Making a Tree from Designed Objects?

its actually refer to john harshman comment.

Wait. You want me to give you an example of something that doesn’t exist?

Sorry, that was too incoherent for any meaningful response.

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yes. if you said that nested hierarchy doesnt exist in vehicles show me how.

you said that there is no problem for evolution to evolve a dog from a fish in a single generation. if so it will not be a problem to evolve a complex eye from non eye.

You’re asking me to do what, exactly? Create a data matrix of cars and trucks, analyze it, and show that it isn’t a nested hierarchy? No, the burden is on you to show that it is. I’d say that it’s obvious.

No, I said no such thing. I said that if such a thing happened, that would not cause a problem for an evolutionary explanation for everything else, because it would be a one-time magic trick unrelated to how anything in the world actually works. You are very, very confused.

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Ironically, I do not necessarily disagree with this. God could have designed through a process of common descent. Why not consider common descent a design principle @scd? That is what, for example, Behe and Denton argue.

This is your mistake, you think the phylogenetic trees inferred from the genetic data should correlate with phylogenetic trees inferred from morphological data. But there is no functional reason that should be so other than as an artifact of the shared genealogical history of the different sets of data. Even for genes that are actually involved in morphological development. Though we can simply exclude such genes from analysis in case you don’t believe this.

But before we even get to that, try to think for a moment about why a phylogenetic tree inferred from one gene, should match the phylogenetic tree inferred from another gene. Or why it should be the case that a tree inferred from morphological data should mach a tree inferred from genetic sequences?

You first have to consider how a phylogenetic algorithm actually works. A historically much used algorithm called Maximum Parsimony basically works like this: What hypothesis of common descent explains the data we see (the gene sequences from different species) using the smallest number of character state changes? A character state change for genetic data is a differences in sequence between similar genes in different species.
So if gene sequence (A) differs from gene sequence (B) by having a G nucleotide instead of a T nucleotide in some location, then that difference is explained by a character state change, as in a mutation. If you only have two genes, one from each species, then of course you don’t know whether the “original” nucleotide was T which then mutated to G, or whether it was T that then mutated to G. But if you have three species, and two of them have G and only one has T, then the simplest (most parsimonious, invoking the least amount of evolution, as in the fewest character state changes) explanation is that the original was G, and then just one of them mutated to T. As opposed to having the original be a T, and then having two independent T->G mutations.

So the hypothesis is that they are different because one of them mutated. So the most parsimonious tree is the one that accounts for the different sequences with the fewest total number of mutations. Hence, Maximum Parsimony.
There are many other phylogenetic algorithms in use today. Another type of algorithm is called maximum likelihood. This algorithm uses something called a substitution model to evaluate how “likely” a particular tree is compared to another. A substitution model is basically a hypothesis that assumes that some mutations are more likely than others. So this maximum likelihood algorithm compares the likelihood of different trees and scores them according to which is the most likely combination of mutations that explains the data we have. If one tree implies that a lot of lower-probability mutations must have happened, and another tree explains the same data with higher-probability mutations, the most likely tree is chosen. Hence, maximum likelihood.

With this understanding in hand, we can proceed to consider the fact that for any given gene sequence, there are an incredible number of different ways to change the gene and achieve the same result/function. Countless gene sequences from different species, despite the fact that they are different in sequence, are known to be functionally equivalent, and can often times even be exchanged with little to no functional significance. Just to pick one examples of this, for a long time cow insulin was used as a substitute for human insulin for human diabetics. And it worked, and the people who used it didn’t turn into cows. The cow insulin protein, despite being different from the human insulin protein, still worked in humans without turning them into cows. So the function was preserved, and it was independent of morphology.

Now the question is, why should this pattern repeat itself for different genes, and morphology too, if evolution didn’t actually take place? If they don’t actually share common descent? What functional reason would there be for having similar tree patterns repeat in other genes shared between the same species too, or in morphological data?

Even If you doubt the fact that there are many different ways to achieve the same functional result, try to consider that we can pick genetic sequences which are known to be completely independent of morphology. To pick an example we can use the enzyme in saliva called salivary amylase.
It’s function is to degrade starch in food you eat.

