The problem with Dawkins' Weasel Program

[GenesForLife]

Of course, my_wan , point mutations aren't the maximal limit of mutation that can take place, the mutational space given the range of processes can range from 1 substitution (point mutations) to whole genome duplications.

[my_wan]

Of course, my_wan , point mutations aren't the maximal limit of mutation that can take place, the mutational space given the range of processes can range from 1 substitution (point mutations) to whole genome duplications.

Yes, I know about gene insertions, frame shift mutations, fusions, etc., but spinoza99 was quoting 10^40,000 odds, which is the genome in its entirety in a single mutation. So the point was that a beneficial mutation can be as simple as a single letter change in the base code, just like a single letter change in the Weasel program. Only for NS there's a minimum of 1 in 4 chance of a given "single letter" mutation the be the best possible result. Of course many such changes have exactly the same function, so the odds can sometimes be even better.

My point was comparative in the biggest possible picture. Once this is understood then the details gets more interesting.

[MrFungus420]

why, if there is a "designer" out there, it's taking so long about it.

Time is relative. Atoms think...

No they don't.

Maybe your arguments would go a little better if you were honest.

[spinoza99]

Wan,

Many of these computer simulations start at the point after the first cell is already constructed. You can't do that. If you can explain how a Ford Mustang 1998 changes into a Ford Mustang 1999 through the mere tweaking of a few parts (one mutation), you have not explained how Natural Selection builds the entire Ford Mustang 1998 in the first place. To build the first organism through undirected processes you need to coordinate a minimum number of genes which are a minimum length. We know that there are certain immortal genes which all organisms share, that number is 500, yet no organism has less than 1600 genes, so the minimum number is somewhere between 500 and 1600, though closer to 1600 than 500. The minimum length of one gene would be the average of those 500 immortal genes. Given that there are 500 genes that ALL organisms share, it is very reasonable to conclude that you cannot construct life without these genes. There is a possibility that you can construct life without these genes but to believe that is to believe in something for which there is no evidence.

Now, regarding the fallacy: "there is only one way to construct life." I have never committed this fallacy and I admit that there are billions (but not gazillions of ways) to construct a one celled organism. The central problem in determining the odds of life is coming up with a method for determining how many functional sequences exist among the possible number of sequences. You mistunderstood me when I said that homologous genes are on average 60% identical. What I did not mean was that humans and chimps have 98% of the same genes, what I meant was that the same gene found in, say, Baker's yeast, and, say, a snake, that one gene, in 60% of the positions we find the exact same amino acid. Some very ancient genes are astonishingly preserved. Let me quote from Albert's Microbiology of the Cell, given to me by dear friend, Genes for life:

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.

There are very many regions of the genome which scientists call ultraconserved regions. (even some areas of the non-coding DNA is very well preserved). I don't know the exact number of how similar these 500 immortal genes are but 60% is a good working number. If we were to hone it to somewhere between 40 and 70% it would not change matters much.

Here are the parameters that I would like this debate to take in the future. I will use an analogy from cars. The first car is usually attributed to Karl Benz in 1885 with his motorwagen which sold on the free market in 1889 (and he lived in Mannheim by the way which is only about an hour from where I currently live). Constructing the first car is similar to constructing the first cell. Changing a car into another completely different car, such as Benz's motorwagen into Ford Mustang 98 is similar to macroevolution, however it must be pointed out that there are many ways to change Benz's car into another car since there are very many cars on the market. Then changing a Ford Mustang 98 into a Ford Mustang 99 is similar to microevolution. Determining the odds of changing a FM 98 into a FM 99 is not an interesting debate. I admit anyway that Natural Selection through random mutations can do this as has been seen with the Ice Fish, the Nylon Bug, animals acuqiring color vision as opposed to black and white vision and other examples. But I also want to point out that NS more often than not changes a Ford Mustang 98 into a Ford Mustang 97 (going backwards) by simply breaking genes. The environment shifts (in the case of parasites a drug is introduced) and the FM 98 is no longer better than the 97, so NS just breaks a few parts, returns it to the 97 which turns out to be a bit better. Debating the odds of turning a Benz into any other functional car is a more interesting debate but still not important. It also a bit harder because we have to determine how many different functional cars can in fact exist, how many parts (genes) they need, etc. But it still is an important debate to combat the standard Darwinian fallacy: "once life gets going NS can do the rest." For the moment however I'm not going to spend my time on it. Suffice it say, Darwinists routinely make the mistake: "because NS can turn a FM 98 into a FM 99, NS can therefore turn a Ford Mustange into a Nissan Centra. To prove this I will quote a rather surprsing admission from a passionate Darwinist, Sean Carroll: "Because decaying genes generally accumulate multiple defects, their inactivation cannot be easily reversed. This means that the loss of gene functions is generally a one-way street. Once gone, these functions will not return." If NS cannot repair a broken gene, there is no reason to believe that NS can build a new gene. The most important debate is calculating the MINIMUM odds of building the first car, the Benz motorwagen.

To calculate the odds of build ing the first cell, I use Stephen Meyer's odds with a few changes. First, he quotes Douglas Axe who invented some method of determining how precise amino acid sequences must be before they are deleterious. I don't know what method Axe use but I use a method that every one can understand and that seems rational: we analyze how many amino acids are necessary in the immmortal genes by determining how many of them are still in the exact same location after 3 billion years and that number is 60%. These genes have been changing for 3 billion years, maybe 10^40 different generations, they have tried many possible sequences and yet they do not exist. The average length of an amino acid in the immortal genes is about 100. 20 raised to 60th power is 10^78 which is very close to Axe's number of 10^74, even though Axe used 150 amino acids. Second, Meyer believes the mininum number of genes is 200 but he does not say where he got that other than that is what most scientists think. I think a more reasonable number is 500 given the fact that there are 500 genes that all organisms share, but 200 does not change matters much. Third, amino acids must first form a peptide bond, yet amino acids can form other bonds. The probability of forming a peptide bond is about 1/2, or if the protein is 100 amino acids long, the odds of all of them forming peptide bonds in one in 10^30. Fourth, amino acids, with one exception, form both left handed and right handed versions. Only the left-handed version are useful for the construction of protein. The odds of a left-handed version being contructed is again roughly 1/2, or the odds of all 100 amino acids being left-handed again is one in 10^30. So to form one gene we add the exponents together 30 + 30 + 78, which is 148, we then multiply that by the 500 necessary immortal genes and get 74,000, making the odds of forming the first cell one in 10^74,000.

I wrote the program, with much higher odds constraints than Dawkins original. Yes his original was 1 in 26, but NS uses a 4 letter alphabet, not a 10^40,000 letter alphabet that number from above tried to pretend. "Reality" is that NS has a 4 letter alphabet, and each beneficial mutation doesn't have to randomly shuffle every letter to get a new person in order to get a beneficial mutation. Even a single letter change (1 in 4, not 1 in 26 like Weasel) can sometimes result in a beneficial mutation.

What you have to factor in is that the human genome is 3.2 billion letters long and of those 3.2 billion letters only a very small number if changed will result in an improvement. There are only 25,000 genes in a human and although I find this hard to believe of those 25,000 20,000 are broken, psuedo genes that don't work anymore. A typical gene in a human is only 1300 letters long. So the number of letters out of the 3 billion that matter are only 6.5 million (1300 * 5000). Then not only do you have to mutate one of those 6.5 million letters you have to mutate it correctly. I don't know what the ratio of correct vs incorrect mutations is but it certainly favors incorrect. But as I have already said those odds are like determining converting a FM 98 into a FM 99.

Question:
1) Are you ready to admit the 10^40,000 is the whole organism sequence, not the odds of a single beneficial mutation?

yes

2) Are you ready to admit that a beneficial mutation can occur by a single letter change in 1 of 4 possible letters, A, G, T, or C?

[/quote]
No, because the odds of forming a beneficial mutation is like determining the odds of changing a Ford Mustang 98 into a Ford Mustang 99, which doesn't matter. You have to determine the odds of building a car in the first place.

This is exactly the same thing as claiming that I must get the *entire* sentence in the Weasel program with a single random mutation!!! That exactly the same thing as claiming a person came into existence from a chemical *accident* in a mud puddle one day!!!! Yet we know that some people have more beneficial mutations than others, so

the odds of a beneficial mutation is not the same as the odds of getting a *whole* person from a single mutation.

correct

Now let's do the same numbers for Weasel. The Weasel program actually defaulted to a 57 (not 109) letter code. DNA has a 4 letter code, A, G, T, and C. See the difference already? Now the *whole* sentence is the polypeptide chain. For "Methinks it is like a Weasel." is a 29 character polypeptide sequence. Hence the odds, as you defined and attributed to Sagan, is 57^29. Lets round this down to 10^29 just to match the NS number base. Yet already 10^29 is already larger than 10^20 from the (10^20)^2000 number. So, if Weasel can do this 2000 times in a row, then the odds are (10^29)^2000 = 10^58,000, which is much bigger than 10^40,000.

I'm not sure I understand exactly what you're saying but it seems like you're saying Weasel can hit 1 in 10^29 odds regularly. I must be misunderstanding something because no one would believe that.

Get this straight, 10^40,000 was *not* the odds of a single beneficial mutation, 10^40,000 is the odds of an *entire* organism, containing 2000 twenty-amino-acid polypeptide chains, from a single mutation!!!

correct

I don't see how you can seriously believe that. If you roll a dice with 10^1,000,000 sides for each second, you will have to roll it 10^1,000,000 times before the odds are 1 that you will get the right number. Seeing as there are only 10^17 seconds in our universe, it is impossible that you could score the right number. If you really believe this then I'm going to have to stop debating with you.

