The problem with Dawkins' Weasel Program

[MrFungus420]

Wan, I don't think this debate can continue to serve a purpose,

Of course not. It never is with a reality denialist like you.

Evolution has been observed. You are arguing against an observed fact.

so this will be my last response. It was a pleasure debating with you and I wish you well.

Essentially all genes have untold countless numbers of different functions,

Many proteins do only one function.

So what? Unless all of them do, your point is not being supported.

Put in the words to Google scholar high specificity of protein and you will get several articles confirming this, here are a few

Hydrogen bonding and biological specificity analysed by protein engineering
[PDF] from unc.eduAR Fersht, JP Shi, J Knill-Jones, DM Lowe… - Nature, 1985 - hekto.med.unc.edu
Tandem SH2 domains confer high specificity in tyrosine kinase signaling
[HTML] from jbc.orgEA Ottinger, MC Botfield… - Journal of Biological Chemistry, 1998 - ASBMB
Human anti-self antibodies with high specificity from phage display libraries.
[HTML] from nih.govAD Griffiths, M Malmqvist, JD Marks, JM Bye… - The EMBO …, 1993 - ncbi.nlm.nih.gov
Cardiac troponin I. A marker with high specificity for cardiac injury
[PDF] from ahajournals.orgJE Adams - Circulation, 1993 - Am Heart Assoc

So, have you actually read any of those, or did you just do a search for "high specificity of protein" and C&P the titles of what popped up?

This is the cooption fallacy

Making up fallacies is not an argument.

What is a fallacy is an argument from ignorance. And that describes your entire argument.

[MrFungus420]

Oh, and my_wan...some very good posts there.

[my_wan]

Wan, I don't think this debate can continue to serve a purpose, so this will be my last response. It was a pleasure debating with you and I wish you well.

That's a pity, but even though I didn't start these threads, I did partake in the debate, and this thread appeared as if tailored from a previous debate of ours that was abandoned. I still feel that the facts needs addressed for a larger audience, and winning a debate or any point of a debate is secondary. I may not a high level of academic For me the truth trumps

Many proteins do only one function. Put in the words to Google scholar high specificity of protein and you will get several articles confirming this, here are a few

Hydrogen bonding and biological specificity analysed by protein engineering
[PDF] from unc.eduAR Fersht, JP Shi, J Knill-Jones, DM Lowe… - Nature, 1985 - hekto.med.unc.edu
Tandem SH2 domains confer high specificity in tyrosine kinase signaling
[HTML] from jbc.orgEA Ottinger, MC Botfield… - Journal of Biological Chemistry, 1998 - ASBMB
Human anti-self antibodies with high specificity from phage display libraries.
[HTML] from nih.govAD Griffiths, M Malmqvist, JD Marks, JM Bye… - The EMBO …, 1993 - ncbi.nlm.nih.gov
Cardiac troponin I. A marker with high specificity for cardiac injury
[PDF] from ahajournals.orgJE Adams - Circulation, 1993 - Am Heart Assoc

"Biological specificity" is not a reference to a singularity of function. "Biological specificity" refers to "complementary molecules", which generally mirror-image shapes that allow them to selectively bind to each other. Yet for any given molecule there are large ranges of other complementary molecules that it can bind to, and any bindable pairing within this large group still involves "biological specificity", because the binding molecules are "complementary".
http://encyclopedia2.thefreedictionary. ... pecificity

I could take each of those references separately and outline the general ranges of bindable molecules being discussed, but the dictionary link I provided should be enough. More general examples include THC (marijuana) which has "biologically specific" neuroreceptors in our brain. That does not mean our brain was "designed" to get high, or that other functional complementary neurotransmitters that these receptors evolved for, with the same "biological specificity", doesn't exist in our body. It merely means we have neuroreceptors that have "biological specificity" (complementary) to THC.

the mistake is in assuming that one particular gene sequence is need for one particular function... just because it has a particular function in a particular instance does not mean an entirely new gene is needed for a new function. ... there an extreme number of different alleles of that given gene which changes the efficiencies of the functions it is capable of.