This enzyme is not involved in making your morphology how it is (it doesn’t cause you to be a member of Homo sapiens), yet it is found in countless animals.

The gene sequence of this enzyme does not cause you to have a spine, nor to have four limbs, nor to have a bony skeleton, nor mammary glands, nor to have hair instead of feathers, nor to have five digits on each limb, nor the patterns of the arrangements of bones in your four limbs, nor to have bilateral symmetry, nor to embryologically develop ass-first (be a deuterostome) or to be multicellular, or for your cells to be eukaryotes.
It does not cause you to be a hominid, or a great ape, or a primate, or whatever other level of classification you can think of. All it does is degrade starch you eat (break up long chains of carbohydrate molecules into glucose monomers). So if you eat a potato, or pasta, or an apple or what have you, the enzyme simply degrades starch into glucose so you can digest it.

You have this enzyme, chimps have this enzyme, gorillas have this enzyme, pretty much all mammals have this enzyme afaik. But the horse version, or the pig version, or the cow or dog or fish version, works just as well as the human version. They each are just as capable of breaking down starch.

So this gene sequence is completely independent from morphology, it is not involved in anything that we could use to classify an organism as belonging to a particular clade using their morphology. Yet when we use a phylogenetic algorithm to infer a tree from the gene sequences from many different species using this amylase gene, we get one that overwhelmingly agrees with the morphological tree.

Even more amazingly, we can just pick other enzymes too also shared among countless species which are also independent of morphology, and independent of each other. Core metabolic enzymes in a pathway responsible for something like RNA or DNA nucleotide biosynthesis. Also completely independent from morphology, and not related to breaking down starch into glucose obviously. Or we can pick genes for enzymes responsible for replicating strands of DNA (DNA polymerases), or for another digestive enzyme responsible for breaking down proteins into amino acids in food. Genes that are even shared among plants, animals, fungi, indeed all eukaryotes, or all known cellular life.

And they’re independent of each other. They are not somehow mutually constraining each other’s gene sequences. Why should it matter with respect to the function of the gene, what kind of phylogenetic tree researchers are able to infer using some particular algorithm of inference? Obviously such a constraint is not what is causing gene sequences to be the particular way they are.

And why should the gene sequences from different genes influence each other in a way that constrains the topology of trees that human researchers infer from them? That is clearly not a constraint that actually operates on genes. The gene sequence of your salivary amylase gene has no bearing on the gene sequence of your DNA polymerase gene, and in so far as some sort of epistatic interaction might actually exist between them, there is no reason to expect this interaction to be of such a nature that it just so happens to constrain them to yield similar trees if subjected to a phylogenetic inference. That would simply not make sense.

So for these gene sequences too, we can submit them to the same algorithm (basically whichever one you choose), and still get pretty much the same tree. Why would that be the case? Remember, they’re all known to be completely independent of morphology, and independent of each other, certainly independent in the sense that their sequences are not constrained by what kind of tree a human systematist can infer from them.
The only sensible constraint that would operate on them are those that preserve function. This is known because we can splice the human(or cow, or pig, or goat, or mouse, or bacterial) variants into fish, and they work just fine and don’t turn the fish into humans or anything else (they remain unaltered), or into fungi, and they remain fungi, or into bacteria, and they don’t suddenly grow a spine and four limbs, or anything like that. Yet we still get a similar tree out when we do the inference from independent sets of data.

The most obvious explanation for the fact that the genes exhibit the same general patterns if subjected to a phylogenetic inference, is because they really do share the same genealogical relationship. The pattern repeats in different sets of data because the different sets of data came to be the way they are through their common evolutionary history. What constrains them to yield similar patterns is the shared constraint of their common descent.

No other explanation makes logical sense. To say that a designer designed it that way, while that is not logically impossible, is equivalent to saying that the designer has created starlight coming to us from distant galaxies “with the appearance of age”, or put fossils in the ground “to test our faith”. You can believe that if you want, but it has rendered your designer deliberately deceptive. The designer would have had to create the pattern expected from common descent, but not expected for any functional reason, simply because… whatever reason you can invent in your head.