Easy, just change the length of the sentence in the Weasel program and do it X number of times, to get those odds. Recall how I explained that a beneficial mutation can be defined by a single letter change in a 4 letter DNA code, giving the odds of a mutation occurring there a 1 in 4 chance of getting the best beneficial mutation for that location.

Ok, you can get those odds, it does not mean that you can score off of them.

The nylon bug was a frame shift mutation, which added 3 letter to the beginning of the sequence. There's a 1 in 64 chance that a 3 letter codon will have a particular sequence. The bug now eats nylon, which didn't exist before 1935 and can only eat nylon and nothing else. It only has a 2% efficiency, but it doesn't matter because no other organism is competing for the nylon food.

Correct, very rarely random mutations can improve on an already existing gene, but it cannot build a gene.

As a matter of fact the smallest life I know of is ∆X174, and has 11 genes. It's a virus that infects bacteria. You said smallest bacteria, but start with bacteria, except to make it sound like life requires more complexity than it does?

viruses aren't life they are just a mechanical device that feeds off of already built life. viruses cannot live without already built life. They are like a parasite that feeds off a car, they are not the precursors of cars.

No evidence you say? The lab experiments are showing that trying "less" complex approaches are more successful.
http://www.wired.com/wiredscience/2009/ ... cleotides/
Here's we create something close to life. Though it doesn't even contain cells, it does self-replicate, compete, and evolves. In fact, while watching it evolve, the newer better version started making the originals go extinct.
http://www.livescience.com/strangenews/ ... -life.html

I'll look into this later

random mutation can cause big changes through mutating one position on one already-built gene, therefore random mutation can design a gene of 200 amino acids.

This is getting a bit silly. This is like saying Weasel is a fallacy, because a random mutation of a single letter, thus it's only claimed that it can produce the whole sentence of 200 amino acids. It only takes one letter change at a time, with only 4 possible letter, for a person to evolve from an amoeba. That's a 1 in 4 chance each mutation takes it in the right direction to get a human. Yet there are other creatures, perhaps as much or more intelligent than us, which could have evolved if the mutations happened differently.

Let's take the first sentence of Dawkins Weasel program

WDLTMNLT DTJBKWIRZREZLMQCO P

That sentence will be discarded by Natural Selection because it does not code for anything.

if you have a living organism, then any given random mutation in a 4 letter code, A, G, T, and C, you have at least a 25% chance of getting the best possible per letter mutation. Not the 1 in 26 per Dawkins, or 1 in 57 per my version.

The mutations are binary, either they're beneficial or they're not. Of the 3.2 billion letters in the human genome very few are beneficial. I would like to hear from you how many of those 3.2 billion are beneficial and why.

Yes, common ancestry is distinct, but common ancestry can't exist without evolution. Even if there was 10 different ancestors, evolution would still require that you have a common ancestry with at least part of the animal kingdom.

Common ancestry cannot exist without change of species. Evolution is a two point hypothesis: all that is needed to acount for ALL the diversity of species is one, natural selection, and two, random mutation. Where Darwin is wrong is that a third is needed: intelligence.

So, what evidence do we have for just evolution, irrespective of common descent? We'll we have genetic algorithms that us the "Random()" function to illustrate how the 4 letter DNA code varies. We have accidental gene fusions and insertion. The nylon bug was a frame shift insertion, so that the functionality of every gene in the DNA sequence was rewritten in a single accident. Algorithms need more evidence though, so we have been tracking the step by step evolution of bacteria in the laboratory for years. We watch each an every mutation that occurs, builds up, and leads to quiet different organisms years later. Not a single letter in every step of the changes missing.

I suppose you're referring to the Lenski experiment. he's been tracking E Coli for about 20 years and to this point no new genes have been built. Only already built genes have been turned off and on.

[GenesForLife]

Nylonase =/= Lenski experiment.

If you want an example of a de novo gene origination from noncoding DNA, here is one

Origination of new genes is an important mechanism generating genetic novelties during the evolution of an organism. Processes of creating new genes using preexisting genes as the raw materials are well characterized, such as exon shuffling, gene duplication, retroposition, gene fusion, and fission. However, the process of how a new gene is de novo created from noncoding sequence is largely unknown. On the basis of genome comparison among yeast species, we have identified a new de novo protein-coding gene, BSC4 in Saccharomyces cerevisiae. The BSC4 gene has an open reading frame (ORF) encoding a 132-amino-acid-long peptide, while there is no homologous ORF in all the sequenced genomes of other fungal species, including its closely related species such as S. paradoxus and S. mikatae. The functional protein-coding feature of the BSC4 gene in S. cerevisiae is supported by population genetics, expression, proteomics, and synthetic lethal data. The evidence suggests that BSC4 may be involved in the DNA repair pathway during the stationary phase of S. cerevisiae and contribute to the robustness of S. cerevisiae, when shifted to a nutrient-poor environment. Because the corresponding noncoding sequences in S. paradoxus, S. mikatae, and S. bayanus also transcribe, we propose that a new de novo protein-coding gene may have evolved from a previously expressed noncoding sequence.

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2390625/

[GenesForLife]

Of course, one more important thing to note is that conservation of sequences and alterations of sequences being detrimental are only features that are necessary after a novel gene evolves to a particular stage and is incorporated into a system. If you want an analogy removing a stone from an arch causes it to collapse only after the scaffolding that was used during construction was removed.

The Mullerian two step explains adequately how such "irreducibly complex" systems can arise. The paper that I have presented above also involves an example where this new gene's protein has become integral to DNA repair, and disrupting its function now will kill the cell, but other close relatives without open reading frames can get by using orthologues to what we see in yeast.

The fact that an allele becomes conserved at some point and further mutation thereof can be deleterious does not imply that they had to be poofed into existence as a whole gene with a conserved sequence at all, learn this elementary lesson once and for all.

[my_wan]

Wan,

Many of these computer simulations start at the point after the first cell is already constructed.

Well duh, you said NS, not abiogenisis. If you are talking about abiogenisis don't say NS, and if you want to talk about NS don't say abiogenisis. We can certainly talk about abiogenisis to, but pretending NS and abiogenisis is the same is just wrong. It's like calling a mechanic an automobile engineer.

Genetic algorithms were never meant to demonstrate abiogenisis, it only illustrates how a very very simply organism can become a very complex organism. That's it, nothing else, and that's all NS is. So yeah, I'll get into the abiogenisis side of it to, but I'm not not going to be too tolerant of confusing the two.

To build the first organism through undirected processes you need to coordinate a minimum number of genes which are a minimum length. We know that there are certain immortal genes which all organisms share, that number is 500, yet no organism has less than 1600 genes, so the minimum number is somewhere between 500 and 1600, though closer to 1600 than 500. The minimum length of one gene would be the average of those 500 immortal genes. Given that there are 500 genes that ALL organisms share, it is very reasonable to conclude that you cannot construct life without these genes. There is a possibility that you can construct life without these genes but to believe that is to believe in something for which there is no evidence.

How how is that a reasonable conclusion? What about Carsonella ruddii, which works fine with 182 genes, with a grand total of 159,662 'letters' (base pairs)? Or φX174 with only 11 genes and 5,386 'letters' (which you apparently ignored from my previous post)? These organisms may require a host, with the smallest known host free organism being Mycoplasma genitalium, with 521 genes. Then we started seeing how many genes we could remove from M. genitalium and have it still work and got even smaller genomes. We can also create entirely artificial DNA and boot up life with it.

Now these are still quiet large for abiogenisis, and most advances are extremely new, but is DNA, cells, or anything we would even define as life, even necessary for NS to work, such as just chemicals? Absolutely not.
http://www.wired.com/wiredscience/2009/ ... catingrna/
This is not life as we know it, but it reproduces and evolves on its own, with nothing but food like all life needs. These were just enzymes that only had a 30 bit information channel, smaller that some of the sentences I tested Weasel with. Yet:

One day, some of the enzymes "went critical" and produced more RNA enzymes than the researchers had put in.

They also soon evolved, driving the originals to extinction (sound familiar):

"Most of the time they breed true, but sometimes there is a bit flip — a mutation — and it’s a different replicator," explained Joyce.

Most of these mutations went away quickly, but — sound familiar? —
some of the changes ended up being advantageous to the chemicals in replicating better. After 77 doublings of the chemicals, astounding changes had occurred in the molecular broth.

"All the original replicators went extinct and it was the new recombinants that took over," said Joyce. "There wasn’t one winner.
There was a whole cloud of winners, but there were three mutants that arose that pretty much dominated the population."

And all this without any cells or any DNA at all, and only a 30 bit information channel in the self replicating enzymes! A computer generally uses 8 bits just to encode a single letter such as A.

So NS doesn't even need life, cells, DNA, etc., to operate chemically. No computer needed. 30 bits is *nothing* for everyday chemical reactions happening in number so large every day that it dwarfs number of living organism that ever existed on Earth.

So your claim that 1600 complete genes are "required" for NS to start is totally wrecked. NS needs zero complete genes to get started. The only thing you can argue is that it's not life, or not how the life we know got started, but it is NS and we don't know if the life we know can evolve from those particular enzyme replicators. Given that most of what we learned is only a matter of months old, arguing 1600 needed genes is an argument from ignorance, i.e., since we don't how it must not be possible. Which is a fallacy of the first order.

Now, regarding the fallacy: "there is only one way to construct life." I have never committed this fallacy and I admit that there are billions (but not gazillions of ways) to construct a one celled organism. The central problem in determining the odds of life is coming up with a method for determining how many functional sequences exist among the possible number of sequences. You mistunderstood me when I said that homologous genes are on average 60% identical. What I did not mean was that humans and chimps have 98% of the same genes, what I meant was that the same gene found in, say, Baker's yeast, and, say, a snake, that one gene, in 60% of the positions we find the exact same amino acid. Some very ancient genes are astonishingly preserved. Let me quote from Albert's Microbiology of the Cell, given to me by dear friend, Genes for life:

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.

