spinoza99 wrote:I'm going to really focus on the central thesis and let the side issues drop. That way we can quickly bring this debate to its conclusion, however, I basically made all of these points before, I'm just restating my arguments and you're not accepting them so I probably won't be continuing this debate. Here are your mistakes:
Fair list of basic issues to debate. It's not that I'm simply rejecting your arguments, I'm trying to explain exactly what is wrong with the actual arguments you provided. Hence I'm not rejecting your arguments by ignoring them, I'm testing your arguments against the observable facts, and the observable facts illustrate exactly *why* you are wrong. So rather than just presume that because I said something different I must simply be disagreeing, look at the reasons why. Because without those observable empirical facts, I would have nothing more than a personal "belief". Personally, the only reason I would debate my personal "belief" of anything is in the hopes that someone could offer the empirical evidence to support or reject it. Yet my argument here is not a "belief", but empirically verifiable facts.
spinoza99 wrote:1. The Richard Dawkins eye fallacy: "a 1% eye is better than no eye at all." The thing is a 1% eye itself is too complex to be achieved by chance alone. The simplest eye that we know of is the Chlamydomonas reinhardtii for which so far 202 genes have been identified:
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1533972/
We developed a procedure to purify the eyespot apparatus from the green model alga Chlamydomonas reinhardtii. Its proteomic analysis resulted in the identification of 202 different proteins with at least two different peptides (984 in total).
Lets compare this to the nylon bug, to show why 202 genes is not a big deal. The nylon bug gene responsible for consisted of ~400 base pairs (not 202 genes). Yet not only did the 400 base pairs work, all the other proteins involved with metabolism also worked, without modification, to also metabolize this new nylon product. So in fact there are many many more than one 400 base pair gene involved in nylon metabolism. So, by your logic, not only was 400 base pairs too unlikely to be "achieved by chance alone", all the other preexisting genes for carbohydrate metabolism also work for metabolizing nylon, even though these same unchanged proteins did not evolve for metabolizing nylon products. Point mutations, leading to different alleles of these genes will almost certainly improve that 2% efficiency over time.
So the mistake is in assuming that one particular gene sequence is need for one particular function. The same genes, other than the one that mutated to break down nylon, in the nylon bug, to process carbohydrate byproducts also works unmodified to process nylon byproducts. Essentially all genes have untold countless numbers of different functions, and just because it has a particular function in a particular instance does not mean an entirely new gene is needed for a new function. Not only is there untold countless numbers of different functions for single genes, there an extreme number of different alleles of that given gene which changes the efficiencies of the functions it is capable of.
Now let's compare this to the 202 proteins in the flagellate green algae involved in the eyespot apparatus. Just because these 202 proteins play a role in eyespot functioning does not mean the functions of same proteins would not still be needed without any eyespot at all. Just like all of the different unchanged proteins used by the nylon bug for metabolism, which now also function to process nylon byproducts. Hence only some very small changes to preexisting functional proteins are needed to add a functional eyespot to the flagellate green algae. Evolution did NOT have to create 202 brand new proteins just to get an eyespot, because those proteins evolved for other functions besides eyespots.
Compare this to the PAX6 gene, which the mouse version or allele of this gene will trigger eye development in fruit flies. This same gene, and alleles of it, is a control gene for other sensory organs and other functions. So evolution didn't have to evolve this gene for sight. It merely had to switch the locus of a preexisting gene sequence to get eye function, rather than the function it evolved for. It then continues to evolve alleles that continued improving eye functionality.
spinoza99 wrote:Ok, NS can not build 202 genes with the knowledge that they would eventually work together. That requires foresight, which is something NS does not have. I'm very skeptical however that you will be able to understand that.
Exactly, NS cannot build genes with "foresight" of the function it will be used for. I also understand that this "foresight" or "intelligence" is what you thesis depends on, which you then presume 202 genes supports this "foresight" thesis. I'm merely trying to explain why it doesn't. And the reason is that those 202 genes didn't have to be those 202 genetic sequences to get the same function, with various efficiencies. Hence countless millions of of different combinations, not just the sequences in those 202, would also work to provide those functions. As evolution continues, and better efficiencies are achieved, then fewer combinations are possible to get that same efficiency. So high efficiency organisms will tend to revolve around a fewer high efficiency sequences, but these high efficiency low probability sequences must come from inheritance rather than accidents.
spinoza99 wrote:2. The fallacy: because NS can get rid of bad mutations it can therefore build new genes. What you are doing is looking at NS's ability to junk a poorly functioning car and saying: see, NS can build cars. This is wrong. This is exhibited with your reply to the Sean Carroll quote.
