Why are We Disagreeing with ID?

[Faizal_Ali]

@colewd

Its not perfectly nested. @John_Harshman had to mark up the diagram with gene loss and gene gain to make it fit a tree.

Unbelievable.

@Rumraket

Think Bill. Think.

And while you’re at it, maybe tell my cat to do my income tax return for me.

[Faizal_Ali]

@colewd

Gene gain and gene loss is almost certainly the wrong hypothesis as it seems exceeding unlikely that these animals could survive this magnitude of random genetic change and not go extinct.

And yet, amazingly, these very animals live and thrive amongst us, with the very genes they would have gained, and without those they would have lost.

Can’t explain that, nope.

[John_Harshman]

The juxtaposition is interesting:

@colewd

I think it is simply hand waving which you accept based on being a true believer.

@colewd

it seems exceeding unlikely that these animals could survive this magnitude of random genetic change and not go extinct.

[colewd (Bill Cole)]

@Faizal_Ali

Can’t explain that, nope.

God is too big a concept…Richard Dawkins.

This is explained by circular reasoning by those who filter data based on Richard’s philosophy.

[lee_merrill]

@Faizal_Ali

How did Behe manage to determine every single protein-protein interaction in every single one of those species and when they arose?

These are the known protein-protein interactions.

@CrisprCAS9

@lee_merrill

So there should be more than one!

How many? If there ‘should’ be three, and we’ve found two, I’d say we’re in a good place. If there ‘should’ be 10^12, and we’ve found two, not so much. And again, we’ve found more than two.

There are about 10,000 protein-protein sites in a cell, writes Behe, and the first cell appeared just about when (geologically speaking) it first could, in about a hundred million years. So one new protein-protein interaction every 10,000 years? But then we read:

“Despite ten million years of evolution with quadrillions of fish under relentless, life-and-death selective pressure, the Antarctic antifreeze protein does not have anything like the sophistication and complexity even of such a simple protein as hemoglobin, let alone that of the stupendous, multiprotein systems that are plentiful in nature. Instead of pointing to greater things, as Darwinists hoped, the antifreeze protein likely marks the far border of what we can expect of random mutation in vertebrates.” (The Edge of Evolution, p. 82)

So one new protein (not a protein-protein interaction) in 10 million years, not a promising rate.

[lee_merrill]

@Faizal_Ali

@CrisprCAS9

How many? If there ‘should’ be three, and we’ve found two, I’d say we’re in a good place. If there ‘should’ be 10^12, and we’ve found two, not so much. And again, we’ve found more than two.

Behe says there should be zero. Any at all are “beyond the edge of evolution.” So that he found even one already sinks his argument.

No, the edge is at a complex of two new protein-protein interactions.

@Rumraket

That still assumes protein-protein binding sites are like the universal solution to all survival challenges or forms of adversity faced by life. That thing over there wants to eat me, what do? Quick, make two arbitrary proteins stick together! That’s stupid.

But protein-protein interactions are elementary to biology. “The cell’s macromolecular machines contain dozens or even hundreds of components.” (Woodson, S. A. 2005. Biophysics: assembly line inspection. Nature 438:566–67)

@Rumraket

Having two proteins stick together isn’t necessarily adaptive. All I’m saying is should that be adaptive then there is almost always a selectable path from no binding to efficient binding, and that in many cases it takes as little as a single mutation to turn some part of a protein’s surface into a binding site.

But to advance, probably new protein-protein interactions will be involved. New structures such as the flagellum, with dozens of parts. But assume you are right! Then a new structure, with say, half a dozen parts, would require the arrival together of 5 new interactions, before selection can select for it. Not a good prospect, for evolution.

[lee_merrill]

@Mercer

The sickle-cell allele doesn’t create a new protein-protein interaction.

It causes hemoglobin to stick to itself, which is a new interaction?

@Mercer

@lee_merrill

and none for p. falciparum

Chloroquine resistance doesn’t involve creating a new protein-protein interaction.

Yes, so no new interactions for p. falciparum.

@Mercer

@lee_merrill

and none (should be one) for HIV.

No, should be five.

References, please?

@Mercer

@lee_merrill

If it’s all that easy to generate new protein-protein interactions.

It is, as the immune system does by random variation (both recombination and mutation) and selection. In just two weeks.