You are essentially claiming that life needs to start with a certain amount of complexity, involving any number of complete genes. I demonstrated above that NS can start without a single gene. It's not considered life, because it doesn't have cells and genes, but there is absolutely no reason to presume NS didn't start well before life developed. In fact, that NS started before cellular life is normally the only reasonable assumption.

You want to pretend that the simplest life we can find today is the simplest cellular life possible. No scientist believes that. So what do you suppose happened to those simpler cellular life forms? Just look at what happened to the original self replicating enzymes above to see your answer. When something better evolved they went extinct, just like happens in all the time in normal living cultures in the lab when a better mutant comes along. Just like what happens when Weasel develops a better sentence eater than the ones before it. This extinction of the simpler, less capable, population of organisms is part of how evolution works. Yet you claim is predicated on the notion that because the simpler versions are extinct, and we don't know what they looked like, it must be impossible for them to exist: wrong. Evolution requires most of them to be extinct, because they can't compete with the more complex life that now exist.

There are very many regions of the genome which scientists call ultraconserved regions. (even some areas of the non-coding DNA is very well preserved). I don't know the exact number of how similar these 500 immortal genes are but 60% is a good working number. If we were to hone it to somewhere between 40 and 70% it would not change matters much.

Yes, many non-coding regions have functions, mostly as regulatory mechanisms of the coding regions. We know about these, we know how to measure them, etc. The level of conservation is even used to determine function, without having to know what that function is. Yet we can take them out of the organism, to create a new smaller organism, and it still survives just fine. Unlike the Irreducible Complexity claim, function can start out as accidents in non-functional DNA, but only have very minimal functionality. The functionality can then evolve to be more important. Like the eyeball stating out as a slightly light sensitive patch of skin, and slowly becoming more functional. It's still has useful function even if it just senses the difference between light an dark.

So even if part of this region we call non-coding is coding some function, it's still only comes to a small part of of non-coding region which is actually coding something. The majority, even with the strictest constraints on conserved regions, remain strictly non-coding. Yet that's pointless, as we can remove these non-coding regions, that are in fact encoding something, and the organism still works just fine.

Here are the parameters that I would like this debate to take in the future. I will use an analogy from cars. The first car is usually attributed to Karl Benz in 1885 with his motorwagen which sold on the free market in 1889 (and he lived in Mannheim by the way which is only about an hour from where I currently live). Constructing the first car is similar to constructing the first cell. Changing a car into another completely different car, such as Benz's motorwagen into Ford Mustang 98 is similar to macroevolution, however it must be pointed out that there are many ways to change Benz's car into another car since there are very many cars on the market. Then changing a Ford Mustang 98 into a Ford Mustang 99 is similar to microevolution. Determining the odds of changing a FM 98 into a FM 99 is not an interesting debate. I admit anyway that Natural Selection through random mutations can do this as has been seen with the Ice Fish, the Nylon Bug, animals acuqiring color vision as opposed to black and white vision and other examples.

No, you can't direct the parameters of the debate that way. I explained why at the top. We can switch from NS to abiogenisis whenever you like, but it's two separate issues. With NS we have life, and only need to explain how it evolves, both to more and less complexity, depending on which allows the organism to better survive.

So we have two separate issues.
1) That evolution (NS) tends to lead to more complex life, in most cases.
2) That abiogenisis needs simpler replicators than we see in the wild today to make sense.
3) Why the simpler life forms no longer exist.
For 1) I have explained via genetic algorithms, nylon bug only being 2% efficient, etc., etc.
For 2) I pointed out above that NS (evolution) even happens with *just* chemistry (self replicating enzymes), no cellular life needed.
For 3) I pointed out how the original non-life self replicating evolving enzymes went extinct as soon as better mutates evolved, just like the Weasel program. I also pointed out how we see this all the time, when watching perfectly normal everyday organisms evolve in the lab.

But I also want to point out that NS more often than not changes a Ford Mustang 98 into a Ford Mustang 97 (going backwards) by simply breaking genes.

Wrong, because when these backwards mutates happen, they don't generally live long enough to reproduce. Just like the original non-life self replicating enzymes went extinct. Remember the quote from the article: "Most of these mutations went away quickly, but — sound familiar?". These were the "backwards" mutations you mentioned, and they went away pretty quickly, without anybodies help. *Only* those mutants that went "forward", and was better than the originals, was able to take over and make the originals go extinct. So just because "backwards" mutants happen much more often does not mean they get to survive very long, for exactly the same reason that that the simplest organisms alive today in the wild tend to be highly complex. That does not mean simpler organisms can't survive if the more complex life wasn't around to keep driving them into extinction.

The environment shifts (in the case of parasites a drug is introduced) and the FM 98 is no longer better than the 97, so NS just breaks a few parts, returns it to the 97 which turns out to be a bit better. Debating the odds of turning a Benz into any other functional car is a more interesting debate but still not important. It also a bit harder because we have to determine how many different functional cars can in fact exist, how many parts (genes) they need, etc. But it still is an important debate to combat the standard Darwinian fallacy: "once life gets going NS can do the rest." For the moment however I'm not going to spend my time on it. Suffice it say, Darwinists routinely make the mistake: "because NS can turn a FM 98 into a FM 99, NS can therefore turn a Ford Mustange into a Nissan Centra. To prove this I will quote a rather surprsing admission from a passionate Darwinist, Sean Carroll: "Because decaying genes generally accumulate multiple defects, their inactivation cannot be easily reversed.

Only Sean Carroll's quote doesn't help you for the reasons I just explained. Because organisms with decaying genes don't live to keep those decays in the population in the long run. Just like all the non-life self replicating enzymes mutates that decayed quickly died. But those few beneficial mutants ended up driving the original normal population into extinction. Geneticist do not deny this decay effect, but you can't use that to claim a dead animal somehow manages to keep its bad mutations in the population. You can't have kids if your dead. The decay goes away because it died. Decay happens in the individuals, which then don't survive in the long run, not the whole population.

This means that the loss of gene functions is generally a one-way street. Once gone, these functions will not return." If NS cannot repair a broken gene, there is no reason to believe that NS can build a new gene. The most important debate is calculating the MINIMUM odds of building the first car, the Benz motorwagen.

Yes, less gene function is generally a one way street, one way to the grave. And since it's in the grave, it's doesn't spread in the population of living organisms. Even if it's not so bad that it kills the organism, or prevents it from reproducing, the kids will not do well either and are less likely to be able to reproduce. The normal versions will continue to thrive though, until a better mutate gets an advantage over the normal organisms. Just like in the non-life self replicating enzymes.

To calculate the odds of build ing the first cell, I use Stephen Meyer's odds with a few changes.

I have already pointed out that NS needs no cells or DNA to get started. NS is then perfectly capable of creating the more complex chemistry that makes cells and DNA, by driving the simpler mutants into extinction. Just like in the non-life self replicating enzymes drove the "backwards" mutants into the grave, while the "forward" mutants drove the original enzymes into extinction.

What you have to factor in is that the human genome is 3.2 billion letters long and of those 3.2 billion letters only a very small number if changed will result in an improvement.

What you have to factor in is that the human genome didn't start with 3.2 billion letters. It almost certainly didn't even start evolution as a cell, or have DNA. The small number of possible improvement in point-like mutations doesn't matter, because like the self replicating enzymes, bad mutations tend to die, while good ones tend to eventually make the normal version go away. Somewhere around 70% of human pregnancies result in miscarriage, most before the woman even knows she's pregnant. That's an awfully lot of "mistakes" going away in the human population before anybody even knew they existed!

There are only 25,000 genes in a human and although I find this hard to believe of those 25,000 20,000 are broken, psuedo genes that don't work anymore.

We haven't done this with people fore obvious reasons, but we strip out *all* these "psuedo genes" in many many different organism just to prove the organism is perfectly normal without them, and they in fact are perfectly normal without these "psuedo genes". We can even create 100% completely man made DNA, and boot up life with it, and they just as normal as natural DNA organisms.

A typical gene in a human is only 1300 letters long. So the number of letters out of the 3 billion that matter are only 6.5 million (1300 * 5000). Then not only do you have to mutate one of those 6.5 million letters you have to mutate it correctly.

Here's the thing, most of the point mutations that occur changes no function at all. Many that are harmful, never get born in the first place, and the woman didn't even know she was pregnant most times. Most 'good' point mutations still makes the same basic protein, just with slightly modified physical and chemical properties. There are lots of ways to make the same basic protein, with only very slight differences.

2) Are you ready to admit that a beneficial mutation can occur by a single letter change in 1 of 4 possible letters, A, G, T, or C?

No, because the odds of forming a beneficial mutation is like determining the odds of changing a Ford Mustang 98 into a Ford Mustang 99, which doesn't matter. You have to determine the odds of building a car in the first place.[/quote]
So, if there are 4 possible letters, A, G, T, and C (at a point mutation), then at least one of those 4 must be the best possible choice. That's means (for a point mutation) you have at least a 1 in 4 chance of getting the best possible choice. Correct?

You are replacing the notion of whole protein mutations with changing a "Ford Mustang 98" to a "Ford Mustang 99", but that's not how it works. If you start with a gene encoding protein X (Ford Mustang 98), and do a point mutation on a letter, you will never get a "Ford Mustang 99". What you will get is another "Ford Mustang 98" (protein X), but with a slighter stronger or weaker glue holding the rear view mirror on, or some other simplistic modification of the original "Ford Mustang 98". You would need lots and lots and lots of point 'letter' mutations to get a "Ford Mustang 99" from a "Ford Mustang 98", period.

