Why are We Disagreeing with ID?

[Rumraket (Mikkel R.)]

@colewd

There is evidentiary argument that supports his claim.

Mhm, sure. Cool story bro.

[Rumraket (Mikkel R.)]

@scd

@Rumraket

No it isn’t. You have no “scientific data” that indicates a specific function “occurs once in about 10³⁰ mutations”

here is one instance:

“Extrapolating from our data and from modest sequence constraints on interhelical turns (23, 28–30), we can estimate that if every position in the protein had been randomized, a library of ≈10^24 members would have been needed to obtain AroQ mutases.”

https://www.pnas.org/doi/10.1073/pnas.191159298

ROFL. So your number was indeed made up, and you went scrambling for something else.

That’s not mutations, those are protein sequences with a particular enzymatic function, which generally aren’t thought to arise de novo particularly often in evolution, but rather evolve incrementally from related ligand-binding proteins. Which is why they write:

Our estimate of the low frequency of protein catalysts in sequence space indicates that it will not be possible to isolate enzymes from unbiased random libraries in a single step. The required library sizes far exceed what is currently accessible by experiment, even with in vitro methods (31, 35). Instead, as in natural evolution, the design of new enzymes will require incremental strategies in which, for instance, a suitable scaffold is first generated, binding and catalytic groups are subsequently added, and the ensemble is optimized in an iterative fashion.

But hey, that’s a functional enzyme sequence 53 orders of magnitude more frequent that what ID-creationists think Axe’s experiments have shown.

[RonSewell (RonS)]

@scd

since we are talking about convergent evolution. so we only need to know what is the chance to get a specific function, and then we can know what is the chance to get it again.

A shark fin and a whale flipper have essentially the same specific function but very different anatomy’s. They are examples of convergent evolution, but that tells us nothing about any comparative probabilities, which, given the aqueous environment, are virtually certain.

[colewd (Bill Cole)]

@Nesslig20

Even within those so-called “created kinds”, you have gene gains and losses. Although, instances of gene gains within these kinds are often re-interpreted as “that gene was originally there in the created ancestor, and every other member of the kind must have lost that particular gene instead”, which is extremely non-parsimonious and this is merely an ad hoc rationalization as it is only invoked as a means to maintain the “no new information can evolve” narrative.

Hi Ness
I would be grateful for any evidence you have for gene variation within “kinds’ or species”.
Best
Bill

[Nesslig20]

@scd

@Rumraket

No it isn’t. You have no “scientific data” that indicates a specific function “occurs once in about 1030 mutations”

here is one instance:

“Extrapolating from our data and from modest sequence constraints on interhelical turns (23, 28–30), we can estimate that if every position in the protein had been randomized, a library of ≈10^24 members would have been needed to obtain AroQ mutases.”

OMG… this figure is only regarding ONE specific function (AroQ mutases), not ANY specific function.

There is also this bit in the article that you sited:

The size of such a library is many orders of magnitude larger than that needed to identify noncatalytic ATP-binding proteins from random sequences (31).

Quoting the abstract from this reference #31:

Functional primordial proteins presumably originated from random sequences, but it is not known how frequently functional, or even folded, proteins occur in collections of random sequences. Here we have used in vitro selection of messenger RNA displayed proteins, in which each protein is covalently linked through its carboxy terminus to the 3′ end of its encoding mRNA1, to sample a large number of distinct random sequences. Starting from a library of 6 × 10^12 proteins each containing 80 contiguous random amino acids, we selected functional proteins by enriching for those that bind to ATP. This selection yielded four new ATP-binding proteins that appear to be unrelated to each other or to anything found in the current databases of biological proteins. The frequency of occurrence of functional proteins in random-sequence libraries appears to be similar to that observed for equivalent RNA libraries2,3.

[Nesslig20]

@scd

@Rumraket

Behe doesn’t have a method. It’s just subjective “it looks designed to me”.

do you think its subjective to detect design by looking at this object?:

(image from wiki).

now, assume that this object can reproduce like a living thing. do you still think its subjective to detect design?

This argument is flawed.

It is indeed fallacious reasoning to say:
“it looks designed to me, therefore it is designed”
…since it’s appealing to subjective intuition.