Even if the above statements are true that does not prove that NS can build an eye of 202 genes. You are basically committing the following non sequitur:

1. Genes have more than one function
2. therefore, NS can build genes

No. We observe, by actually watching stuff evolve in the laboratory, that genes can evolve. We then look at the specific sequence that lead to it, not just the start and end but everything in between to, and see that: Oh, this gene that had this function is now also (without modification) doing this function after this new gene evolved. Just like the nylon bug evolved to eat carbohydrates, but when one gene mutated to metabolize nylon all the other unmodified genes involved in metabolizing carbohydrates are now taking part in a different function, metabolizing nylon byproducts provided by the mutated gene.

So you have the logic backwards, and we can actually observe the mutations that produce new genes step by step, and then notice all the other unmodified genes are now involved in doing a different function, even though they're the 'exact' same gene that did the other function before.

Evolution did NOT have to create 202 brand new proteins just to get an eyespot, because those proteins evolved for other functions besides eyespots.

This is the cooption fallacy, see my response to Genes for life.

To GenesForLife you stated: "Co-option was developed as a Darwinian response to ID." No, Co-option came from what we actually observe, and can demonstrate as many times as you want. When the nylon bug mutated one gene (created a new gene), the byproducts from metabolizing nylon, provided by this new gene, are not the same byproducts that used to come from carbohydrates. Yet the other genes (unmodified proteins) that had the job of organizing and incorporating the carbohydrate byproducts are now take on a different function to deal with the nylon byproducts, even though they are the un-mutated original proteins.

Calling co-option a fallacy is like saying a wooden or concrete floor that can both function to break glass is a fallacy. To then accuse researchers of "inventing" broken glass, when the glass hits the floor and shatters, of inventing it merely to reject ID, is absurd beyond reason. Cooption is NOT an "idea", cooption is something we actually observe.

evolution didn't have to evolve this gene for sight. It merely had to switch the locus of a preexisting gene sequence to get eye function, rather than the function it evolved for.

You need foresight for that, which NS does not have.

No, all you have to do is let the "not as good" random events die on their own, and the "better" random events have the babies to replace the dead bad ones. Thus the mutations don't know which are good and bad. That only comes later when the bad ones fail to make babies of their own, and the good ones have the babies to replace the bad loses.

Ok, NS can not build 202 genes with the knowledge that they would eventually work together. That requires foresight, which is something NS does not have. I'm very skeptical however that you will be able to understand that.

Just like the nylon bug didn't know it was going to need hundreds of genes to work together to process nylon byproducts. But guess what? Hundreds of the exact same unmodified genes that "work together" to process carbohydrate byproducts also "work together" to process entirely different nylon byproducts (co-option), and only needed 'one' of those genes to mutate to break down nylon into the byproducts the other unmodified genes could use, even though they never evolved to use them.

As evolution continues, and better efficiencies are achieved, then fewer combinations are possible to get that same efficiency. So high efficiency organisms will tend to revolve around a fewer high efficiency sequences, but these high efficiency low probability sequences must come from inheritance rather than accidents.

You're just assuming that NS can achieve efficiency

No, we don't need to assume it. Not only can we emulate the process, but we actually watch, and record step by step, the process of evolution of actual living organisms as they "achieve efficiency". It's like dropping glass on the floor, watching it break, then accusing me of only "assuming" the glass broke. It's just flat out wrong.

2. The fallacy: because NS can get rid of bad mutations it can therefore build new genes. What you are doing is looking at NS's ability to junk a poorly functioning car and saying: see, NS can build cars. This is wrong. This is exhibited with your reply to the Sean Carroll quote.

I said: here's proof that NS cannot build genes
you said: NS can discard defective genes

No.
You say: Mutations are bad, so NS cannot build genes.
I say: Mutations many get bad mutations and die off, others get neutral and good mutations and live, while the good mutations build up, even though they are more rare, while the bad ones simply die off leaving the resources for to good ones to continue.

I never said "Mutations are bad, so NS cannot build genes," and you know better than that. I demand you apologize for such a blatantly false statement. I clearly quoted Sean Carroll as saying: "NS cannot repair genes."
You're still saying the same thing: NS can destroy bad genes, therefore it can build genes.

I would apologize, except as I'll explain, what I did was apply your reasoning to your argument the way you applied it to mine to see how you would respond. Because, due to your responses to my previous attempts, I wanted to see what you would consider a reasonable response. So if I owe you an apology, you owe me one.