But again, I mean inside a cell, new protein-protein interactions.

[Faizal_Ali]

@colewd

@Faizal_Ali

Can’t explain that, nope.

God is too big a concept…Richard Dawkins.

This is explained by circular reasoning by those who filter data based on Richard’s philosophy

https://examples.yourdictionary.com/examples-of-sarcasm.html

[CrisprCAS9]

Why is that you respond to every request for evidence with an unsupported and inevitably false claim by Behe? Behe is either so poorly educated on the subject of biochemistry that his musings can be ignored, or he is being deliberately dishonest. Such is further supported in your response here:

The first cell wouldn’t need the interactions of a modern cell, and the rate of new interactions in a primitive cell would not need to be similar to the rate of new interactions now. Further, his point of comparison provides no evidence of ‘new’ protein-protein interactions in need of explanation, merely that proteins do in fact interact. How many of them interacted weakly before selection increased that affinity? Anyone with an understanding of biochemistry would tell you ‘nearly all’. And if they aren’t ‘new’, then Behe’s thesis doesn’t apply. So nearly as I can tell, it doesn’t apply to any actual system in biology.

So try again: How many ‘new’ interactions should there be? And support your number with an actual, reputable source.

[scd]

@Rumraket

And independent origin of a similar function is vastly different from independent origin of a similar sequence

so how you explain convergent evolution? if we know that function X is rare as one in 10^30 sequences then what is the chance to get that function twice?

@colewd

As I said above the pattern does fit Behe’s method of design detection.

@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?

[Dan_Eastwood]

@scd

so how you explain convergent evolution? if we know that function X is rare as one in 10^30 sequences then what is the chance to get that function twice?

I find this statement very curious. Normally when we see an event that occurs more often, we think it has a higher baseline probability of occurring. Only in ID (and related) claims is an event thought to be less likely the more often it occurs.

@scd

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

In this case we recognize the objects as watches, we know that humans make watches, and that humans exist. We inter design by humans, but we do not infer that humans exist - we already know that humans exist.

@scd

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

Yes. For reasons stated just above.

It also raises the question of why this alleged Designer doesn’t make watches.

[Dan_Eastwood]

@scd

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

More, what you see in biology reflects your own suppositions. I do not object to your beliefs. I only assert this does not amounts to a scientific claim.

[RonSewell (RonS)]

@scd

assume that this object can reproduce like a living thing.

It might be a good idea to stick a little closer to reality, as that seems to be enough of a challenge.

[Mercer (John Mercer)]

@lee_merrill

@Mercer

The sickle-cell allele doesn’t create a new protein-protein interaction.

It causes hemoglobin to stick to itself, which is a new interaction?

Objectively false. It merely changes the affinity:

https://www.cell.com/biophysj/fulltext/S0006-3495(04)73875-8

Lee, protein binding is not a digital, binary phenomenon, no matter what Behe says.

@lee_merrill

@Mercer

Chloroquine resistance doesn’t involve creating a new protein-protein interaction.

Yes, so no new interactions for p. falciparum.

How would you possibly know without looking? Isn’t that a textbook case of bearing false witness?

@lee_merrill

@Mercer

@lee_merrill

and none (should be one) for HIV.

No, should be five.

References, please?

Let’s see how you do with the one above. The evidence, not words. Do you understand the difference?

@lee_merrill

@Mercer

@lee_merrill

If it’s all that easy to generate new protein-protein interactions.

It is, as the immune system does by random variation (both recombination and mutation) and selection. In just two weeks.

But again, I mean inside a cell, new protein-protein interactions.

What, precisely, would be your justification for limiting consideration to intracellular interactions? Aren’t extracellular ones just as important?

[Rumraket (Mikkel R.)]

@scd

@Rumraket

And independent origin of a similar function is vastly different from independent origin of a similar sequence

so how you explain convergent evolution?

Natural Selection.

Despite an almost infinite number of different possible cars in the space of all possible cars, given the same landscape the BoxCar2D simulation will converge on extremely similar cars as the best one for that landscape every time:

https://rednuht.org/genetic_cars_2/

Just let it run with the same parameters and with enough generations you’ll see convergence towards the same car setup every time you run the simulation anew.