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@Rumraket I agree except that God could have designed us through a process of common descent. This would produce the same pattern.

Yes if God designed using common descent, then common descent would be true, and the explanation for why we see the evidence we expect if common descent was true, is that common descent actually happened. It is not that God created each species deceptively to look like common descent happened yet it didn’t.

I have to wonder why you need to stick God in there anyway. It still has that strange quality of unnecessary rationalization. It’s sort of like saying that when it rains, while gravity usually takes care of it, once in a while God gives particular drops of water special attention and steers them down towards particular locations. Why would anyone believe that?

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I didn’t say that God is nudging inconsequential things. Nor did I say there is scientific evidence.

I’d rather say that God providentially governs all things, including evolution, and I know this from evidence outside of science. Now, however, we are moving to theology, which may or may not be your desire to engage.

Wow, that sounds convincing. Air of mystery and spookiness.

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Let’s be clearer: The method evaluates the conditional probability (which is what “likelihood” means) of observing the observed data given a model of evolution and a particular tree. Then one chooses as best the tree that makes the observed data most likely.

Carry on.

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We could have a whole thread on whether there is such a thing, and if so what it would be.

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Okay, I see I got it wrong. I thought it was scoring the probability of the tree, given the data and the substitution model. But you’re saying given a substitution model the algorithm is trying lots of different trees to see which tree makes it more likely that we end up with the kind of data we have.

I have a question of terminology for you. Could one say that maximum parsimony is a kind of “minimum evolution” algorithm? It seems to me that is essentially what it does, prefer trees that, so to speak, invoke the least amount of evolution to have occurred.

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There was a considerable controversy over that many years ago. But sure, it is. However, there’s a distance method called by that name, and some people want to avoid conflating the two.

yep, but you realy think that its work in the same efficiency? i doubt it.

actually we get many different result by checking different genes. see here for instance:

https://www.nature.com/news/phylogeny-rewriting-evolution-1.10885

we cant know it for sure. its seens logical that a fish insulin for instance will have a gene that is more similar to other fishes since they may share similar diet, environment etc.

Do you have any interest in testing this hypothesis? If this hypothesis were true, we should see correlations between diet and insulin sequence. If this is not true, you would need to drop it as an explanation and find another specific factor (not merely “environment”).

scd: yep, but you realy think that its work in the same efficiency? i doubt it.

It doesn’t matter what I think, that’s just what the evidence shows: ’Human’ insulin versus animal insulin in people with diabetesmellitus

Background:
Human insulin was introduced for the routine treatment of diabetes mellitus in the early 1980s without adequate comparison of efficacy to animal insulin preparations. First reports of altered hypoglycaemia awareness after transfer to human insulin made physicians and especially patients uncertain about potential adverse effects of human insulin.

Objectives:
To assess the effects of different insulin species by evaluating their efficacy(in particular glycaemic control) and adverse effects profile (mainly hypoglycaemia).

Search strategy:
A highly sensitive search for randomised controlled trials combined with key terms for identifying studies on human versus animal insulin was performed using The Cochrane Library , MEDLINE and EMBASE. We also searched reference lists and databases of ongoing trials.

Selection criteria:
We included randomised controlled clinical trials with diabetic patients of all ages that compared human to animal (for the most part purified porcine) insulin. Trial duration had to be at least one month in order to achieve reliable results on the main outcome parameter glycated haemoglobin.

Data collection and analysis:
Trial selection as well as evaluation of study quality was performed by two independent reviewers. The quality of reporting of each trial was assessed according to a modification of the quality criteria as specified by Schulz and by Jadad.