Here you come along and say:
“I can look at these watches. They look designed to me. We also know they are designed, so “looks designed to me” is an accurate inference.”

This also is faulty reasoning. Just because fallacious reasoning CAN lead to a correct conclusion, that doesn’t mean it isn’t fallacious reasoning. It’s just that you can come to a correct conclusion IN SPITE of the fact that the reasoning you used was fallacious. This is rather like an “inverse fallacy fallacy”.

The actual reason why we know these watches are designed is not because they “look designed”. Rather, it is because we are already aware of where they come from.

To hammer down the point of why “looks designed to me” is fallacious reasoning; instead of looking at watches, let’s apply it to this example below:

This “looks” designed, doesn’t it? This structure is even called the “Giant’s causeway” since celtic legends say this was build by actual giants. Well, is it designed?

[Tim]

@scd

not in this case, since we are talking about convergent evolution. so we only need to know what is the chance to get a specific function, and then we can know what is the chance to get it again.

You are still committing the Texas Sharpshooter.

You are:

1. assuming that the “specific” pair of converging organisms is the only pair that could have potentially converged. Evolution is contingent, and with a slightly different set of circumstances, we could have had a flying cousin of the Rodents, rather than the bat we know, that is a flying cousin of Carnivores and Ungulates, as the mammalian clade that converged on flight along with birds.

2. assuming that (for example) the “specific” series of mutations that historically caused the ancestors of the bat to gain flight are the only series of mutations that could possibly have done this. Just as there’s ‘more than one way to skin a cat’, it seems reasonable that there’s ‘more than one way to wing a bat’.

[Dan_Eastwood]

@scd

@Dan_Eastwood

By that criteria we would conclude that human’s designed (at least some of) nature, which is absurd.

no. we can conclude design. not a specific designer.

You stated …

@scd

humans also make gears and motors.

This is true. Further, we know of no other source for gears and motors.

Therefore, your argument implies that gears and motors found in nature are made by human.

Observing gears and motors in nature, we might hypothesis that nature can produce gears and motors roo*ie: Nature is the Designer).

[Tim]

Is it me or is 1 in 10³⁰ become the new 42 – the ultimate answer to Life, the Universe and Everything – i.e. the answer to all questions?

As we are talking about specifics, what is 1 in 10³⁰ the specific probability of? What specific evidence is it based on? And what specific argument derives this number from this evidence?

[colewd (Bill Cole)]

@Rumraket

Mhm, sure. Cool story bro.

Here is one that I think you should remember. You should also remember this discussion is about bacteria where this is the most likely possibility of seeing a protein sequence evolve in a population.

Axe (2004) and the evolution of enzyme function

@Rumraket

But hey, that’s a functional enzyme sequence 53 orders of magnitude more frequent that what ID-creationists think Axe’s experiments have shown.

As you know it depends on the protein. Some vertebrate proteins may be orders of magnitude more difficult then what Axe has quoted. Proteins in the WNT beta catenin pathway are likely more challenging then beta lactamase.

Evolution is a limited explanation unless it can account for the worst case.

[RonSewell (RonS)]

@colewd

I would be grateful for any evidence you have for gene variation within “kinds’ or species”.

Brown and blue eyes.

There is existing variation in all populations.

[Rumraket (Mikkel R.)]

@colewd

As you know it depends on the protein. Some vertebrate proteins may be orders of magnitude more difficult then what Axe has quoted. Proteins in the WNT beta catenin pathway are likely more challenging then beta lactamase.

Back to making stuff up again you have no idea whether is true, and in any case evolution doesn’t have to invent a particular function de novo, as they can evolve incrementally by combining parts of other proteins and so on.

[Nesslig20]

@colewd

Hi Ness
I would be grateful for any evidence you have for gene variation within “kinds’ or species”.
Best
Bill

The genus Oryza experienced…

…an average of 51.5 de novo genes per million years

Unless you think that every single species (including the domesticated rice species) within that genus were all uniquely created, then this would suffice.

https://www.nature.com/articles/s41559-019-0822-5

With kind regards,
Ness

[Rumraket (Mikkel R.)]

