I couldn’t possibly be detecting any irony, could I?
The idea of exaptation and the similarities of the bacterial injectisome to the bacterial flagellum helped me to accept biological evolution after having been a YEC for a sizable chunk of my life. Learning about the neutral theory of evolution and neutral drift and that evolution can and does produce complexity were factors as well.
Sorry, you have not cited any real problems, just interesting puzzles at best.
I’m not familiar with each of the above, and don’t have time to research further at present… but briefly, can you clarify for me…
- which of the above are direct evidence of common descent?
versus
- which are direct evidence of the mechanism of unguided natural selection working on unguided natural variation?
This goes back to the point toed above… “evolution” can refer to the process of common descent, or the Darwinian mechanism… the core difference that sets ID and others apart from the bio logos/“evolutionary” position is not dispute about common descent, (hence why a common-descent-affirming, “evolution” believing scientist like Behe and others are fully supported and embraced by the ID side, but whose ideas are more or less persona non grata at Biologos.)
But from my amateur and cursory glance at your list, they all appear to be arguments for common descent, which is not my dispute.
@T_aquaticus
I’m not ignoring anything. I am asking for specific examples of DNA differences that result in differences in embryonic development, and why you think those DNA differences can not be produced by evolution.
As I said in my previous response, we may not be in a position to do this yet. But even if we were and showed it was highly improbable to occur, you’d likely plead sharpshooter fallacy. But what we know already about gene regulation shows any constructive changes are extremely unlikely to arise opportunistically.
From extrapolations we estimate that 8.2% (7.1–9.2%) of the human genome is presently subject to negative selection and thus is likely to be functional, while only 2.2% has maintained constraint in both human and mouse since these species diverged.
So from this you infer that approx. 90% of the genome is evolving at a rate consistent with neutral mutations. However, how did they derive their estimate? By comparing genomic sequences of different mammals. Most of their 10% is focused on protein-coding sequences, so it is not surprising that there is relatively little changes in sequence, even between different species. However, they then assume that the differences between mammals in non-coding sequences implies that these sequences are subject to ‘turnover’, which you imply (I don’t think the authors actually say so) means susceptible to neutral mutation. But this extrapolation is based on assuming that eg humans and mice have diverged from a common ancestor. And, the question to ask is: much of the non-coding sequences are repeats; wouldn’t repeats have been randomised by neutral mutations? (Another indication that their rationale is unsound is that, because they conclude these non-coding sequences are mutable, they conclude that a large proportion of this could be deleted without impacting on fitness (p8). Whereas we know that much of non-coding regions are required for eg packing of DNA.) So, I’m going to look into this further, but I think these differences between the non-coding regions of different mammalian (and other vertebrate?) groups may provide further genomic evidence against common ancestry. So thank you for drawing it to my attention!
@T_aquaticus
They say explicitly that neutral mutations only evolve neutrally in 5% of the genome. It isn’t saying that neutral mutations can only occur in 5% of the human genome. Neutral mutations and evolving neutrally are two different things.
It explicitly states that neutral mutations can evolve non-neutrally.
Agreed. But even taking this into account (and the paper discusses various examples) she still concludes that only about 5% of the human genome is susceptible to neutral evolution, as my previous quote, and this is from the subtitle of her paper
Just 5% of the human genome is subject to neutral evolution,
So it’s hard to maintain as you do that she doesn’t mean it.
@T_aquaticus
Why would it have to be two specific bases? Do you think there is only one such interaction possible in the human genome? If so, I would love to see that evidence.
For example, how many combinations of two mutations in the modern human genome can result in a beneficial phenotype? Don’t you have to know this number before you can calculate probabilities of one such interaction being found?
Based on what we know about the length of control sequences for genes, which I mentioned last post, how many two-specific bases do you think will lead to a beneficial phenotype, and why?
@T_aquaticus
The problem is your calculated probability. You are also ignoring the parallel nature of sexual reproduction which can combine beneficial mutations from separate genetic backgrounds into the same genetic background. For example, let’s say there are 100 possible beneficial mutations that are not linked (i.e. are far enough apart in the genome to allow recombination). The odds of getting these 100 mutations is not 100 times the probability of getting 1 of them. Rather, these 100 mutations will occur in different individuals within the population. As these beneficial mutations increase in frequency you will start to get an accumulation of beneficial mutations due to sexual reproduction. This greatly increases rate at which evolution occurs.
