thus largely matching the real phylogeny. This is no comfort for your theories.

True. Then again it isn’t intended to. However, the fossil record is consistent with common descent but inconsistent with separate creation. If it were consistent with separate creation you would be able to identify the basic types, which you haven’t managed in even a single case. Nobody else has either.

“Universal common design” is nearly meaningless except as a synonym for “god did it”. But how did god do it? It could have been through guided evolution and common descent. They’re fully compatible. Both Michael Behe and Michael Denton agree with that.

Then you shouldn’t have equated common design with guided evolution. See how your shifting personal definitions cause confusion?

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I don’t know since I am relying on secondary sources. Here is a snippet of the article though…
“However, with a growing number of instances of pseudogene-annotated regions later found to exhibit biological function, there is an emerging risk that these regions of the genome are prematurely dismissed as pseudogenic and therefore regarded as void of function.”

There are different types of convergence and I was specifically referring to functional convergence, which involves what Winston has suggested in his model.

I cannot provide a detailed account of those examples because Old earth Baraminology has not been fully developed yet. But, here is an idea of what those examples might be for now:

The sudden appearances of Avalon, Cambrian fauna, Ordovician, Nekton animals, Odontodes vertebrates, Land vertebrates, Insects, Dinosaurs/birds, placental mammals, Genus Homo, and Humans

Because it is consistent with the origin of life model that I showcased in a recent topic.

Well, HGT does two things to phylogenetic patterns from the study I showed you before:

“We conclude that the observed phylogenetic pattern reflects both vertical inheritance and biased HGT and that the signal caused by common organismal descent is difficult to distinguish from the signal due to biased gene transfer.”

Sure, but why is this a point of contention?

I think you meant to say this is NOT talking about…If so, I have already conceded this, which is why I am invoking Winston’s model to explain the rest of the data.

Quantum tunneling is how he did it. Here is a snippet of an article you should read:

"In summary tunnelling has guided us via prominent examples to biochemistry where quantum tunnels are important infrastructures in the world of functional molecules: spontaneous mutations in DNA, enzymatic reactions and especially energy transduction pathways are highly influenced, supported and even enabled by quantum tunnelling. The transition probability of the tunnelling concept from the field of organic chemistry [123] to biochemistry [124] has significantly increased within the past years while, at the same time, the conceptual barrier between chemistry and biology has become smaller and has begun to disappear [125] (see also Pross, 2013, in this issue).

Quantum Tunnelling to the Origin and Evolution of Life (nih.gov)

I bolded that part to illustrate why you cannot separate the origin of life from evolution, which is also why Universal common design and descent have to be mutually exclusive models. (ex. General relativity and Newton mechanics)

You have to stop citing papers you haven’t read. It’s just rude. I refuse to discuss a claim based on your poor scholarship.

No, he’s not talking about convergence of any sort. Separate creation is not compatible with convergence, which is a feature of common descent.

Exactly. You can’t provide an account at all. And it will never be fully developed. This is you once again relying on hypothetical future information to support your argument. That isn’t cricket.

I have pointed out previously that none of these are identified as basic types. I have also pointed out previously that Avalon isn’t even a taxon; it’s a location. Similarly, Ordovician is a time period, Odontodes are teeth, and none of them is a family, which you have previously said is what basic types are. And I have further pointed out that many of these supposed basic types are nested within each other, so at most one of those nested groups can be a basic type. This is you once again reposting an incoherent claim without ever addressing previous criticisms.

It’s also consistent with many other irrelevant notions. Consistency is not a good guide to relevance.

Yes, that’s because the HGT they observe largely follows the true phylogeny. This is not useful to your claims.

Because I said that horizontal transfer is rare in eukaryotes, and tens to hundreds of genes out of roughly 20,000 would be considered rare. In other words, that paper supports my claim, not yours.

No, I said what I meant. What?

But that’s not what it means. You must try harder not to be incoherent.

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Completely wrong.