[nwrickert (Neil Rickert)]

@scd

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

They look designed to me. And, yes, that’s a subjective judgement, because I did not base that conclusion on clear objective criteria.

[scd]

@Dan_Eastwood

In this case we recognize the objects as watches, we know that humans make watches

humans also make gears and motors. and yet we find gears and motors in nature. so by using that criteria we should conclude design in nature.

@Dan_Eastwood

Only in ID (and related) claims is an event thought to be less likely the more often it occurs.

@Rumraket

Despite an almost infinite number of different possible cars in the space of all possible cars, given the same landscape the BoxCar2D simulation will converge on extremely similar cars as the best one for that landscape every time

natural selection cant help here if that specific function occurs once in about 10^30 mutations. so its actually meaningless in that case.

@nwrickert

They look designed to me.

great. so we can detect design.

@nwrickert

And, yes, that’s a subjective judgement

i dont think so. im sure that anyone who will see that image will conclude the same.

[Rumraket (Mikkel R.)]

@lee_merrill

@Rumraket

That still assumes protein-protein binding sites are like the universal solution to all survival challenges or forms of adversity faced by life. That thing over there wants to eat me, what do? Quick, make two arbitrary proteins stick together! That’s stupid.

But protein-protein interactions are elementary to biology.

So, again, that still assumes protein-protein binding sites are like the universal solution to all survival challenges or forms of adversity faced by life.

That thing over there wants to eat me, what do? Quick, make two arbitrary proteins stick together! That’s still stupid.

@lee_merrill

@Rumraket

Having two proteins stick together isn’t necessarily adaptive. All I’m saying is should that be adaptive then there is almost always a selectable path from no binding to efficient binding, and that in many cases it takes as little as a single mutation to turn some part of a protein’s surface into a binding site.

But to advance, probably new protein-protein interactions will be involved.

But to advance to what? Effective resistance? Sand colored mice? Peppered moths? There are countless adaptations that do not require protein-protein interactions so it is obviously stupid to argue that the fact one did not evolve in response to some arbitrarily picked selection pressure means they can’t evolve in general. That just obviously doesn’t follow.

@lee_merrill

New structures such as the flagellum, with dozens of parts.

T-URF13 too! VPU1! Which we know evolved.

@lee_merrill

But assume you are right! Then a new structure, with say, half a dozen parts, would require the arrival together of 5 new interactions, before selection can select for it.

That’s another assumption that there’s some structure that has no functional intermediates. You just can’t help yourself by making assumptions about imaginary hurdles evolution has to pass through.

@lee_merrill

Not a good prospect, for evolution.

I agree that your entirely hypothetical and imaginary piece of complete fiction would be a big problem for evolution to overcome. It would also be a problem to travel across the ocean if boats and planes were impossible. It’s just boats and planes aren’t impossible.

[lee_merrill]

@CrisprCAS9

So try again: How many ‘new’ interactions should there be? And support your number with an actual, reputable source.

I think Behe is a reliable source, though admittedly my number was very back-of-the-envelope. But there being only a few known new interactions implies that placing the edge of evolution at a complex involving two new protein-protein interactions is reasonable.

[lee_merrill]

@Mercer

@lee_merrill

It causes hemoglobin to stick to itself, which is a new interaction?

Objectively false. It merely changes the affinity:

https://www.cell.com/biophysj/fulltext/S0006-3495(04)73875-8

Lee, protein binding is not a digital, binary phenomenon, no matter what Behe says.

Well, at your reference I read “Sickle cell disease is caused by a mutant form of hemoglobin, hemoglobin S, that polymerizes under hypoxic conditions. The extent and mechanism of polymerization are thus the subject of many studies of the pathophysiology of the disease and potential treatment strategies.”

And Behe talks about protein binding affinity, he does not treat it as binary.

@Mercer

@lee_merrill

Yes, so no new interactions for p. falciparum.

How would you possibly know without looking?

Well, I trust that Behe knows where to look. And again, if someone has a refutation, I expect we would have heard about it on Panda’s Thumb or somewhere similar.

@Mercer

What, precisely, would be your justification for limiting consideration to intracellular interactions? Aren’t extracellular ones just as important?

Yes, I only chose the cell to make it clear I meant traditional evolutionary processes, not including the immune system…