What you then need to take into account is the probability of those specific 100 coming together within a population of a given size (and without others that might counter the effect of some of them).
@T_aquaticus
If none of these coordinated mutations for development can even be cited, then what’s the point?
Taking account of what we do know, rather than relying on what we don’t (evolution of the gaps).
@T_aquaticus
I know what it means.
If you know what fixation means then you’ll agree that ‘fixed’ mutations are susceptible to change. And if so, then why do you keep repeating that fixation will happen. That’s not in question.
They are all evidence of both. #3 would need to be fleshed out to cover common descent a bit better.
That isn’t the case. For example, a designer could take an adaption from a mammal species and add it to a bird species, or vice versa. This would violate a nested hierarchy. So the nested hierarchy is both a piece of evidence for common descent and unguided natural evolutionary mechanisms. The pattern of transitions and transversions is the same because it is the fingerprint of unguided mutations that we see happening in modern life. The pattern of endogenous retroviruses evidences the unguided insertion of viral sequences and the pattern of inheritance consistent with common descent. The pattern of transitional fossils links in with the nested hierarchy, so again both common descent and unguided natural processes. Genetic equidistance links in with unguided accumulation of mutations resulting in genetic distances consistent with both a nested hierarchy and common descent.
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And I would likely be correct.
Let’s say I had a deck of cards. I shuffle them and then deal them out one at a time face up. The probability of getting that specific order of cards is 1 in 52!, or 1 in 8x10^67. That is an extremely unlikely outcome, and yet I got it on the very first try. In fact, I will get an equally improbable outcome every time I do the same experiment.
The same for mutations. Any time mutations occur it will result in an extremely improbable outcome. Every. Single. Time. And for the same reasons that my card example produces improbable outcomes.
It’s not an assumption. It’s a conclusion based on mountains of evidence.
Not if those repeats are from relatively recent transposon insertions which make up a large chunk of the non-coding intergenic DNA sequence.
That’s not what I understood. You seemed to be saying that neutral mutations could only occur in 5% of the genome which is not what the paper said.
I have no clue of how that could even be calculated which is why I am extremely skeptical of those who claim they can, which is most of the ID/creationist crowd.
If they are all beneficial, it’s extremely likely. As each beneficial mutation increases in frequency it will be more and more likely to be found with the other 99 beneficial mutations that are also increasing in frequency.
What coordinated mutations for development do we know of?
All mutations are susceptible to change.
When a mutation occurs there are 3 general results. The mutation can almost immediately disappear from the population. The mutation can increase in frequency a bit and circulate at a low or medium frequency. The mutation can increase in frequency to the point where it is found in all individuals in a population. You seem to think that only the first situation happens.
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Appreciate the thoughts as always; i’m tight on time at present, but briefly one quick observation…
if i understand rightly, this is true only for those sections of otherwise similar sections of DNA. Orphan genes unrelated across species can’t even be claimed as having such patterns, no? as such, the pattern of mutations between homologous sections of DNA are evidence that mutations in those sections are indeed explicable by said natural processes… a process that no ID proponent denies to my knowledge.
In other words, if i understand rightly, an ID proponent that supported common descent, but who hypothesized that humans were intentionally designed at a specific point in time through specific larger non-homologous modifications of DNA in a proposed CHLCA, while keeping the other ~95-98% of the genome untouched, would expect just such a pattern of mutations to occur along the homologous DNA over the corresponding ages as the species continued to diverge.
So again i’m not sure how this demonstrates the efficacy or mechanism of unguided variation/selection regarding those parts of DNA that are actually under discussion?
You are making the assumption that orphan genes are not in regions with otherwise similar sections of DNA. There are many cases where orphan genes are the product of just a handful of mutations that produce a new transcript. Two species can share the same stretch of DNA with just a few differences while only one of those species will have a gene within that stretch of DNA. When they say that it is a new gene they are saying that the DNA is only transcribed in one species.
There are also cases of orphan genes that are due to indels (the portmanteau of insertion and deletion). In this case, we would not be comparing substitution mutations which are the transition and transversions. However, the distribution of indels is also as random as the substitutions.