Here's why: I inform you about specific examples where a new gene results from NS, the nylon bug. You accuse me of claiming that, because NS can get rid of defective genes, it must be able to create new genes. If I owe you an apology, why do you not owe me an apology for claiming new genes are possible "because" NS can destroy genes, rather than what I actually said that we actually know the exact mutations that have created new genes, like the nylon bug mutation?

Getting rid of the bad mutations in a population, not individuals as they just die off, is merely one of the many functions NS is capable of. A "complementary" function is to replace those that die with mutations that do survive. Just like proteins, NS is capable of more than one sub-function. NS is merely the superset of all those sub-functions.

You essentially said that with: "NS repaired that mutation by killing that organism." Discarding bad genes is not building genes.

It didn't "repair" it, it removed it from the population of self replicators, so these bad mutations do not continue to self replicate. But the neutral good mutations do continue replicate,

You've provided no evidence that good mutations occur other than mere point mutations. Sequencing 150 amino acids is a lot different than a mere point mutation. I'm still waiting for NS explanation of Titin, a protein with 27,000 amino acids.

I intentionally stuck primarily with point mutations to make the workings of genetic algorithms as intuitive as possible, as the OP was about Weasel. Yet I have also demonstrated that countless different gene sequences can do the same function, and that the same gene sequence can do countless different functions. Just like all the unmodified proteins in the nylon bug switched from carbohydrate byproduct processing to nylon byproduct processing, without mutating. While the nylon mutation created an entirely "new" gene consisting of ~400 amino acids. Yet hundreds of other unmodified proteins in the nylon bug still work together with that one "new" gene to do things they never did before that new gene mutated. They work together because each one (without mutation) is capable of countless different functions, and get forced into these new functions when a "new" gene is added to the mix, even when they are not very good at that function. Like the nylon bug only being 2% efficient a metabolizing nylon.

I could add examples, such as the chromosome fusion that separates our genetic makeup from most other primates, but you asking how NS got so many functions to work together, as if that one sequence, or one group of proteins, was the only way to get them to work together. The fact that the nylon bug proteins still work together, when the very thing they worked together to do drastically changed, proves that function cooption (which you called a fallacy) is how it's works. It also proves that untold trillions of different combinations would also work. So the random accident didn't just have to pick just 1 good accident out of 10^40,000, but some percentage of 10^40,000 would also work.

population A may have 25% die before replicating, while population B will may have 35% die before replicating ... Hence the whole population is NOT binary, even though the individuals are.

The fallacy you're making here is: 1. Population A is not binary 2. therefore, all populations are not binary. There are many mutations which result in 100% death, especially those which concern the translation of DNA. If you can't translate DNA, you can't exist.

There is no such thing as a natural binary population. We create them in the laboratory sometimes, by making a population, or different populations, all clones of each other, to observe how mutations (evolution) act in the colony to erase the binary functions.

It is *impossible* for a mutation that kills the organism to spread to the entire population in a constant environment. Why? Because, in order for it to spread to the entire population, it must allow the organism to live and reproduce enough to overtake future generations with that mutation. That can't happen if the mutation killed them. NS does not allow *any* I may have to ever spread to you. If I die without kids, then no mutation I have will ever have any bearing on your kids, your kids kids, and so on. Mutations that kill do not spread in the population, period.

There is only one way to get a bad mutation spread to every person, which depends on the fact that good and bad are not binary. That is to change to environment to one people can't live in, and needs mutations that would have killed people in the old environment to survive in the new environment. Now what was good is bad, and what was bad is good. Good and bad mutations are not binary.

Many spiders depend on this mechanism, where the more food they catch the more young they create, but catching the food reduces the food available for others to catch. So even one extra bug, due to a protein allele involving a single DNA letter making the add an extra web rung,

What you're assuming is: 1. a point mutation can confer advantage to a species 2. therefore, only point mutations are needed to create new genes.

It's much more complicated than that.

Yes, it's much more complicated than that, which is why I mostly stuck with point mutation to make it more intuitive.

There are many other types of mutations, other than point mutations, that can create new genes. Yet point mutations can and demonstrably do create new gene. It was a single letter mutation (insertion of "T") in the nylon bug that re-wrote the entire gene sequence, frame shifted to an entirely new gene. Thus, proof that a point mutation can create a new gene.