New models may include new terms, or they may use existing terms to describe a novel idea or process. They rarely reuse existing terms while meaning something different, because that can make it harder to understand. They especially don’t reuse existing terms from the same field to mean something other that the usual meaning in a context where the usual meaning could also apply, because that leads to total confusion. They should never reuse existing terms without explicitly stating that they are doing so and including the new definition. Doing so guarantees that a model will be misunderstood.

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No, that is not the meaning of falsification.

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Hi Chris
I re read the paper this morning and don’t think this model is very different than prior models as it is based on Fisher/Wrights work.

It is different from other work that involves gene duplication as it uses NC regions as the point of origin for de novo genes. These models are very difficult to test as they predict results in greater than 100k years for quickly replicating organisms.

The other issue with models like this is figuring out the real correlation between fitness and new function. Behe’s work showed that blunting of genes can improve fitness.

What exquisite detail in this paper do you think predicts the origin of new functional sequences?

Best
Bill

You test models against data when the timescales are greater than can be experimentally assessed. That’s how they test models in geology and astronomy.

The model in that paper is consistent with rates of gene gain on geological timescales inferred from comparative genetics.

Behe has done no work to show this, it was already known. Behe has instead used this already established knowledge (gained from other people’s work) as a premise in his attempt to argue that this is effectively the only mode of evolution.

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Are these the species they used to generate the model? How many mutations do you think they allotted for discovery of a new gene? How would these estimates translate to what we see in the Howe diagram?

Unbelievable.

That’s in the paper, Bill.

Very well. Taking the slowest rate among those numbers (4.6 * 105 years), and extremely conservatively(and totally unrealistically) assuming sequential evolution of each new gene (meaning for each additional new gene, the previous one has to evolve first, so half-way through the establishment of one gene another can’t start evolving from another locus), that still gives us ~889 new genes in 400 million years.

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That’s per lineage, of course. Counting all lineages, the diagram encompasses around 1.3 billion years. Say 2600 new genes. And that’s just from non-functional sequences, and doesn’t count the genes arising from duplication.

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The model time-step calculated in column 3 is the time it takes for 1 mutation to occur in a locus of 100 bp

From the paper.

Are you claiming new genes form from a single mutation in 100 BP of DNA?

Here, let me correct this sentence for you.

I cannot provide a detailed account of those examples because Old earth Baraminology has not been fully developed yet don’t have a theory yet, just a few vague ideas that are not falsifiable.

Maybe this will help you understand why scientists, members of a community built on the foundation of falsifiability, are skeptical of your “theory.”

HTH,
Chris

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Not in general, no, neither is the paper. A new gene arises when the fitness contribution from a locus passes a so-called genic threshold.

Gene birth model

We use the Wright-Fischer framework to model well-mixed populations of fixed size N , composed of asexually reproducing haploid individuals. For each individual i , we consider the fitness contribution Fi of a single locus in its genome. Here, fitness represents exponential growth rate, which is equivalent to the quantities considered in experiments that measured DFEs (e.g., Böndel et al . ( 2019 )). We describe a locus as genic if it consistently contributes a fitness advantage above a predetermined genic threshold.

It is thus not really a matter of the number of mutation or the size of the locus, but the total fitness effect of mutations that occur in that locus. This is an entirely reasonable simplification, since a locus can of course be very far from, or very near, to a functional gene, and thus could involve the accumulation of many small-effect, or just a single large-effect mutation to transform it into a beneficial gene.

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The simulation runs for thousands of such steps. Why would you think the paper claims a single mutation creates a new gene?

HTH,
Chris

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I could hazard a guess.

If this paper passes peer-review it should give ID Creationists conniptions.

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Isn’t this what your estimate is based on? 4.6x10^5 years for P.tetraurelia to generate a mutation in in 100bp.

If we use Arts low end number for a functional search these waiting times are way! too long.

The assumption has to be that function is very close to the NC sequence. Do you agree?