I'm not sure I understand exactly what you're saying but it seems like you're saying Weasel can hit 1 in 10^29 odds regularly. I must be misunderstanding something because no one would believe that.

What I said was that would be the odds of the Weasel program getting the whole sentence right on the first try. The 10^40,000 odds you quoted is the odds of getting a person from an amoeba with one big mutation. Neither the Weasel program nor NS works by shuffling the deck of DNA sequences in a single generation. And I started this response explaining why NS doesn't even need any DNA at all to get started, much less organize so much at once that you get 10^40,000 odds against it. I also explained what happened to those simpler life forms.

Ok, you can get those odds, it does not mean that you can score off of them.

Easy, if I can "score off" 10^29, which I have, I can simply repeat the program 2000 times and that comes to 10^58000. I don't think I run the Weasel program 2000 times, but I run it at least several hundred times. Recall, your 10^40,000 depended on creating 20 different whole proteins (while I showed above that NS does even need 1), which also form about 2000 enzymes, which the non-life enzyme in the example at the top was a single enzyme. DNA is not the only way to produce these enzymes. So I am perfectly justified in comparing the 2000 to simply running the Weasel program 2000 times, and get the 10^29 sentence every time.

Correct, very rarely random mutations can improve on an already existing gene, but it cannot build a gene.

Weird, the "Ford Mustang 99" (gene) is not merely an improvement on the "Ford Mustang 98", but a whole new Mustang with just a few common parts. Every single modification between the two are different mutation. A gene is nothing more than a "unit of heredity", regardless of how that heredity is encoded. Enzymes are created artificially and naturally all the time without DNA, and the non-life self replicating enzyme, referenced at the top, evolved without DNA. What is the "gene", or "unit of heredity", in that case?

viruses aren't life they are just a mechanical device that feeds off of already built life. viruses cannot live without already built life. They are like a parasite that feeds off a car, they are not the precursors of cars.

So what if they feed off life, doesn't every living organism on Earth have to feed off of something? Don't try to goo without supper for too long. A viruses environment can simply do things our environment can't do for us, yet we need what our environment provides to protect and grow our young just like a virus. It basically lays eggs in our cells the way flies lay eggs in a dead carcass.

Let's take the first sentence of Dawkins Weasel program

WDLTMNLT DTJBKWIRZREZLMQCO P

That sentence will be discarded by Natural Selection because it does not code for anything.

So, any reasonable assumption is that life must start with chemistry, not life. Chemistry does not need life to work, but life needs chemistry to work. So it stated with some meaningless random chemical reaction, thus no life needed.

The mutations are binary, either they're beneficial or they're not. Of the 3.2 billion letters in the human genome very few are beneficial. I would like to hear from you how many of those 3.2 billion are beneficial and why.

No, there not binary, the "law of the excluded middle" does not apply. First off there is 3 choices, not 2. Good, bad, and neutral, but the "law of the excluded middle" doesn't even apply to those 3 choices. A mutation can be good in one way, while being bad in another. It might only be a little good or bad, or a lot good or bad, or any combination of a little, a lot, good, bad, or neutral. Most certainly NOT binary.

Common ancestry cannot exist without change of species. Evolution is a two point hypothesis: all that is needed to acount for ALL the diversity of species is one, natural selection, and two, random mutation. Where Darwin is wrong is that a third is needed: intelligence.

There's that intelligence thing again, like in the other thread. I could accept thinking about that if you could provide one reason to. NS does in FACT account for ALL the diversity of species, but does not account, or even try to account, for were life came from. That's a separate research agenda.

If you can explain the me how a deadly mutation can be just as successful at having kids (while dead), as the good mutations i'll listen. But merely saying bad mutations are more common gets you nowhere. Are you saying that the best mutations can't have enough kids to make up for all the dead bad mutations. Remember, many less adapted organism could survive fine, if they didn't have to compete with better adapted organisms. And we understand how that works with nothing more than randomness. So why do you insist it needs more than randomness?

I suppose you're referring to the Lenski experiment. he's been tracking E Coli for about 20 years and to this point no new genes have been built. Only already built genes have been turned off and on.

Since a gene is a "unit of heredity" and the beneficial mutations were inherited by the next generation that took over the population in Lenski's cultures, then yes new gene functions were created. Not merely tuned on or off. How do we know they weren't merely turned on and off? Because we have the exact genetic sequence of each generational variation.

But my point was that you don't *need* a new protein to have beneficial mutations. But you were quoting the odds of new proteins as the odds of getting a beneficial mutation, wrong. Lenski's experiments documented loads of beneficial mutations, that even drove some of the previous organisms to extinction. Nor do you even need proteins for NS to work, only chemistry. If you keep making tiny changes to one kind of protein then eventually you can end up with something so different you have to call it a new protein, but there's only so many different basic types.

[my_wan]

Add a few comments on the Sean Carroll pic quotes:

No need to reverse them if the critter is dead...

Note it says all "domains" of life, not all life. Might want to look up what "domain" means.

[Tero]

Can we get back to flipping coins, excluding parallel experiments and "you can't get something from nothing?" This stuff is just too spooky, I need Ray Comfort to comfort me. And tell me I'm special.

[my_wan]

Can we get back to flipping coins, excluding parallel experiments and "you can't get something from nothing?" This stuff is just too spooky, I need Ray Comfort to comfort me. And tell me I'm special.

I need to see how well my banana fit my hand about now to..

[JOZeldenrust]

my_wan, your WOT was one amazing post.

[Ronja]

my_wan, from the nosebleed section:

[spinoza99]

Wan,

I appreciate you taking the time to answer my statements carefully. I enjoy debating with you and respect you as an opponent. I'm also glad that you stopped making subjective statements about the quality of my ideas, that always helps. Most of this debate is bogged down in side issues and many of the arguments I'm making now are simply repeats of old arguments so we're starting to say the same thing, which means this debate cannot go on much longer. However, I have identified some major areas of misunderstanding that really need to be cleared up.

You said: "if there are 4 possible letters, A, G, T, and C (at a point mutation), then at least one of those 4 must be the best possible choice." In the histone H4 for example 100 of the 102 positions none of the mutations are beneficial, none are neurtral, but all of them are deleterious. (I'm only talking about changes in the amino acid structure not the DNA, because amino acids is the only thing that matters). This is a very fundamental misunderstanding on your part. If you look at the sequence of the Histone H4 you seem to think that you can mutate any of it and that has a 1 in 4 chance of getting the best improvement. The histone either works or it does not. You can't improve on it. It just coils up the DNA so that I can fit in the nucleus. Let me give an example from language:

Would you tell me what colour that is

In the above sentence there is only one mutation that can be neutral, remove the u in color. Every other mutation destroys the sentence. There are 10^37 different ways to change that sentence, and only one of them results in a neutral mutation, everything else is deleterious.

Do you admit that that is what the Ultra Conserved Regions of the genome are like?

You also failed to understand the Sean Carroll quote that NS cannot repair genes, so why then do you believe that it can build genes? You wrote in response:
"Yes, less gene function is generally a one way street, one way to the grave. And since it's in the grave, it's doesn't spread in the population of living organisms." Of course less gene function leads to the grave, that is certainly not proof that NS can build a gene. To say: I don't believe NS can repair a gene, but I believe NS can build a gene, is just a pure contradiction. I can't learn anything from someone who makes such an assertion.

I said: here's proof that NS cannot build genes
You said: broken genes kills organisms

Do you see how you did not answer my point?

What you have to factor in is that the human genome is 3.2 billion letters long and of those 3.2 billion letters only a very small number if changed will result in an improvement.

What you have to factor in is that the human genome didn't start with 3.2 billion letters. It almost certainly didn't even start evolution as a cell, or have DNA. The small number of possible improvement in point-like mutations doesn't matter, because like the self replicating enzymes, bad mutations tend to die, while good ones tend to eventually make the normal version go away.

The point is the 3.2 billion letters are there right now, and to find the golden mutations among that sea of 3.2 billion letters is not something chance can do.

You want to pretend that the simplest life we can find today is the simplest cellular life possible. So what do you suppose happened to those simpler cellular life forms? Just look at what happened to the original self replicating enzymes above to see your answer. When something better evolved they went extinct, just like happens in all the time in normal living cultures in the lab when a better mutant comes along. Yet you claim is predicated on the notion that because the simpler versions are extinct, and we don't know what they looked like, it must be impossible for them to exist: wrong. Evolution requires most of them to be extinct, because they can't compete with the more complex life that now exist.

This is wrong. The weak do not die out when something stronger arises. Look at cats, the littlest cats are still around, in spite of panthers and tigers. Look at fish: fish range from sharks to fish as small as 1cm. Look at snakes: anacondas have not rendered even the littlest snakes extinct. Life is teeming with numerous tiny creatures. Large creatures never obliterate the small. If predators eliminated their prey, then there would be no predators. Extinctions mainly occur because the environment changes not because a new species arises, though of course there are exceptions: just look at all the species homo sapiens have eliminated, though even there man has eliminated species not by methodically killing them but by ruining their habitat.

***************

Side issues:

To build the first organism through undirected processes you need to coordinate a minimum number of genes which are a minimum length. We know that there are certain immortal genes which all organisms share, that number is 500, yet no organism has less than 1600 genes, so the minimum number is somewhere between 500 and 1600, though closer to 1600 than 500. The minimum length of one gene would be the average of those 500 immortal genes. Given that there are 500 genes that ALL organisms share, it is very reasonable to conclude that you cannot construct life without these genes. There is a possibility that you can construct life without these genes but to believe that is to believe in something for which there is no evidence.