They would need to explain why those modifications are inconsistent with unguided mutations and why we don’t see those same modifications in other more distantly related species. This is where the nested hierarchy comes in.
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Very appreciated, thanks. this was somewhat similar to when i started exploring… early in my life i was exposed to a creation science proponent saying something to the effect of, “what are the odds that even one protein could form…” or the like. at the time, i dismissed this observation entirely, i simply retorted (in my mind) that, sure, the odds may be astronomical, but we’re not talking a single opportunity… but potentially billions and billions of attempts over billions of years…
it wasn’t until i actually did the math, and understood exactly what ~10^130 possible combinations actually meant that i began to understand how irrelevant billions and billions of opportunities over billions of years were when were talking that level of magnitude…and how prohibitive the numbers are we were talking.
On a completely different topic, you may have the background to help discuss something particularly interesting to me regarding the design behind the tRNA molecules in the protein synthesis process… would you have the time/inclination/expertise to discuss further? if so i can start a new thread and/or private discussion, so as not to derail this present thread.
There has been some discussion of mutations that lead to changes in gene expression. I decided to quickly look at what the literature is saying about lactase persistence in humans. This is the condition where humans continue to produce the lactase enzyme into adulthood instead of stopping production during childhood.
It turns out that there are a lot of different mutations responsible for this phenotype. It’s not a case of one lucky mutation and only one mutation that can produce this phenotype. Also, these mutations cluster to a region well upstream of the gene for lactase, about 13-14,000 base pairs upstream. At least 6 mutations have been thoroughly studied and are verified to functionally change lactase expression, and their geographic distribution is pretty interesting.
This is why I am very skeptical of claims that these types of mutations are extremely rare and almost impossible for evolution to produce.
Also in the paper:
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You’re still trapped by meaningless numbers which have absolutely nothing to do with nature whatsoever. No matter how good the science is, you utterly ignore it for the sharpshooter fallacy, after following every rational step. Ah well, that’s evolution for you. There was obviously survival value in that kind of flawed, superstitious reasoning, or the larger cognitive mechanisms that have that as a by product.
can you explain why you refer to evolution as an unguided process?
@T_aquaticus
That is an extremely unlikely outcome, and yet I got it on the very first try.
Come on, you must know that’s not a relevant analogy. Surely you don’t need me to have to point out that it’s a question of what works. Playing cards, any order will work; but for biological systems, only specific orders work – you must have come across ‘specified complexity’ many times before.
@Leyton
But this extrapolation is based on assuming that eg humans and mice have diverged from a common ancestor.It’s not an assumption. It’s a conclusion based on mountains of evidence.
The presumed evolution of mice and men from a common ancestor is based on some evidence. But there is also clear contrary evidence, notably substantial differences in embryonic development, including the formation of extraembryonic membranes which I’ve already mentioned.
This seems to be a common misperception by some participants on this forum: you/they are so convinced by the evidence consistent with evolution (though I suspect that for some/many, one of these would have been the similarities of the phylotypic stage, before I mentioned the different ways these form) that you refuse to take seriously any contrary evidence. I suspect that one of your criticisms of ID is that it isn’t susceptible to falsification, yet when it comes to evolution you won’t take seriously the possibility of falsification.
@Leyton
But even taking this into account (and the paper discusses various examples) she still concludes that only about 5% of the human genome is susceptible to neutral evolution,That’s not what I understood. You seemed to be saying that neutral mutations could only occur in 5% of the genome which is not what the paper said.
Please explain what you see is the difference between these.
@T_aquaticus
I have no clue of how that could even be calculated which is why I am extremely skeptical of those who claim they can, which is most of the ID/creationist crowd.
how many two-specific bases do you think will lead to a beneficial phenotype, and why?
It’s you who’s suggesting that constructive changes in development might been achieved through two specific mutations. I’m suggesting that, based on what we know about the length of control sequences and of transcription factors that interact with them, a significantly higher number of coordinated mutations would be required. Constructive changes could be achieved by only a couple of mutations only if, by good luck, the rest of the changes were already in place.
@T_aquaticus
If they are all beneficial, it’s extremely likely.
But that’s the point! It is very unlikely that single mutations will effect a constructive change in development. The point is that several specific mutations would be required to do this; you want them to arise independently but then bring them together by good luck.
