The problem with Dawkins' Weasel Program

[Gawdzilla Sama]

It keeps killin' me chickens.

[my_wan]

It keeps killin' me chickens.

Don't fret, just copy and paste more chickens

Time for me to to paste another another chicken or two

[Gawdzilla Sama]

It keeps killin' me chickens.

Don't fret, just copy and paste more chickens

Time for me to to paste another another chicken or two

[my_wan]

It keeps killin' me chickens.

Don't fret, just copy and paste more chickens

Time for me to to paste another another chicken or two

Now I'm skeered...

[Gawdzilla Sama]

"You can't get fresher chicken."

[Ronja]

Ronja,

It can happen that:

species A with population 1000 due to mutation X reproduces zero.
species A with population 1000 without mutation X reproduces >= 1

This does not make sense - do you suggest that mutation X somehow manages to happen in the whole population in one generation?

[my_wan]

Ronja,

It can happen that:

species A with population 1000 due to mutation X reproduces zero.
species A with population 1000 without mutation X reproduces >= 1

This does not make sense - do you suggest that mutation X somehow manages to happen in the whole population in one generation?

Seeing that I already explained this to spinoza several times, perhaps letting spinoza answer you should be humorous.

[GenesForLife]

High five, Ronja.

[spinoza99]

Nope, heard of co-fecking-optation?

Co-option was developed as a Darwinian response to ID. Darwinists desperate to save their theory from being falsified invented a new theory to deal with irreducible complexity. Here is the essential fallacy of cooption:

1. NS can give tools new functions
2. Therefore, NS can build tools

Co-option does not explain how the tools are built in the first place.

you've described 3 genes, Shh, Wnt and Pax6, what about the other 199?

[spinoza99]

Gene Duplication, Gene insertion , retroposition, retrotransposition, mutator DNA and viral integrase driven gene formation, all of which do generate genes.

All of those processes just in some way or another manipulate an already built gene. It's like saying the cut and paste function writes new words.

So we're saying life can create stuff with a "cut and paste function"? Almost correct, it's actually a "copy and paste function" and it's call self replication. Are you denying that we a "self replicators"?

I was wrong. When I said "All of those processes just in some way or another manipulate an already built gene. It's like saying the cut and paste function writes new words," that was a false statement and I apologize.

This is what I should have said: there are mechanisms by which genes can be shuffled around, deleted, duplicated, transposed, I especially love horizontal gene transfer where the genes of one organism gets transferred into another. This does not explain how the amino acids are correctly sequenced. This would be like saying that a typewriter can write English all by itself. A typewriter can put letters on paper, but it can only spell words correctly through intelligence. You need intelligence to take a gene of 100 amino acids, duplicate it twice, combine it into a gene of 200 letters, delete 20 letters, then change the spelling of another 30 or so letters to get a brand new gene.

[spinoza99]

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.

Essentially all genes have untold countless numbers of different functions,

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

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

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.

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.

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.

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

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.

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.

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.

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.

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.

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?

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. 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.

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.

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.

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.

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.

[Ronja]

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.
...

Pity - I have not read the whole thread in detail, but based browsing through it and on you latest posts, you do not appear to have grasped the essentials of NS yet. As you seem to be especially interested in abiogenesis and eyes (at least), may I recommend these books:

Richard Dawkins: "The Selfish Gene"
Among other things it explains the role of abiogenesis as the first step towards life - for more detail, the Wikipedia articles on the issue are not half bad (meaning that today's versions of them are well written and have solid sources):
http://en.wikipedia.org/wiki/Abiogenesis
http://en.wikipedia.org/wiki/Miller%E2% ... experiment

IMO the book explains the gene centered view of evolution much better than the Wikipedia article, but also the article can be worth reading http://en.wikipedia.org/wiki/Gene-cente ... _evolution

Dawkin's "The Extended Phenotype" is maybe an even better written book, but The Selfish Gene should be read first, IMO.

Andrew Parker: "In the Blink of an Eye" is somewhat speculative, but presents the idea well that for a multi-cell organism, even just one cell that, based on a mutation, reacts to light can offer an evolutionary advantage over a multitude of organisms that have nothing with which to detect the difference between light and dark. Also with this subject, the Wikipedia page is pretty good: http://en.wikipedia.org/wiki/Evolution_of_the_eye

Or, if you do not mind following link after link for more details, this summary/overview type article can be valuable: http://en.wikipedia.org/wiki/History_of ... ry_thought


Also Daniel Dennett's "Darwin's Dangerous Idea" is a good book. It lays the foundation for how something as complex as our own consciousness can arise completely based on simple, automatic functions. Dennett further explores the issue in "Consciousness Explained", which is a rather demanding book (it took me two years to get through, but I found it well worth the effort).


I wish you serendipity in your search (for to me you appear a searcher, though this may be because I am one myself), i.e. both luck in bumping into useful information/ideas, and wisdom to recognize them, however initially strange they may seem.

[GenesForLife]

Nope, heard of co-fecking-optation?

Co-option was developed as a Darwinian response to ID. Darwinists desperate to save their theory from being falsified invented a new theory to deal with irreducible complexity. Here is the essential fallacy of cooption:

Bzzzz, since the recruitment of genes for other purposes has been observed in real life, this is not a fabrication, do learn this elementary fact first.
Co-optation has been observed.

Secondly, the Mullerian two step that deals with the evolution of irreducible complexity, was postulated in the Nineteen-twenties by Muller, which trashes any assertion that the addition of new parts to a system (by co-optation of new genes produced by mutation) to evolve novel systems could, if that new part was rendered essential by strong positive selection, would make the system irreducibly complex, and the fact that this was proposed nearly seventy years before Behe came up with his putrid nonsense of Irreducible Complexity drives a Chunnel Tunneling Device up the exhaust port of that particular assertion.

1. NS can give tools new functions
2. Therefore, NS can build tools

Bzzz, care to try to understand what is actually being said instead of engaging in the propping up of duplicitous strawmen?
Co-optation means that evolution does not require foresight.

Mutation is not equal to selection, when are you going to start acknowledging this fact in the posts you make?

Co-option does not explain how the tools are built in the first place.

And where did I claim co-optation builds genes?

you've described 3 genes, Shh, Wnt and Pax6, what about the other 199?

[/quote]

Wnt, Pax6 and Shh are all pathways, pathways that perform other cellular functions, but are co-opted for eye production, again this is a clear example of

[1] Co-optation happening.
[2] Selection not needing foresight.

Next time I suggest you learn to read and analyse what is actually being said before you go spouting errant nonsense.

[GenesForLife]

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.

Essentially all genes have untold countless numbers of different functions,

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

One function =/= one phenotype.

Do you know how signalling pathways, especially those involved in embryonic development work?
Hint - there is a chapter in MBOC5 on embryonic development, look some of that up, and then read about pathways.
If you want to read about genomic regulatory networks I can sort a copy of "The Regulatory Genome" out for you.

[Ronja]

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