How how is that a reasonable conclusion? What about Carsonella ruddii, which works fine with 182 genes, with a grand total of 159,662 'letters' (base pairs)? Or ∆X174 with only 11 genes and 5,386 'letters' (which you apparently ignored from my previous post)? These organisms may require a host, with the smallest known host free organism being Mycoplasma genitalium, with 521 genes. Then we started seeing how many genes we could remove from M. genitalium and have it still work and got even smaller genomes.

Carsonella ruddii works in a symbiotic relationship with its host, it can't exist without its host. But I don't want to sound too dismissive of this information. I admit that this is an interesting find and a point for the Darwinists. However, I won't really start to believe in life arising by a combination of chance and necessity until see life based on a paradigm of 5 amino acids which form proteins no longer than 10. And can function with 10 genes, that would be odds of 1 in 10^80 which is not really reasonable but it is certainly more reasonable that 1 in 10^40,000. Essentially your atheist faith is relying on a hopeful monster: you're just waiting for an organism with a set of 5 amino acids, that forms proteins of 10, that has a set of 10 genes. This certainly will not be found in our lifetime.

We can also create entirely artificial DNA and boot up life with it.

Right, a pure act of ID

This is not life as we know it, but it reproduces and evolves on its own, with nothing but food like all life needs. These were just enzymes that only had a 30 bit information channel, smaller that some of the sentences I tested Weasel with. Yet:

"Most of the time they breed true, but sometimes there is a bit flip a mutation and it s a different replicator," explained Joyce.

I get the feeling that you're not even aware of ID arguments. Do you read ID literature? Anyway, I don't have the tools necessary to understand the RNA world hypothesis, nevertheless I will quote from people who do:

In vitro RNA selection does not demonstrate that complex ribozymes could have arisen naturally in a prebiotic soup, because the in vitro experimental conditions are wholly unrealistic, revealing at every turn the fingerprints of intervening intelligence. RNA World researchers have taken their own engineering of ribozymes as analogous to plausible prebiotic processes, when in fact the two situations are profoundly different. Indeed, aspects of ribozyme engineering, together with other lines of evidence, support a very different view of biological origins from that advocated by RNA World researchers.

http://www.arn.org/docs/odesign/od171/ribo171.htm

If you want to continue to debate the RNA world then I suggest you find someone more competant than myself to do it with, because I as yet do not understand it fully. Stephen Meyer has a whole chapter devoted to critiquing the hypothesis in the Signature of the Cell. I suggest you read that chapter, if not the whole book.

So your claim that 1600 complete genes are "required" for NS to start is totally wrecked.

I did not put the figure at 1600, rather between 500 and 1600, though I'm aware that ID proponents accept the 200 figure, which is still gives us odds of around one in 10^40,000.

NS needs zero complete genes to get started.

unlikely. I doubt even passionate Darwinists would support that claim.

You are essentially claiming that life needs to start with a certain amount of complexity, involving any number of complete genes. I demonstrated above that NS can start without a single gene. It's not considered life, because it doesn't have cells and genes, but there is absolutely no reason to presume NS didn't start well before life developed. In fact, that NS started before cellular life is normally the only reasonable assumption.

You did not demonstrate above. You quoted a flawed experiment by Joyce.

There are very many regions of the genome which scientists call ultraconserved regions. (even some areas of the non-coding DNA is very well preserved). I don't know the exact number of how similar these 500 immortal genes are but 60% is a good working number. If we were to hone it to somewhere between 40 and 70% it would not change matters much.

Yes, many non-coding regions have functions, mostly as regulatory mechanisms of the coding regions. We know about these, we know how to measure them, etc. The level of conservation is even used to determine function, without having to know what that function is. Yet we can take them out of the organism, to create a new smaller organism, and it still survives just fine. Unlike the Irreducible Complexity claim, function can start out as accidents in non-functional DNA, but only have very minimal functionality. The functionality can then evolve to be more important. So even if part of this region we call non-coding is coding some function, it's still only comes to a small part of of non-coding region which is actually coding something. The majority, even with the strictest constraints on conserved regions, remain strictly non-coding. Yet that's pointless, as we can remove these non-coding regions, that are in fact encoding something, and the organism still works just fine.

It's true that we can take the non-coding regions out of the genome and the organism can function just fine. I think it's too early in our research of the genome to comment on what these are or what their implication is. Jonathan Wells has a book coming out on the subject soon which I encourage you to read

http://www.amppubgroup.com/press/discov ... -junk-dna/

Like the eyeball stating out as a slightly light sensitive patch of skin, and slowly becoming more functional. It's still has useful function even if it just senses the difference between light an dark.

Even genes for life admits that the simplest eye needs 202 genes to function. Getting 202 genes to coordinate is extremely difficult for random mutation to accomplish. If the odds of forming one gene are one in 10^100, than the odds of 200 genes all working together is one in 10^20,000

But I also want to point out that NS more often than not changes a Ford Mustang 98 into a Ford Mustang 97 (going backwards) by simply breaking genes.

Wrong, because when these backwards mutates happen, they don't generally live long enough to reproduce.

backwards mutations only work in desperate circumstances such as the existence of disease. For example, if malaria is killing everyone, and if one person can break their hemoglobin gene (syckle cell anemia) then the malaria can no longer set up shop in the red blood cell and kill the person. Once malaria goes away, that person, or race with the broken gene will soon die off.

There are only 25,000 genes in a human and although I find this hard to believe of those 25,000 20,000 are broken, psuedo genes that don't work anymore.

We haven't done this with people fore obvious reasons, but we strip out *all* these "psuedo genes" in many many different organism just to prove the organism is perfectly normal without them, and they in fact are perfectly normal without these "psuedo genes".

I'm not saying that it's not true that only 5 of the 25 thousand human genes work, I'm just saying that it's rather amazing.

We can even create 100% completely man made DNA, and boot up life with it, and they just as normal as natural DNA organisms.

The answer to this question will not be answered in our lifetimes.

You are replacing the notion of whole protein mutations with changing a "Ford Mustang 98" to a "Ford Mustang 99", but that's not how it works. If you start with a gene encoding protein X (Ford Mustang 98), and do a point mutation on a letter, you will never get a "Ford Mustang 99". What you will get is another "Ford Mustang 98" (protein X), but with a slighter stronger or weaker glue holding the rear view mirror on, or some other simplistic modification of the original "Ford Mustang 98". You would need lots and lots and lots of point 'letter' mutations to get a "Ford Mustang 99" from a "Ford Mustang 98", period.

This is a semantic dispute on when is a panther not a panther, so I'll ignore this.

Ok, you can get those odds, it does not mean that you can score off of them.

Easy, if I can "score off" 10^29, which I have, I can simply repeat the program 2000 times and that comes to 10^58000. ... I am perfectly justified in comparing the 2000 to simply running the Weasel program 2000 times, and get the 10^29 sentence every time.

Again, I must be misunderstanding something because if the odds of scoring a correct mutation are one in 10^29, then you will never hit it because there have only been 10^17 seconds in our universe's history.

Correct, very rarely random mutations can improve on an already existing gene, but it cannot build a gene.

Weird, the "Ford Mustang 99" (gene) is not merely an improvement on the "Ford Mustang 98", but a whole new Mustang with just a few common parts.

I would say it's barely a new mustang with many common parts. That's why I chose that particular car. It's like the difference between tigers and panthers.

A gene is nothing more than a "unit of heredity", regardless of how that heredity is encoded. Enzymes are created artificially and naturally all the time without DNA, and the non-life self replicating enzyme, referenced at the top, evolved without DNA. What is the "gene", or "unit of heredity", in that case?

A gene is a sequence of (in humans) on average 450 amino acids, though I understand that one gene does not equal one protein, rather one gene equals one polypeptide chain.

viruses aren't life they are just a mechanical device that feeds off of already built life. viruses cannot live without already built life. They are like a parasite that feeds off a car, they are not the precursors of cars.

So what if they feed off life, doesn't every living organism on Earth have to feed off of something? Don't try to goo without supper for too long. A viruses environment can simply do things our environment can't do for us, yet we need what our environment provides to protect and grow our young just like a virus. It basically lays eggs in our cells the way flies lay eggs in a dead carcass.

Phototrophs use the sun, organotrophs use other animals, lithotrophs use the earth. Some people use the words autotrophs and heterotrophs but I like the other words because their better related to their latin root. (I can read latin, sort of)

The mutations are binary, either they're beneficial or they're not. Of the 3.2 billion letters in the human genome very few are beneficial. I would like to hear from you how many of those 3.2 billion are beneficial and why.

No, there not binary, the "law of the excluded middle" does not apply. First off there is 3 choices, not 2. Good, bad, and neutral, but the "law of the excluded middle" doesn't even apply to those 3 choices.

The law of excluded middle does apply: beneficial means good, not beneficial means neutral or bad.

A mutation can be good in one way, while being bad in another.

Then it's neutral.

Common ancestry cannot exist without change of species. Evolution is a two point hypothesis: all that is needed to acount for ALL the diversity of species is one, natural selection, and two, random mutation. Where Darwin is wrong is that a third is needed: intelligence.

There's that intelligence thing again, like in the other thread. I could accept thinking about that if you could provide one reason to.

Very simple. What was the source of all information before 1953? Intelligence. What did we find in 1953, the DNA code, information. Therefore, DNA is constructed by intelligence.

If you can explain the me how a deadly mutation can be just as successful at having kids (while dead), as the good mutations i'll listen. But merely saying bad mutations are more common gets you nowhere. Are you saying that the best mutations can't have enough kids to make up for all the dead bad mutations.

No, what I'm saying is that because the number of bad mutations is so large, then the odds of getting a successful mutation are so low. Again, look at the histone H4, 102 positions, only 2 of them are neutral, all the rest are bad.