@Tim

As we are talking about specifics, what is 1 in 1030 the specific probability of? What specific evidence is it based on? And what specific argument derives this number from this evidence?

I really have no idea. It’s difficult to relate the idea of a function to the frequency by which a mutation would result in it. How does that work exactly?

In any case let’s play with that number. It is estimated a cubic meter of sea water contains approximately 10¹² bacteria. The total volume of Earth’s oceans comes out at 1.335x10²¹ liters. Assume the typical bacterium divides once every 4 hours, and have been doing so for 4 billion years, and assume an average rate of mutation of 1 in 1000 cell divisions, I get ~8.76x10⁴² total mutations in the history of life on Earth.

That means that function that only occurs once in every 10³⁰ mutations could have occurred ~8.76x10⁴²/10³⁰ = 8.72 trillion times.

¯_(ツ)_/¯

[scd]

@Rumraket

That’s not mutations, those are protein sequences with a particular enzymatic function, which generally aren’t thought to arise de novo particularly often in evolution, but rather evolve incrementally from related ligand-binding proteins.

true. but i will argue that its not that different. if we know that specific function is so rare in sequence space, then we can conclude that we do need a huge number of mutations in order to get a specific function twice by convergent evolution. now, since many biological systems needs at least few proteins, we can conclude that the chance to get a specific biological system twice (or even the same function with different structure) should be extremely small.

@Tim

You are still committing the Texas Sharpshooter.

see above.

@Nesslig20

There is also this bit in the article that you sited:

this refer to a different protein/function which can bind an ATP. which is very different from AroQ mutases. actually, its not even a functional protein, since there is no protein that only bind ATP. ATP binding by itself do nothing in the cell. so if we are talking about a protein that needs 3 binding sites (such as the aminoacyl-tRNA synthetase) we are talking here about one in 10^36 mutations to get that protein.

@Nesslig20

The actual reason why we know these watches are designed is not because they “look designed”. Rather, it is because we are already aware of where they come from.

which is again also true for gears and motors.

@Nesslig20

This “looks” designed, doesn’t it?

not necessarily. It’s just a simple structure in relation to say a watch.

@Dan_Eastwood

This is true. Further, we know of no other source for gears and motors.

i dont think so. if gears exist in nature, and we know that human didnt made nature- we can conclude that other designer was involve.

[John_Harshman]

@colewd

I would be grateful for any evidence you have for gene variation within “kinds’ or species”.

In order for that to happen, you would first have to identify at least one kind. Would you care to?

[colewd (Bill Cole)]

@Nesslig20

Unless you think that every single species (including the domesticated rice species) within that genus were all uniquely created, then this would suffice

Hi Ness
I do think that plants maybe able to generate some de novo genes through recombination resulting in some exon changes based on Turf study. I have seen this and other examples. I have not seen anything like this for vertebrates. Have you?

Best
Bill

[John_Harshman]

De Novo Genes Arise at a Slow but Steady Rate along the Primate Lineage and...

De Novo Origin of Human Protein-Coding Genes

[John_Harshman]

@colewd

I do think that plants maybe able to generate some de novo genes through recombination resulting in some exon changes based on Turf study. I have seen this and other examples. I have not seen anything like this for vertebrates. Have you?

In other words, any examples you come up with to counter Bill’s claims will be dismissed as irrelevant for some ad hoc reason.

[RonSewell (RonS)]

@colewd

I have not seen anything like this for vertebrates.

Antifreeze genes in codfish…

De Novo Gene Evolution of Antifreeze Glycoproteins in Codfishes Revealed by Whole Genome Sequence Data

Gene gain:

Most likely, codfish afgp s arose from entirely non-coding DNA making them type I de novo genes

and gene loss:

Moreover, afgp has been subsequently lost in one lineage of codfishes, analogous to the loss of afgp in non-Antarctic notothenioids.

See also: Molecular mechanism and history of non-sense to sense evolution of antifreeze glycoprotein gene in northern gadids

Evolution of an antifreeze protein by neofunctionalization under escape from adaptive conflict

The development of blood antifreeze opened a new niche for these fish, and that in turn altered the landscape of selection on other features. Sean Carroll is featured in this YouTube:

The Icefish Has Clear Blood