@Leyton
Taking account of what we do know, rather than relying on what we don’t (evolution of the gaps).What coordinated mutations for development do we know of?
As above, what we are learning about is how development proceeds at the genetic level; and it’s this knowledge that’s showing how unlikely it is that constructive changes could be achieved opportunistically.
@T_aquaticus
You seem to think that only the first situation happens.
When I first mentioned neutral mutations (Dec 22) it was to point out that the probability of their fixation is only 1/2N and that fixation would take much longer than a mutation with a selective advantage. So from the start I have clearly indicated that I know fixation of neutral mutations occurs.
But why do you pin so much hope on them? As I’ve already mentioned, apart from eg synonymous mutations in protein-coding sequences, neutral mutations are likely to be as random as any sequence – almost by definition. As indicated above, I think your hope is that via neutral mutations much of a beneficial change can be put in place cryptically, so that only one or two mutations would then be required to have a beneficial effect such as a constructive change in development. But your premiss is pie in the sky (or fairies in the garden).
How many specific orders, and how did you calculate this number?
Also, specified complexity doesn’t mean anything. It’s just a term that’s thrown out there. It isn’t a measure of anything.
You have never demonstrated that this is evidence against common ancestry.
Here are 29 potential falsifications of the theory of evolution:
It’s explained pretty well in the paper:
And:
The author is clearly saying that neutral mutations do occur in the 95% of the genome that does not evolve neutrally. What is being described is neutral mutations hitchhiking with beneficial mutations because they are close to one another in the physical genome. Neutral mutations and neutral evolution are two different things, sometimes related but not necessarily synonymous.
No, it isn’t. It can happen, but I don’t see how it is necessary for every case.
What makes mutations coordinated? How many are you suggesting? Where is the evidence?
Evidence?
Evidence?
If 5 neutral mutations occurred in a 1,000 base pair promoter sequence, why would that promoter sequence suddenly become random?
We also see single mutations upstream of the human lactose gene that confer an advantage.
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@T_aquaticus
How many specific orders, and how did you calculate this number?
The point is that specific orders (even if some variation is possible) are required, so your card shuffling is not a valid analogy.
@T_aquaticus
Also, specified complexity doesn’t mean anything. It’s just a term that’s thrown out there. It isn’t a measure of anything.
Rubbish! What specified complexity means is that any order won’t do, it has to be specific (even if not 100% specific). Every gene is an example of specified complexity, and it won’t go away just because you don’t recognise it.
@T_aquaticus
You have never demonstrated that this is evidence against common ancestry.
Different embryonic development in supposedly related groups, such as different vertebrate classes, is a clear example. It is certainly against evolutionary expectation, and is prima facie evidence against common ancestry, which can be avoided only if realistic scenarios / mechanisms (not relying on good luck) can be proposed to explain how the development of a common ancestor could have diversified, and the complexity of embryonic development is prima facie evidence against that.
@T_aquaticus
Here are 29 potential falsifications of the theory of evolution:
And, of course, they only mention possible falsifications that they believe have not been demonstrated!
But let’s look at some of the things they say:
This article is specifically intended for those who are scientifically minded but, for one reason or another, have come to believe that macroevolutionary theory explains little, makes few or no testable predictions, is unfalsifiable, or has not been scientifically demonstrated.
So perhaps it’s worth my saying that I think macroevolution sets out to explain much (I’m not belittling it), it does make testable predictions, and it is falsifiable. And, whilst some evidence supports macroevolution, this does not prove it, and it is susceptible to falsification.
Though gradualness is not a mechanism of evolutionary change, it imposes severe constraints on possible macroevolutionary events. Likewise, the requirement of gradualness necessarily restricts the possible mechanisms of common descent and adaptation, briefly discussed below.
I agree with that.
However, whether microevolutionary theories are sufficient to account for macroevolutionary adaptations is a question that is left open.
Sounds reasonable.
[this follows immediately] Therefore, the evidence for common descent discussed here is independent of specific gradualistic explanatory mechanisms. None of the dozens of predictions directly address how macroevolution has occurred, how fins were able to develop into limbs, how the leopard got its spots, or how the vertebrate eye evolved.