Main results:
Altogether 2156 participants took part in the 45 randomised controlled studies that were discovered through extensive search efforts. Though many studies had a randomised, double-blind design, most studies were of poor methodological quality. Purified porcine and semi-synthetic insulin were most often investigated. No significant differences in metabolic control or hypoglycaemic episodes between various insulin species could be elucidated. Insulin dose and insulin antibodies did not show relevant dissimilarities.

scd: actually we get many different result by checking different genes. see here for instance:

Let me explain why this doesn’t mean what you think it means. Phylogenetic trees are like measurements, they don’t have to match exactly to still be significantly similar. And so similar in degree the only good explanation is that they are that similar because they underwent the shame genealogical history.

To see what I mean, Imagine I give you two ultra-sensitive thermometers to measure the temperature in my living room to test the hypothesis that there’s a relatively uniform temperature everywhere in the room. And they agree to the 6’th decimal place, where they disagree. They each measure 20.0330413 and 20.0330415 degrees C. Does this cast a significant doubt on the uniform temperature of the room?

Or I give you two thousand normal thermometers and place them all over the room, and most of them measure 20 or 21 degrees, and once in every 100 thermometers, there’s on that says 26, and one that says 17. Does that cast doubt on the hypothesis? We have to answer such questions using statistics.

The disagreement between phylogenetic trees is not of such a magnitude that they cause doubt on the general conclusion that species share common ancestry. They are still incredibly similar.

From Douglas Theobald’s 29+ Evidences for macroevolution article we find Prediction 1.3: Consilience of independent phylogenies

When two independently determined trees mismatch by some branches, they are called “incongruent”. In general, phylogenetic trees may be very incongruent and still match with an extremely high degree of statistical significance (Hendy et al. 1984; Penny et al. 1982; Penny and Hendy 1986; Steel and Penny 1993). Even for a phylogeny with a small number of organisms, the total number of possible trees is extremely large. For example, there are about a thousand different possible phylogenies for only six organisms; for nine organisms, there are millions of possible phylogenies; for 12 organisms, there are nearly 14 trillion different possible phylogenies (Table 1.3.1; Felsenstein 1982; Li 1997, p. 102). Thus, the probability of finding two similar trees by chance via two independent methods is extremely small in most cases. In fact, two different trees of 16 organisms that mismatch by as many as 10 branches still match with high statistical significance (Hendy et al. 1984, Table 4; Steel and Penny 1993). For more information on the statistical significance of trees that do not match exactly, see “Statistics of Incongruent Phylogenetic Trees”.

The stunning degree of match between even the most incongruent phylogenetic trees found in the biological literature is widely unappreciated, mainly because most people (including many biologists) are unaware of the mathematics involved (Bryant et al. 2002; Penny et al. 1982; Penny and Hendy 1986). Penny and Hendy have performed a series of detailed statistical analyses of the significance of incongruent phylogenetic trees, and here is their conclusion:

“Biologists seem to seek the ‘The One Tree’ and appear not to be satisfied by a range of options. However, there is no logical difficulty in having a range of trees. There are 34,459,425 possible [unrooted] trees for 11 taxa (Penny et al. 1982), and to reduce this to the order of 10-50 trees is analogous to an accuracy of measurement of approximately one part in 10^6.” (Penny and Hendy 1986, p. 414)

scd: we cant know it for sure. its seens logical that a fish insulin for instance will have a gene that is more similar to other fishes since they may share similar diet, environment etc.

First of all I think “knowing for sure” is a red herring. We don’t know anything “for sure”.

But it doesn’t matter what you think sounds logical, what matters is what the molecular biology of living organisms is really like, and it isn’t what your intuitions tell you is “logical”. The whole point of my post was to show you that your intutions here are wrong.

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Of course, humans can significantly alter their diets, and their insulin gene sequence doesn’t change. It is possible to live on high protein, or high fat, or high carbohydrate diets, and it doesn’t change the insulin gene sequence. It affects your metabolism, and how your body responds to insulin (some diets can lead to diabetes of course), but it doesn’t change the sequence of the gene.

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its just one possible explanation out of many. so im not sure about that.

That doesn’t appear to have held up over the last 6 years. Why would you cite something from the gossip section and not an actual scientific paper?

If you’re looking for truth, do you quit after finding one thing you can use as ammunition, or do you keep looking?