I said: here's proof that NS cannot build genes
you said: NS can discard defective genes
No.
You say: Mutations are bad, so NS cannot build genes.
I say: Mutations many get bad mutations and die off, others get neutral and good mutations and live, while the good mutations build up, even though they are more rare, while the bad ones simply die off leaving the resources for to good ones to continue.
spinoza99 wrote:You essentially said that with: "NS repaired that mutation by killing that organism." Discarding bad genes is not building genes.
It didn't "repair" it, it removed it from the population of self replicators, so these bad mutations do not continue to self replicate. But the neutral good mutations do continue replicate, and those good mutation replications, although more rare, will replace the population losses from the dead bad mutations. That's why I brought up how 70%+ of all pregnancies are miscarried. That doesn't prevent successful pregnancies.
spinoza99 wrote:Next you basically said Sean Carroll was wrong with: "NS has also evolved ways of repairing at least some damage," and there is no evidence for that. You're just looking at, say, the editing system in the nucleus which edits false transcriptions and saying: look, NS did that. This is essentially Darwin of the gaps, you don't know how the editing system arose so you assume NS did it. I, on the other hand, recognize the need for foresight in the construction of it, so my argument is not an argument from ignorance, yours is.
I did not say NS repaired the damaged DNA, I said that NS evolved the mechanisms to repair some of the DNA damage you acquire over your lifetime. You are not evolving. Once your received your share of mutations at the time you were conceived, that's it for you. The only way NS will continue is for you to have kids, replicate. Then those mutations the kids receive at birth is the mutations define NS. Most will not make it, just as 70%+ of pregnancies are miscarried, but the ones who do will replicate and replace the ones who don't. Once you are gone without kids, it's up to other people to replicate to fill in the population losses.
spinoza99 wrote:3. not understanding the binary nature of functioning.
You seem to think there is some law of excluded middle which prevents anyone from building dichotomies. This is wrong. Either an organism reproduces or it doesn't.
This binary function ONLY works for what actually happens to a particular organism. Consider two separate populations of a particular species with functional genetic differences, but each population is exactly identical (clones) of each other. Now any individual will either replicate or die before replicating (binary). However, population A may have 25% die before replicating, while population B will may have 35% die before replicating, as a direct result of the genetic differences. Yet both populations, so long as they remain separated, will still replicate enough for the population to survive. If you mix the populations to create a single population, the 75% group will overtake the 65% group over time, but the whole population still continues to survive.
Hence the whole population is NOT binary, even though the individuals are. NS is NOT binary, because it only describes what happens to the whole population. That's why I keep telling you that you can't say that just because a bad mutation occurred in some individual that kills it means that this mutation will kill the whole population. Mutations do not occur in whole population, only individual at conception, and the only way for this mutation to spread throughout the population is if that individual has kids, that has kids, that has kids, etc., till those descendants eventually take over the whole population. Meaning everybody else's kids didn't make in somewhere down the line.
spinoza99 wrote:Several protein sequences will result in the organism not passing on its genes. You, on the other hand, think that even if a sequence is 1% functioning, then it will still pass on its genes 1% of the time. This is wrong. This is the central problem with Dawkins Weasel program. He thinks that the change of one letter will result in the organism being preserved.
So what if a protein sequence does prevent an individual organism from passing on its genes? It just means somebody else's kids, with better mutations, will have the kids to keep the population alive. Which means that mutations can't kill the population.
The Weasel program is even more linear than NS involving DNA. It's not a one letter change that allows the organism to be preserved. It is being able to eat more of the food sentence that allows survival, leaving those less able to eat the food sentence to starve to death. Many spiders depend on this mechanism, where the more food they catch the more young they create, but catching the food reduces the food available for others to catch. So even one extra bug, due to a protein allele involving a single DNA letter making the add an extra web rung, or a greater preference for night lights, can drive the local population to consist of primarily that one spiders offspring.
spinoza99 wrote:On the contrary an immense amount of parts have to be in place in order for an organism to begin to survive. You seem to think that a chain of 10 amino acids can evolve into an organism with 200 genes. There is no evidence to support this. I have already stated this fact several times, so this will be the last time that I attempt to force you to understand that.
The problem with this claim is that an equally immense number of ways the parts can be arranged to still get the same function, with varying efficiencies. It is only the high efficiency functions, we see after 4 billion years of evolution, that are SEEM improbable if you mistakenly assume that these functions required the more precise high efficiencies from the beginning. But we know they don't, just like the nylon bug didn't.
spinoza99 wrote:4. The RNA world. Actually I do have the knowledge to critique your understanding of Joyce's experiment. The big problem with these experiment is the right-handed amino acids. Life only uses left-handed amino-acids.