Remember, many less adapted organism could survive fine, if they didn't have to compete with better adapted organisms. And we understand how that works with nothing more than randomness. So why do you insist it needs more than randomness?

Intelligence can routinely select the right choice out of a set of 10^30, randomness can't.

Lenski's experiments documented loads of beneficial mutations, that even drove some of the previous organisms to extinction.

I'll read up more on the Lenski experiment and get back to you.

[my_wan]

Wan,

I appreciate you taking the time to answer my statements carefully. I enjoy debating with you and respect you as an opponent. I'm also glad that you stopped making subjective statements about the quality of my ideas, that always helps. Most of this debate is bogged down in side issues and many of the arguments I'm making now are simply repeats of old arguments so we're starting to say the same thing, which means this debate cannot go on much longer. However, I have identified some major areas of misunderstanding that really need to be cleared up.

It was predictable that that the debate would come back full circle, so I'll readdress those.

You said: "if there are 4 possible letters, A, G, T, and C (at a point mutation), then at least one of those 4 must be the best possible choice." In the histone H4 for example 100 of the 102 positions none of the mutations are beneficial, none are neutral, but all of them are deleterious. (I'm only talking about changes in the amino acid structure not the DNA, because amino acids is the only thing that matters). This is a very fundamental misunderstanding on your part. If you look at the sequence of the Histone H4 you seem to think that you can mutate any of it and that has a 1 in 4 chance of getting the best improvement. The histone either works or it does not. You can't improve on it.[/quote]
Let's suppose histone can't be unproved on (doubtful). So how is histone any different from the Weasel program after constructing the entire sentence, such that you can't improve on it? All mutations after that are bad? Yet keep running Weasel after the sentence is complete and you will see that bad mutations keep occurring, but is not conserved any more than anything was conserved while it was evolving to begin with.

So what your argument depends on is not that a *presumed* "perfect" can only mutate badly, but the claim that such mutations will build up in the population, wrong. Just as they will not build up in the Weasel program. We know that, due to genetic variations, some people are more prone to radiation damage than other. Yet the higher incidence of cancers and such in this subset of the population these mutations occurred in, these mutations will disappear from the population over time, only the be replaced by more bad mutations that'll start getting removed through disease. The healthy population will always be the majority if living organisms for this reason. Just like the Weasel program that keeps running after the sentence is perfect.

So one last issue to address is, does the *presumed* perfect gene sequences need to be perfect to be beneficial? No! Even those people we know to have detrimental mutations are still able to repair damaged DNA better than no repair at all. The only reason you are calling their genetic sequence less than "perfect" is because most people have an even better one. Even a tiny bit of repair is better than no repair. Yet you are calling 102 point mutation "one" mutation, wrong. That bad mutation would have been a good mutation, if everybody else's gene sequence was even worse. The less functional DNA (bad) sequences are still useful, and even preferential, to what came before. And what (now bad) came before provided an advantage that allowed those organisms to outcompete the ones that didn't have it.

So no, it's not just "one" mutation, and good verses bad is relative. The best gets the survival advantage, and the less adapted can survive just fine until something better comes along to outcompete them, and drives them toward extinction.

It just coils up the DNA so that I can fit in the nucleus. Let me give an example from language:

Would you tell me what colour that is

In the above sentence there is only one mutation that can be neutral, remove the u in color. Every other mutation destroys the sentence. There are 10^37 different ways to change that sentence, and only one of them results in a neutral mutation, everything else is deleterious.

So, you still presuming that the sentence "Woold you teel me waat colour that is" wouldn't survive without "Would you tell me what colour that is" to out compete it. Just like many people who do have bad mutation cannot repair their DNA as well as others. but can still repair some of their DNA errors. Just like the nylon bug is only 2% efficient, and these 2% bugs WILL become extinct when a mutation comes along that is better than 2% efficient. Just like the Weasel program.

So your 10^37 (rounded down without punctuations from 5.2*10^37) becomes 1 in 52 odds, just like the Weasel program. There is no such thing as either function or no function (law of the excluded middle). You start with very poor function, say 25 like the nylon bug, and continue to get point mutations (1 in 52 with your character set, 1 in 4 minimum with DNA character set) that adds efficiency incrementally. Histone is far from 100% efficient, and starting with the best sequence available at this time and claiming ALL point mutations are bad is a non sequitur, because that bad mutation was in fact a good mutation before the even better one randomly occurred, as that bad mutation still allowed some repair.

Do you admit that that is what the Ultra Conserved Regions of the genome are like?

No I don't deny that, but I do deny that before that last "point" mutation of those 102 existed to begin with it wasn't beneficial to have the other 101, or the other 100 before that, and so on. Because repair is beneficial even if it's not as good as provided by all 102. What makes a region "Ultra Conserved" is not something 'planned' by the mutations, but gets conserved after the fact because the organisms that didn't have them tend to die more than those that have all 102. We aren't running DNA test on all the dead people, or on the the kids of those dead people that never existed because their patents didn't live long enough to have them. That's the only reason it looks conserved, as we only do DNA test on people who actually exist. Yet still we find people in which these mutations are not conserved in, because the random mutations are still happening. Being conserved does not prevent or effect these random mutations, it only makes them more likely to die.

You also failed to understand the Sean Carroll quote that NS cannot repair genes, so why then do you believe that it can build genes? You wrote in response:
"Yes, less gene function is generally a one way street, one way to the grave. And since it's in the grave, it's doesn't spread in the population of living organisms." Of course less gene function leads to the grave, that is certainly not proof that NS can build a gene. To say: I don't believe NS can repair a gene, but I believe NS can build a gene, is just a pure contradiction. I can't learn anything from someone who makes such an assertion.

Your mixing populations with individuals. If an individual has a deadly mutation, then that individual dies, and the rest of the population continues without that mutation. Hence, NS repaired that mutation by killing that organism. NS has also evolved ways of repairing at least some damage, which is beneficial so that organism gets to live and have kids, and passes this repair mechanism along to the population. You can call dying not repairing it if you wish, but for the rest of the population genetics the problem is fixed. Just not fixed for the organism that died because of it.

I said: here's proof that NS cannot build genes
You said: broken genes kills organisms

Do you see how you did not answer my point?

I did answer, it fixed the bad mutation by killing it. While the rest of the population, without that mutation has babies to take their place. Yet, as I have pointed out, a gene that gives a 2% efficient function will survive just fine, until a mutation comes along that is more efficient. Then, due to competition, the 2% efficient organism can't continue surviving so well and will die off.

Your "proof" depends on the claim that, say histone for instance, needs all 102 sequences to work. Wrong, as we know some people don't have all 102 and still get some function from it, though not as efficient as all 102. So NS does NOT have to get all 102 point mutations to add beneficial functions. A mild 2% efficiency only becomes a disadvantage when 3%, 5%, 10%, etc., randomly comes along later and the number of points increases from few to many as this efficiency continues to increase. Claiming it needs all 102 just to have any beneficial function at all is just false, as pointed out that people with defective versions can still repair their DNA with less efficiency.

The point is the 3.2 billion letters are there right now, and to find the golden mutations among that sea of 3.2 billion letters is not something chance can do.

This depends on the same argument that histone needs all 102 point mutations to have any function. Right now it needs those 102 to be able to compete with organisms that have all 102, but if everybody only had 98 of them it would still be beneficial, and those with 98 would survive just fine until some random mutation produces 99 or 100, etc, that made that function even more efficient. That's why we do see the simple organism that once existed to show us exactly what process it took. And your pretending because these simpler organisms don't exist they never did. Like pretending a 2% efficient nylon bug never existed once a 10% efficient nylon bug drives them into extinction.

So no, NS cannot shuffle 3.2 billion letters and get anything meaning. It starts with something much much simple, that almost certainly doesn't even have cells or DNA, and slowly adds complexity bit by bit, or a few bits at a time in some cases. Then, as this complexity is added, the simpler versions get driven into extinction. Just like what happened to the original non-life self replicating enzymes I linked. Just what will happen to 2% efficient nylon bugs when more efficient versions come along. Just like what happen to better Weasel sentences when something even better came along with the Random() function.

This is wrong. The weak do not die out when something stronger arises. Look at cats, the littlest cats are still around, in spite of panthers and tigers. Look at fish: fish range from sharks to fish as small as 1cm. Look at snakes: anacondas have not rendered even the littlest snakes extinct. Life is teeming with numerous tiny creatures. Large creatures never obliterate the small. If predators eliminated their prey, then there would be no predators. Extinctions mainly occur because the environment changes not because a new species arises, though of course there are exceptions: just look at all the species homo sapiens have eliminated, though even there man has eliminated species not by methodically killing them but by ruining their habitat.

And in what way do you suppose big cats compete with little ones. Is a tiger going to waste energy chasing mice, no. Is a little house cat going to hunting on the African plains? I don't think so. To keep even one big cat from driving another big cat into extinction, they take different ecological niches, hunting styles, terrain, strategies, etc., etc. Hence they do not even have the same habitat, even when you see them together. The extinction effect requires a common ecological niche, like nylon bugs in the same food medium, cats with the same hunting styles and terrain of choice, etc. It's basic ecology. The existence of something in north America is not going to drive something in Africa to extinction, and the same rules apply to different ecological niches in the same habitat.

Big fishes generally need little fishes, meaning that if they start driving their food into extinction then they start starving themselves, giving the little fishes a chance to survive again. So you can't drive you food source to extinction without also driving yourself to extinction, which then allows your food source to thrive again. This is a well known cyclic effect. Just look at the boom bust cycle that occurs between rabbits and foxes, wolves and deer, etc. Predation is actually part of keeping the system healthy and stable. Just research the damage Elk have done to habitats in the western US, due to the lack of Wolves to eat them.