If your accusing me of saying point mutations are the only way new genes are created it would at least as bad as what you wanted me to apologize for. I would say that point mutations are generally more involved in optimizations of gene sequences than creation, but once enough point mutations occur it still eventually becomes a different gene. Even changing only one letter at a time can eventually rewrite the entire sequence.

On the contrary an immense amount of parts have to be in place in order for an organism to begin to survive. You seem to think that a chain of 10 amino acids can evolve into an organism with 200 genes. There is no evidence to support this. I have already stated this fact several times, so this will be the last time that I attempt to force you to understand that.

The problem with this claim is that an equally immense number of ways the parts can be arranged to still get the same function, with varying efficiencies.

This runs in pure contradiction to the Albert quote which I will quote for you again because apparently you chose to ignore it the first time: the amino acid sequence
of histone H4 from a
pea and from a cow differ at only 2 of the 102
positions. This strong evolutionary
conservation suggests
that the functions of histones involve nearly all of their
amino acids, so that a change in any position is deleterious to the cell. This sug-
gestion has been tested directly in yeast cells, in which it is possible to mutate a
given histone gene in utero and introduce it into the yeast genome in place of the
normal gene. As might be expected, most changes in histone sequences are
lethal; the few that are not lethal cause changes in the normal pattern of gene
expression,
as well as other abnormalities.

I didn't ignore it. My response is here, and several responses here, and GenesForLife added to my response here. Perhaps I didn't respond in a way that suited you, but simply accusing me of not responding gives me no clue how to correct that. I'm not sure how to improve on that previous response, except to go into the detailed role of histone in enzyme activity accomplished through covalence modification and circle back around to the same response.

Early life forms didn't have the enzyme complexity to regulate of todays species. But once a regulatory mechanism evolved and dominated, then later complexity built on top of that, optimized, then built on top of again, places increasing constraints on the specific underlying mechanism to remain the same. So the earliest (surviving) sequences will be the most similar, but does not mean that was the only form before that histone sequence evolved. If you look at the other forms of histone, besides histone H4, you will see lesser and lesser constraints on the efficiency of the sequence, because there is less complexity evolved on top of it since it evolved. Just look at all the variants in the whole range of histone proteins.

In fact, it appears to me, you are trying to use the fact that NS shows that all life on Earth had a common ancestor as a way of trying to demand something besides a common ancestor must exist or NS must be wrong. Any early optimizations that initially do not require very detailed constraints on the sequence, will acquire detailed constraints on that sequence as more and more complex biological systems evolves to use this preexisting function.

Moreover, the so called 60 immortal genes are roughly 60% identical in all species. So if there are so much tolerance in their protein folds then why don't those other protein folds exist?

You mis-applied the 60%. It's not that 60% of these genes are identical, it's these genes sequences are 60% identical, i.e., that is "AAAAA" is 60% identical to "BBAAA", which does not mean they are the same. Thus they are not identical in different species, and vary by 40% between species.

4. The RNA world. Actually I do have the knowledge to critique your understanding of Joyce's experiment. The big problem with these experiment is the right-handed amino acids. Life only uses left-handed amino-acids.

So, I continuously referred to them as "non-life", and it's perfectly possible for people and all life to exist with right-handed amino acids. We only use left-handed amino-acids because that's what our surviving ancestors used, and we inherited.

False, people cannot exist with right-handed amino acids.

If people can't exist with right-handed amino acids, why would you suppose then that any mystery exist as to why the life that succeeded is only left-handed? Couldn't the same reason people can't be made from right-handed amino acids be the same reason life evolved left-handed? I'm open to being wrong about chemical chirality, but if so isn't that reason enough that life has right-handed amino acids?

Given that we all had a common ancestor, even us and trees, wouldn't that mean that if we consisted of right-handed amino acids that you would be making the same argument against left-handed amino acids? You can't demand we be both and still have common descent.

Second, the odds of getting all left-handed amino acids 100 times in a row is 1 in 10^30. There is not enough time to go through all those failed sequences.