So, I continuously referred to them as "non-life", and it's perfectly possible for people and all life to exist with right-handed amino acids. We only use left-handed amino-acids because that's what our surviving ancestors used, and we inherited. It, as you say below, is merely a 50/50 random shot whether or not people evolved with left or right-handed amino acids, and we stay that way because we inherit the amino acid handedness from our parents.
What you are totally avoiding is how their evolution does exactly what evolution predicts, and refutes your claims about bad mutations.
spinoza99 wrote:That right there should tell you something, and the ratio between them is 50/50. So the first thing an origin of life researcher does is try to get rid all of those obnoxious right-handed amino acids.
But wait, your criticizing Joyce's experiment for NOT getting rid of them. Yet in the same breath accusing researchers of getting rid of them. See why I don't see these criticisms as being a very honest representation of the actual empirical lab results? It sounds to me like accusing researchers of whatever you want to accuse them of in order to claim whatever you want about the results.
Above you are rejected results because they did NOT partake in ID, or forcing what you want to happen. That's the whole idea behind Joyce's experiment, randomize everything from perfectly natural non-life chemicals and see what spontaneously happens on its own. So your accusing researchers of doing something you rejected their results for not doing. While pretending that random amino acid handedness we inherited requires a guarantee of the handedness must be what we inherited from a random event to be admissible.
All the while totally ignoring the way these spontaneous self-replicators evolve with new and better versions driving the originals to extinction, in spite of most mutations being bad, and the more numerous bad mutations dying off, exactly as NS predicts. Exactly as the Weasel program does. All without any researcher choosing what lives and dies. The same empirical data we see when we watch cultures of actual life evolve in the lab. Why has this empirical data been ignored, only to accuse researchers of doing what you accuse Joyce of not doing?
spinoza99 wrote:Second, amino acids form other bonds other than peptide bonds, but only peptide bonds are used for forming life. That's another thing the origin of life researcher tries to get rid of. So right there INTELLIGENCE is manipulating nature to form a result. When you write: " 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!" that's certainly true, but the chemist also, with his intelligence, manipulates the situation to get the results he desires. That's not spontaneous generation.
So here are are back to accusing researchers of manipulating what you accused Joyce of not manipulating.
Could peptide bonds be because those first chemical reactions that formed bonds other than peptide bonds failed to self replicate? Oops, bad mutation, you die. So now the stuff still left to replicate uses peptide bonds. Duh... It's like saying because we are not dinosaurs that dinosaurs can't ever have existed.
spinoza99 wrote:5. The Nylon bug. I'm glad you gave more information on this because you have shown me that this is the classic breaking of genes which become beneficial because of extraordinary circumstances. In this case, a gene was broken, i.e., no longer being able to eat carbohydrates so it then could use nylon to survive. This is the classic Darwinian fallacy which can be summed up as follows: "NS can destroy a bridge, thus preventing an enemy from attacking it, therefore, it can build a bridge."
So breaking the "bridge" to the carbohydrate food didn't build any "bridges"? So I guess the "bridge" to nylon food is just a figment of our imagination? This is getting sillier by the minute.
No. We do not say NS builds "bridges" because it can destroy bridges, we say NS builds "bridges" because we watch it build "bridges" in exquisite detail, the same way we watch in exquisite detail as the more numerous bad mutations dissolve from the populations with each generation of living organisms in the lab.
Get this straight: This is not a claim based on watching the opposite, it is what we see directly.
spinoza99 wrote:6. Wrong math. "Notice how the three triple point letters CGA, CGC, and CGG all code for Arg? This means that many point mutations, swapping individual letters, have no effect on what the nucleotide string codes for. So the odds are actually better than the 1 in 4 I quoted for "point mutations"."
The question was not whether a mutation was better, but which mutation is the best. If it is already the best possible letter, then any equivalent letter, leading to the same codon, is not a bad mutation. Hence there's a much better than 25% chance that a point mutation will not be harmful, or even meaningful. Yet if you have a point mutation (A, G, T, or C ) in a codon that is CGT, and the best possible mutation is Arg, then you effectively have a 100% chance that a mutation of T will be a good mutation. Though, for a random mutation in the whole codon, it's still a 25% chance of getting the best mutation.
spinoza99 wrote:No the odds are not 1 in 4. Here's what you're doing wrong. Let's take the sentence: "We hold these troths to be self-evident." What are the odds of repairing the misspelling of "troths" by chance? You seem to think they are 1 in 26. They are not. Chance does not know which letter is misspelled. Therefore, the odds are 26 raised to the 39th power, since there are 39 characters. What you have to do is take how many mutations occur in the genome, let's say 20 in a genome 2 billion letters long, those 20 mutations can occur in any of the 2 billion letters.