To prevent extinctions, different animals must take different balancing niches, in which they are all dependent on each other. Even Elk populations depend on Wolves eating them to keep the Elk populations and their habitat healthy. Just because you have two cats does not mean they depend on the same ecological niche, even when they live in the same habitat. Compare lions and leopards in the same regions in Africa. It's quiet easy to distinguish their habitats or niches, so they both can survive even though they both go after the same game to a large extent. They certainly couldn't do this if they tried taking the same ecological niche.

If you have multiple food sources in the same petri dish, or predation on one or more of the organisms, many different organisms can live within a self balancing ecology. It's works as if the different groups was part of a larger organism, working together to maintain a balance. Yet let one, in one particular niche, get an advantage on its own species, and you'll see the original population of that species get replaced with the new variant. Same thing happens in your biology, when gain a new genetic advantage that makes certain other beneficial mutation obsolete, like hair on people after we started making our own to use whenever we needed it.

***************

Side issues:

Carsonella ruddii works in a symbiotic relationship with its host, it can't exist without its host. But I don't want to sound too dismissive of this information. I admit that this is an interesting find and a point for the Darwinists. However, I won't really start to believe in life arising by a combination of chance and necessity until see life based on a paradigm of 5 amino acids which form proteins no longer than 10. And can function with 10 genes, that would be odds of 1 in 10^80 which is not really reasonable but it is certainly more reasonable that 1 in 10^40,000. Essentially your atheist faith is relying on a hopeful monster: you're just waiting for an organism with a set of 5 amino acids, that forms proteins of 10, that has a set of 10 genes. This certainly will not be found in our lifetime.

Yes, but there is no animal that doesn't require something that acts like a host in many ways, even if it's just the solar output from the sun, soil chemistry, or some sort of food and energy source. We all require Earth and its life as a host in some ways.

We can also create entirely artificial DNA and boot up life with it.

Right, a pure act of ID

No argument here, but why didn't you address the argument, rather than the extending factoid added for completeness?

I get the feeling that you're not even aware of ID arguments. Do you read ID literature? Anyway, I don't have the tools necessary to understand the RNA world hypothesis, nevertheless I will quote from people who do:

In vitro RNA selection does not demonstrate that complex ribozymes could have arisen naturally in a prebiotic soup, because the in vitro experimental conditions are wholly unrealistic, revealing at every turn the fingerprints of intervening intelligence. RNA World researchers have taken their own engineering of ribozymes as analogous to plausible prebiotic processes, when in fact the two situations are profoundly different. Indeed, aspects of ribozyme engineering, together with other lines of evidence, support a very different view of biological origins from that advocated by RNA World researchers.

http://www.arn.org/docs/odesign/od171/ribo171.htm

Oh, I am very aware, and your not doing yourself any favors going there. Since you aren't proclaiming any particular proficiency, I'll just just point the fundamental issues with your link. It is true that many such experiments involve extremely open ended presumptions about initial condition (early Earth), and the notion that many of these long purification sequences represent realistic early Earth can be as convoluted as very complex organisms happening all at once by accident. Not always very realistic. So I'll give you this argument with respect to the "rational design" approach mentioned. However, we do know that a simply reducing atmosphere with some electrical discharges produces many of the amino acids naturally, without any DNA. We know you do not need DNA to get these amino acids, which can even be found on meteors that never came in contact with Earth. So what is this paper claiming about the The "irrational design" approach?

So the existence of these chemicals is a well established natural phenomena, independent of anything requiring a lab or life to produce. It says these "partially randomized RNA molecules, which are screened -- "selected" -- for functional activity of a desired sort." You can call these RNA snippets "partially randomized" if you want, but the fact is that these RNA snippets are a natural part of the non-life environment. What about the "desired functional activity"? Naturally you are looking for 'self replication' where it's never been seen before. Thus falsely implying that desired result is somehow having the chemist tell the chemicals how to act. False. A chemist only learns what chemistry does, and can't define what chemistry does. The rules of chemistry can't be changed by a chemist!

Now for the elephant in the room, "selected". NS "selects" what life exist, not by selecting what lives, but by the environment "selecting" what dies without reproducing. So when a self replicator spontaneously shows of in this chemical soup, a soup that we already know is a natural part of the non-life environment, "selected" merely means letting them self replicate per NS. So this "selected" in this article as if "selected" means not NS. In fact NS REQUIRES selection, just not an intelligent selection, much like the chemist was initially ignorant of the chemical process that created it, and NS is ignorant of which mutations will survive and which will dies till after they either die or have kids. NS *IS* a "selection" process, just not an 'intelligent' "selection" process, and this article pretending otherwise is totally bogus.

If you want to continue to debate the RNA world then I suggest you find someone more competant than myself to do it with, because I as yet do not understand it fully. Stephen Meyer has a whole chapter devoted to critiquing the hypothesis in the Signature of the Cell. I suggest you read that chapter, if not the whole book.

So your suggested reading material is from Stephen Meyer, whos "prayers" convinced him to devote his life to "destroying Darwinism"? Even with his book "Icons of Evolution" completely and totally destroyed with empirical factual data, I still have my ears open for any arguments he can propose that ask interesting questions. Yet all I'm seeing from him is the same, if it was a bad mutation that killed this one individual organism, it must be bad news for the whole population. No it was good news for the whole population that that dead individual can't effect the genetic makeup of the whole population. Why? Because it's dead or dying!

I did not put the figure at 1600, rather between 500 and 1600, though I'm aware that ID proponents accept the 200 figure, which is still gives us odds of around one in 10^40,000.

Ok, but my same argument applies even if it's only 100. You still can't pretend that all 100 is needed to have NS. The effective "genes" (in a stricter sense of its definition), of the self replicating nonlife enzyme I linked, consisted of a 30 bit channel. Since that is a base 2 system, that a 1 in a billion chance (1,073,741,824). So if you have multiples trillions of chemical reactions occurring in any given second, on any given planet, then such a reaction *must* naturally occur sometime, somewhere, period, with a probability of essentially 100%. This is all NS needs, which can then use NS, and other random accident, to increase complexity.

It's unlikely, and apparently too restricted, to assume this is the right starting process for life on Earth. But the fact remains than NS has been demonstrated with *only* a 30 bit information channel. There's also no reason to presume an accidental swap of a base element will not lead to extra valence bonds that increases the information bandwidth of these self replicators. Life almost certainly didn't begin with a full cellular structure as seen today.

NS needs zero complete genes to get started.

unlikely. I doubt even passionate Darwinists would support that claim.

It's already been demonstrated, in the link I provided. You do not need life to get NS. Life, as we define it, needs genes and cells, NS does not. And as long as you have NS, then you have a mechanism to allow life to evolve. Assuming you must have life, as we define it, to have NS is wrong.

You did not demonstrate above. You quoted a flawed experiment by Joyce.

Note my rebuttal above, concerning the term "selected" in the "irrational design" approach your linked article stated? In fact you are now claiming that it is flawed because "selection" was involved. Yet NS *IS* a selection process. Joyce's enzymes *are* in fact self replicators which evolve per NS, even if the information channel size presently appears stuck at 30 bits. "Selection" is not a "flaw", it *is* what NS is. The chemist neither knew it would "go critical", or has any say so whatsoever in the chemical laws that made it "go critical".

But even if we suppose this is ID as you claim. What are the odds of it happening by accident. Well, it has a 30 bit base two information channel. That gives odds of 1 in 1,073,741,824. Given that the number of non-life chemicals undergoing a reaction at any given time dwarfs a billion, the odds of some form of NS is essentially 100%. But even if we take this as 1 in a billion per planet per billion years, life in the galaxy is essentially a certainty. Even more so for the entire Universe. There's about 100 billion stars in this galaxy alone, and even more galaxies than that. So even one in a trillion is essentially a certainty that life will happen naturally.

So your 10^40,000 odds is wrecked, even if Joyce's enzyme is entirely and completely a product of ID.

It's true that we can take the non-coding regions out of the genome and the organism can function just fine. I think it's too early in our research of the genome to comment on what these are or what their implication is. Jonathan Wells has a book coming out on the subject soon which I encourage you to read
http://www.amppubgroup.com/press/discov ... -junk-dna/

Now you back to the guy whos prayers told him to ""destroy Darwinism", and linking directly to the Discovery Institute to boot. In fact he said that "destroying Darwinism" was his motive for studying Christian theology at Yale in the first place. So he made up his mind what the truth was, went to seminary (not biology) to justify it, and now writing books to that effect. What doe he have to say about the age of Earth:

I think the earth is probably four-and-a-half billion or so years old. ... But the truth is I have not looked at the evidence. And I have become increasingly suspicious of the evidence that is presented to me and that's why at this point I would say probably it's four-and-a-half billion years old, but I haven't looked at the evidence

So even hasn't even looked at such basic evidence.

Yes, I do read these peoples work. Want some humor? Read the court minutes of the Kitzmiller trial. Behe, in that trial, even admitted to the judge that "astrology" was science.

"I kind of feel like Zsa Zsa Gabor's fifth husband. As the old adage goes, I know what to do, but I just can't make it exciting."

Even genes for life admits that the simplest eye needs 202 genes to function. Getting 202 genes to coordinate is extremely difficult for random mutation to accomplish. If the odds of forming one gene are one in 10^100, than the odds of 200 genes all working together is one in 10^20,000

What is this "genes for life" you keep referring to? And give me some reference to this claim. The PAX6 is not just responsible for eyes, but is a control gene for all sensory organs. So here you have a variant of the same gene used for touch, so this gene and its variants has a function even without eyes. Give me some reference and I'll address the 202 gene coordination more fully, but the fact is this same gene in reused over and over again for lots of functions other than eyes. What about the "mutations" of this "same" gene that provides other functions?

backwards mutations only work in desperate circumstances such as the existence of disease. For example, if malaria is killing everyone, and if one person can break their hemoglobin gene (syckle cell anemia) then the malaria can no longer set up shop in the red blood cell and kill the person. Once malaria goes away, that person, or race with the broken gene will soon die off.