This can be demonstrated to be wrong, shown here:
http://www.newscientist.com/article/mg1 ... ehind.html
What this shows is that when you dilute amino acids, then whether you start a left to right mixture of 100:1 or a 100:99 mixture, you end up with almost entirely with the left handed mixture. In essence, even a tiny difference in proportions gets amplified when diluted. Hence even if the number of left-handed amino acids outnumbered the right handed amino acids by 1 part in a billion, you still end up with a near certainty, upon dilution, of left handed reactions.

Besides, you don't need to left-handed amino acids 100 times in a row, you just need to get 1, which reacts to make a single molecule with 2 left-handed amino acids, which later reacts with another left handed pair to make a molecule of 4, which can later react with another singles molecule of 4 left handed versions making 8. After only 7 of these interactions you can have an amino acid molecule containing 128. The dilution effect merely makes nearly all such interaction the same handedness.

We do not say NS builds "bridges" because it can destroy bridges, we say NS builds "bridges" because we watch it build "bridges" in exquisite detail, the same way we watch in exquisite detail as the more numerous bad mutations dissolve from the populations with each generation of living organisms in the lab.

This is just a Darwin of the gaps argument. 1. I see a beautifully constructed bridge. 2. I don't know how it was built 3. Therefore, NS built it.

"Darwin of the gaps argument"!!! So I watch ants build an ant bed, and you say: (para-quote) "This is just a Ants of the gaps argument." to explain the ant bed!!! We watch and see it happening step by step, count the mutations and see that they are random, without a pattern or intelligence, then watch as the bad stuff from these random mutations die off, and watch as the good stuff from these random mutations has babies and dominates the population. We watch it, like watching a glass break on the floor, and we do not call the floor the "floor of the gaps" to explain the broken glass!!!

I on the other say 1. I see a beautifully constructed bridge 2. It required foresight 3. Intelligence is the only thing that has foresight 4. Therefore, intelligence did it.

Yes I know, and you are welcome to try and support that. But if we watch Johnny clean his supper plate, and you have another explanation of why the plate has no food left on it, claiming what we actually observed Johnny do is just a "Johnny of the gaps" makes your so called evidence worthlessly WRONG, and exceedingly silly.

No the odds are not 1 in 4. Here's what you're doing wrong. Let's take the sentence: "We hold these troths to be self-evident." What are the odds of repairing the misspelling of "troths" by chance? You seem to think they are 1 in 26. They are not. Chance does not know which letter is misspelled. Therefore, the odds are 26 raised to the 39th power, since there are 39 characters. What you have to do is take how many mutations occur in the genome, let's say 20 in a genome 2 billion letters long, those 20 mutations can occur in any of the 2 billion letters.

Yes, and I showed above how for a given codon, it still come to a 25% chance of the best codon for a random whole codon string. Since codons are the informations carriers the sentence "We hold these troths to be self-evident.", needs to be broken up like "We ,hol,d t,hes,e t,rot,hs t,o b,e s,elf,-ev,ide,nt."where "rot" it the only one that contains a possible advantageous mutation. However, because all the other triplets have other letter that result in the same code (like DNA), even if the mutation occurs somewhere beside "rot" doesn't mean it's going to be a bad mutation, as it can also be neutral. The effect per codon triplet is what matters.

I said: the odds of spelling sentence X is 1 in 10^39 whereas you think they are 1in 26
you said: the odds of a sentence Y are Z
In other words, you didn't defend yourself but made an irrelevant assertion.

Her's what you don't seem to get. If the first letter "W" mutates to "g", then it's sisters will eat the food and it'll starve to death. Same for the other bad mutations. Only when that one good mutation finally does come along it gets to eat the food and have the babies. Now those babies start having babies and eating all the food that the sentence with 1 wrong letter would have eat. So there baby rate will fall behind, for lack of food, and the complete sentence becomes dominate.

The 1 in a billion odds is the result of 30 a bit information channel. .. why? Because the bit sequence that Joyce's spontaneously produced replicators had is not the only random sequence of those bits that would produce a working self replicator

Did it form a cell that self-replicated and passed on its genes? no.

[/quote][/quote]
Are you trying to imply that I called Joyce's self replicators life? I included "non-life" in essentially every reference to it for a purpose. Yet it did self-replicate, and a gene is "a unit of heredity of life", and Joyce's self-replicators have units of heredity, without life. So:
Did it form a cell that self-replicated and passed on its units of heredity? Yes!!!!
And went on the optimize, via random mutations, these units of heredity on their own, just like NS predicts.