Yes, and I showed above how for a given codon, it still come to a 25% chance of the best codon for a random whole codon string. Since codons are the informations carriers the sentence "We hold these troths to be self-evident.", needs to be broken up like "We ,hol,d t,hes,e t,rot,hs t,o b,e s,elf,-ev,ide,nt."where "rot" it the only one that contains a possible advantageous mutation. However, because all the other triplets have other letter that result in the same code (like DNA), even if the mutation occurs somewhere beside "rot" doesn't mean it's going to be a bad mutation, as it can also be neutral. The effect per codon triplet is what matters.
spinoza99 wrote:7. more wrong math.
spinoza99 wrote:spinoza99 wrote: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).
You're going to have to explain again how you got that 1 in a billion figure because it doesn't make any sense. I don't expect however that you will be more clear the second time.
The 1 in a billion odds is the result of 30 a bit information channel. A bit is binary so each bit has 2 choices like a coin. So the odds of 30 bits of information is the same as flipping a coin 30 times and getting all heads , i.e., 1 in 2^30 or (1,073,741,824).
However, it would be a mistake to assume this is the odds of Joyce's self-replicators spontaneously forming. For the same reason your 10^40,000 odds is mistaken. Why? Because the bit sequence that Joyce's spontaneously produced replicators had is not the only random sequence of those bits that would produce a working self replicator. If it was it couldn't evolve even better arrangements of those bits, as they actually did. In fact the 1 in the 1 in 2^30 odds presumes that "1" represents the only possible arrangement of bits for it to spontaneously self replicate. This can't possibly be true because many many other arrangements of those same bits also self replicate. Just like many many more than 1 of 10^40,000 possible arrangements of human DNA can also self replicate. If it was only that "1" possibility, then evolution, with or without intelligence, is not possible.
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side issues
spinoza99 wrote:my_wan wrote:spinoza99 wrote: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?!!!!!
Since you use so many exclamation points I suppose I'm obligated to respond. What I said was correct, I really don't see why you can't see it. Malaria kills humans by taking up residence in the red blood cells and feeding off of the hemoglobin. Sickle cell amenia basically renders the red blood cells dysfunctional therefore the malaria cannot feed off of it and therefore the human becomes immune to malaria, thus giving it an advantage. If the malaria were to disappear that same human would no longer be at an advantage but would be less fit due to its sickle cell disease.
Ok, maybe I misread this. We'll see. Yes, without Malaria AND once people without the sickle cell gene takes over the population, then people with the sickle cell will eventually die off. However, if everybody has the sickle cell gene, after malaria is extinct, then this gene is no more going to kill everybody off than it did before malaria went extinct. It's not the sickle cell gene that will kill them off, it is the inability to compete with the population growth of people without the gene that kills them. Same way Joyce's self replicators survived fine, until better replicators came along.
spinoza99 wrote:my_wan wrote: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?
I've been reading for quite a while that in the human one in every 100 million results in a mutation, 100 million divided by 3 billion would be 30, and I've read that from about 3 different authors but now in Genetics 101 by Greenwood he claims that it should be just 3 mutations per human:
genetics 101 wrote:Overall, the DNA polymerase mismatches one in every 100,000 nucleotides. The proofreading function of the polymerase corrects all but 10 percent of these. Of this remaining 10 percent, mismatch repair systems found in many cells are capable of recognizing and repairing 90 percent. Thus, the replication machinery is responsible for an uncorrected mutation in only one nucleotide per billion.
Your numbers seem basically right, but I'm not sure how you are interpreting it. When you say "one in every 100 million results in a mutation", 100 million what? It seems like you are thinking 100 million people, which is not correct.
The human genome has about 3 billion base pairs, with a mutation occurring in about 1 in 100 million of them (that don't get corrected). That indeed gives a mutation count of about 30. But, people are diploids, and the mutations important for NS are the ones you are born with. So you receive approximately 30 mutations from each parent for a total of about 60 mutations.
The usual number given of about one in 30 million base pairs give a per person rate of about 100 to 200. Certain, presumably more direct, measure with human sequencing of parents and children puts it closer to 60. These may be subject to sample size issues, but I took the conservative approach to avoid overstating the point. The variability of mutations rates in people can vary quiet a bit as a result of their genetic heritage, family. As I've already mentioned, some people are better at repairing errors than others. It's certainly more than 3, which appears to be 10% of 30 when that 30 has already into account the 90% that get repaired, and also fails to account for us being diploids.
. And then when they come back, they can