But then this ‘question that is left open’ is used as cop-out to ignore any macroevolutionary changes that microevolutionary processes can’t explain! So any potential falsification of evolution due to its lack of explanation for macroevolution is ruled inadmissible. Any difficulties are swept under the rug of ‘we know evolution is true because we can demonstrate microevolution’.
So what about their ‘Prediction 2.4: Ontogeny and development of organisms’ ?
Because morphological cladistic classifications of species are generally based on derived characters of adult organisms, embryology and developmental studies provide a nearly independent body of evolutionary evidence.
The macroevolutionary conclusion is that the development of an organism is a modification of its ancestors’ ontogenies (Futuyma 1998, pp. 652-653). Early in the 20th century, developmental biologist Walter Garstang first stated correctly that ontogeny creates phylogeny. What this means is that once given knowledge about an organism’s ontogeny, we can confidently predict certain aspects of the historical pathway that was involved in this organism’s evolution (Gilbert 1997, pp. 912-914). Thus, embryology provides testable confirmations and predictions about macroevolution.
All of their ‘Confirmations’ and ‘Potential Falsifications’ relate to similarities of later embryonic development of vertebrates, notably after the phylotypic stage. Whereas the earlier the development, the more likely we would expect it to be similar for groups derived from a common ancestor. So a clear potential falsification of common ancestry is that the earliest stages of development might be found to be different. Which they are!
Indeed, it is clearly illogical (even disingenuous) to cite similarities of later development as evidence of common descent, but not recognise that differences of early development are evidence against common descent.
Further, as I’ve pointed out here previously, the fact that the actual embryos (rather than extraembryonic tissues) are derived from different parts of the blastula, means that the embryos are not homologous (at least not in an evolutionary sense). So their examples of: mammalian ear bones and reptilian jaw; mammalian pharyngeal pouches and fish branchial arches; snake and whale hindlimbs; are not even comparing homologous tissues.
@Leyton
It’s you who’s suggesting that constructive changes in development might been achieved through two specific mutations.No, it isn’t. It can happen, but I don’t see how it is necessary for every case.
Example??
@T_aquaticus
What makes mutations coordinated?
When several are required for a beneficial effect.
@T_aquaticus
If 5 neutral mutations occurred in a 1,000 base pair promoter sequence, why would that promoter sequence suddenly become random?
What you’re hoping for is that a gradual accumulation of neutral mutations will suddenly cause a beneficial effect.
The point is that you have to know how many specific orders will work before you can claim how probable it is for those specific orders to be found.
All you have done is replace specified complexity with specific order while not giving any way to measure either.
The theory of evolution states that lineages change over time. Why do you finding those changes is somehow evidence against the theory?
The how is mutations and selection.
The difference between micro and macroevolution is analogous to the difference between micro and macroeconomics. Microeconomics describes how an individual interacts with the economy. Macroeconomics are the larger trends that emerge from the sum of individual interactions. Microevolution is what happens in populations with mutations, selection, and other mechanisms. Macroevolution is the result of those populations interacting with each other and the environment.
It’s the pattern of both the similarities and differences that matter. That’s what you continue to miss. If there was a species that shared derived features with birds and mammals this would actually falsify the theory. For example, a species that had feathers, three middle ear bones, cusped teeth, teats, and flow through lungs would be a serious problem for evolution.
The overarching piece of evidence is the nested hierarchy. The fact that both similarities AND differences fall into this pattern is evidence for the theory.
And I will say this again. It’s a bit silly to point at how life changes over time and use this as evidence against a theory that describes how life changes over time.
If the earlier stages of development change that doesn’t mean the end product is no longer homologous.
The mutations that confer lactase persistence is a great example, and I discuss it in a previous post.
And we see evolution producing those mutations, so what is the problem?
Why can’t it?
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What is wrong with simply adaptation?
“Specified complexity” strikes me as a discreet and intentional ID begging of the question, subtly inferring specification, therefore stamped engineering blueprint, therefore designer.
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Incorrect. The only specific orders required are the ones on how to make the different cards. 350,000 different species of beetles demonstrates that the number of allowed variations are enormous – like the number of different games which can be played with the cards, all following the rules which make the game work.
Can you explain to me why you ask? Not that it needs to be said of course. That it is unguided. As that is completely implicit and never needs to be said.
happy new year !
how do you guide / control a process?