Here you say "that person, or race with the broken gene" as if they are the same thing. No, the race will not die off just because the gene is "broken". If they did, then it wouldn't be an advantage for surviving malaria!!! Listen to your own words here!!! You are saying that by making a deadly disease go away, the "bad" mutation that made it possible to survive this deadly disease will wait till after the deadly disease becomes extinct to kill everybody!!!! If the mutation is going to kill everybody, why would it wait on a deadly disease to go extinct to do so?!!!!!

We can even create 100% completely man made DNA, and boot up life with it, and they just as normal as natural DNA organisms.

The answer to this question will not be answered in our lifetimes.

Already been done:
http://www.impactlab.net/2010/05/21/art ... irst-time/
It's merely (mostly) just a copy of life we already know, yet every piece of DNA it contains is manmade in the lab. No living DNA was used. They even used the equivalent of “watermarks” in the artificial DNA to show it was entirely man made. It was injected into a cell with no other DNA present and it low lives.

Not in our lifetime? You massively underestimate what were doing!!!!!

This is a semantic dispute on when is a panther not a panther, so I'll ignore this.

But wait. YOU said that a good mutation requires the whole panther, whole protein, whole gene sequence, etc., etc. Though it's hard to pen down exactly which as I have allowed you to use the word "gene" in a very general sense, while you keep using it interchangeably with protein, cars, etc.

Yet you still have not acknowledged that two panther have any number of point mutations that can both be good and bad, while they remain panthers. In fact you average around 60 mutations, about 30 from each parent, from your parents. That's 60 genetic difference that you go from neither of your parents. That would help explain why many pregnancies never last long enough for the woman to ever even know she was pregnant, but why aren't you dead if they are always so bad?

Again, I must be misunderstanding something because if the odds of scoring a correct mutation are one in 10^29, then you will never hit it because there have only been 10^17 seconds in our universe's history.

Yes, you are missing something. The point. The 10^29 is the odds of shuffling every gene in the entire sequence randomly and getting a functional organism. But NS works by making only tine changes to individual letters or small groups of letters. Hence you can have a million different versions of the same protein (panthers you refused comment on), and every one of them will work. Only some will will work better than other, and the ones that work better tend to stay alive in the population longer. Many protein variants that don't work so well for one thing, will turn out to be and improvement somewhere else.

Your still falsely pretending that a "mutation" involves "whole" proteins and other such wholisms. A mutation in a protein does not mean you will get a new protein (panther), but merely another variant of the same protein with a little more efficiency for some thing or a little less for other functions. Protein function is not something that either gets turned on or off with different variants of the *same* protein. The variations mere lead to varying efficiencies for this or that function.

I would say it's barely a new mustang with many common parts. That's why I chose that particular car. It's like the difference between tigers and panthers.

So, since you have approximately 60 genes that didn't come from either of your parents, but came from mutations, does that mean you are a different model of human that your parents was? Even the efficiency with which some of your proteins operate is different from either of your parents, but it's still the same protein, and you are still the same kind of human. Tigers and panthers are not the same kind of cat.

So quit pretending that a mutation of a gene that makes a protein makes it a different kind of protein the way tigers and panthers differ. Such mutations often only changes efficiency, if anything at all, not protein types. Or other whole genetic sequence constructs. The function is *NOT* either turned on or off, many in betweens exist at different efficiencies.

A gene is a sequence of (in humans) on average 450 amino acids, though I understand that one gene does not equal one protein, rather one gene equals one polypeptide chain.

Here is a gene segment:

Now, we are talking about "mutations". When a point "mutation" occurs the whole "gene" does not change. Rather one of the four bases change, Adenine, Guanine, Thymine, or Cytosine (A, G, T, or C). There are no other changes that occur in a point mutation. Hence the proteins created by a sequence of these these point mutations is still generally the protein. But you keep talking (giving odds) as if ALL the bases were randomly shuffled and ended up with a new functional protein, wrong. Point changes (mutations) occurs only at individual bases, which doesn't tend to produce new proteins. On slight variants the way you are a variant of your parents, containing DNA sequences that came from neither of your parents (about 60 differences).

So you can't talk about whole proteins, or even whole polypeptide chains, as if they are a single mutation!!!!! Or gives odds as if only one of those variants actually works!!! There are millions of different variants of a given gene that gives the same function, just with different variation in efficiency. Point mutations operate at the level of single letter, not genes. Though the latter can occur in some cases also, they are not point mutations.

The law of excluded middle does apply: beneficial means good, not beneficial means neutral or bad.

So what happens when a mutations that will kill you 25% of the time, but give you a 60% chance of surviving a disease that is going around your species? Oh yeah, you said above it would save peoples lives, then if the deadly disease went extinct the same thing that saved everybody who lived would suddenly go extinct..

The fact is whether or not something is beneficial or not depends on the environment you have to survive in, and DNA doesn't pick, nor can it plan for that environment. It only allows you to be born because you parents at least survived long enough to have you. So it must be good enough at that environment for your parents to do that.

A mutation can be good in one way, while being bad in another.

Then it's neutral.

Wrong. In one environment a mutation might kill 25% of people who have it, but give a 60% chance of surviving a disease that other people will mostly die from. So whether or not this is a good or bad mutation depends on what diseases you will be in danger of contacting. Domestic dogs have evolved a lot of traits that only help them get food from people. Yet few of these dogs could survive in a world without people. Why are we such wimps compared to many other large animals, not because being stronger is a bad mutations, but because being smarter is a better mutation, and the energy spent on getting strength from food is better off feeding the energy demands of the brain.

Not even function is either on or off. Why can't we smell as well as a dog? Why can't a dog smell as well as their parents? These are all mutants, which didn't turn smell off, but merely changed the efficiency of smelling.

Very simple. What was the source of all information before 1953? Intelligence. What did we find in 1953, the DNA code, information. Therefore, DNA is constructed by intelligence.

So when Pluto was discover by intelligence in 1930, that means Pluto was created by intelligence? Above you say mixing some natural chemicals in a dish is an intelligent act by chemist, so the chemical reaction must be the result of the chemist intelligence (ID). So was Pluto the intelligent creation of the astronomer?

No, what I'm saying is that because the number of bad mutations is so large, then the odds of getting a successful mutation are so low. Again, look at the histone H4, 102 positions, only 2 of them are neutral, all the rest are bad.

And that is exactly why I ask you to look at the Weasel program more close. Yes, the number of bad mutations is larger, but so is the number of dead people who never had kids compared to the live who did. When 1 person fails to live long enough to have kids, then that leads to thousands that never existed because of it in the fairly near future. Are you counting all those dead and would have but don't people when you see so few bad mutations in living people? Are you counting the 70%+ of pregnancies which are miscarried? That billions and billions of people that would have existed but don't, because evolution is a random lottery and they win. Hundreds of million of times more people than ever existed throughout history were never born because their parents didn't win the evolutionary lottery. Are you counting them when you you go: Well umm how come not everybody is dying . They are, and if you go into the future far enough, and people don't go extinct like most other animals have, and still restricted to earth, then only one female and one male from today will be a direct ancestor of everybody alive for some point of time the future.

Why didn't the roughly 60 mutations you have, that you didn't get from your parents kill you? Are you counting the 2 or 3 people that didn't make it through pregnancy when you count how lucky you are? It's the only *real* way to count all these bad mutations, by counting all those who don't exist.

Intelligence can routinely select the right choice out of a set of 10^30, randomness can't.

See, you still ignoring that randomly shuffling a 10 character set and randomly laying out the sentence "Me thinks it is like a weasel." has odd of 10^30. But see, life doesn't need the whole sentence, life only needs a tiny percentage, like the 2% efficient nylon bug. So even one letter "Mx_xxxxxx_xx_xx_xxxx_x_xxxxxxx" is over 3% efficient, which is more than what the nylon bug needs right now. NS needs even less than life does, even for chemistry. Yet you even responded to this crucially important point above by saying: We'll that just asking when a panther is not a panther so I'll not bother with an answer. So when id protein X not protein X? If you have two versions of protein X, one at 2% efficiency, the other at 5% efficiency it does not makes it a different protein, only a different variant of the same protein like the different panthers. Not a panther and a lion.

I'll read up more on the Lenski experiment and get back to you.

You also need to figure out why it is that Weasel does not have information about the sentence, only the "Random()" function provides Weasel with all information it uses and why evolution does not need to code a singular protein variant sequence all at once, because a protein (or polypeptide) sequence which is different is still often the same protein with the same functions, just with different efficiencies.

You would be better off going back to the original language thread, as you are only hiding the same argument behind evolution, while mistaking whole proteins as something *point* mutations create.

[GenesForLife]

Even genes for life admits that the simplest eye needs 202 genes to function. Getting 202 genes to coordinate is extremely difficult for random mutation to accomplish. If the odds of forming one gene are one in 10^100, than the odds of 200 genes all working together is one in 10^20,000

Can you demonstrate where exactly I said "The simplest eye needs 202 genes to function"?

In which logically consistent universe is

"The article is plain wrong, Chlamydomonas reinhardtii, which has NO pax6 , has an eyespot which can regulate movement towards light in the absence of a nervous system, requiring the involvement of just 202 genes." which was demonstrated to pooh-pooh your assertions of eyes requiring thousands of genes in this thread http://www.rationalia.com/forum/viewtop ... 2&start=60 equal to what you said that I admitted? You have been reported for quote mining.