To suggest that I made the claim it was life would be a lie, or to suggest that because is is not life means it's not subject to NS is a lie. But why else would you choose the term "gene", except to imply one or the other of these lies? Is this OP not about the algorithmic legitimacy of Weasel?

[my_wan]

This may be leading off topic, but given the the OP originator disavowed continuing I'll say it.

Is spinoza (channeling) Behe? http://rationalia.com/forum/viewtopic.p ... 74#p697017

This apparent "channeling" is something of an interest of mine, and in part what I get out of debating with spinoza. I even construct responses that may help illicit rebuttals that helps me articulate these ideological constructs. The similarities you see here I used to study in terms of "Modern Mythology", but recently it has began to fit better in the psychological construct of teleological reasoning. Even the study of "Modern Mythology" can be subsumed into a set of teleological predicates. This is my explanation of the apparent "channeling" effect, even when not intentional.

My original move to the teleological framework was inspired by Bethany Heywood at Queens University Belfast, and I got a copy of her dissertation this scientificamerican.com article is based on:
People with Asperger's less likely to see purpose behind the events in their lives

This article unwittingly illustrates just how ubiquitous teleological reasoning is. Note when it says:

As compared with 34 neurotypical people, those with Asperger’s syndrome were significantly less likely to invoke a teleological response—for example, saying the event was meant to unfold in a particular way or explaining that God had a hand in it. They were more likely to invoke a natural cause (such as blaming an illness on a virus they thought they were exposed to) or to give a descriptive response, explaining the event again in a different way.
[...]
The atheists, as expected, often invoked anti-teleological responses such as “there is no reason why; things just happen.” The people with Asperger’s were significantly less likely to offer such anti-teleological explanations than the atheists, indicating they were not engaged in teleological thinking at all.

Then the same articles sums the results by saying:

These results support the idea that seeing purpose behind life events is a result of our mind’s focus on social thinking. People whose social cognition is impaired—those with Asperger’s, in this case—are less likely to see the events in their lives as having happened for a reason.

So let's sum up the way this article was presented:
1. Study: Neurotypical atheist group states 'no reason'.
2. Study: Asperger’s group states 'natural cause'.
3. Article: Claims study says Asperger’s see "no reason".
Hence the article claims about the study directly contradict the results of the study. Why?

Now let's compare this to the idea of "real" magic. "Real" is magic that can't be done, because if it could be done it wouldn't be "real" magic. But magic that can be done is not real magic. No matter how outrageous an effect you invent, like a scientific principle that lets you walk through walls, it's not real magic. So how can we possibly define "real" magic, that also fits teleological reasoning and spinoza's thesis?

The answer is: Effects which have no other cause than someone's intention. In fact, the entire scientific revolution was predicated on replacing intent with cause. That is:
Methodological Naturalism = Cause and Effect.
Metaphysical Naturalism = Intention and Effect.

Consider that prior to the scientific revolution, the reason used to justify the 'belief' that a vacuum was impossible, supporting Aristotle's "nature abhors a vacuum", was that God is everywhere and if a vacuum existed God couldn't be everywhere, hence a vacuum was impossible.

What this shows is that the modern theistic concept of "supernatural", as something outside of and separate from nature, was invented after the scientific revolution to get God out of those damn scientist way. A way of moving the goalpost so to speak.

What spinoza, and organizations like the Discovery Institute seek to do is reimplement intent as a causal force in nature, and the only way to attempt that in this day is to play games with the meaning of randomness and "attentional bias".

Several types of cognitive bias occur due to an attentional bias. One example is when a person does not examine all possible outcomes when making a judgment about a correlation or association. They may focus on one or two possibilities, while ignoring the rest.

Note the red, and how spinoza insist on the law of the excluded middle?
In some debates "God of the Gaps" is just were such hypotheses are forced when someone challenges them to attend to those missing "attentional" elements of their argument.

The similarity between spinoza's thesis to Behe's is simply a product of the way teleological reasoning, a form of reasoning that ALL neurotypical people do implicitly even when rejecting it, when applied to natural phenomena is forced into being expressed as a nature of randomness fitted onto binary logic. All such arguments *must* look similar for this reason. It's the *only* way to force fit supernaturalism, theistic or otherwise, within a natural world.