What is an ID proponent's basis of comparison? (edited)

So, leaving out living things for a moment, how many bits is an igneous rock (let's say, the size of a baseball), or a star (let's say, the sun)? Are these things designed or not? I mean, they're pretty complex, depending on how you look at them.Also, where does this 400 bits estimate come from? No one ever denied that. We know humans can make things. Pretty darn complicated things. But just because we can replicate something we find in nature doesn't mean that thing in nature was intelligently designed. Houses are not proof that an "intelligent being" made caves. Algorithms obviously need input by definition, obviously. But why "intelligent input"? How can an algorithm recognize the difference between input from an intelligent source and input from an unintelligent (a-intelligent?) source?

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

Evolution (actually random mutations) produces new biological functions all the time:
Bacterial resistance to antibiotics or bacteriophage
The ability for some human adults to digest lactoseJust to name a couple extensively documented ones.It is incorrect to state that evolution is not directed. Evolution IS directed, by natural selection. The same way the flow of a river is directed by gravity and the surrounding landscape. However, there is no end goal of complexity (which is why >99% of life on the planet is microorganismal).

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

That table so conveniently leaves out resistance gained by the PRODUCTION of beta-lactamases, which cleave the beta-lactam ring of penicillin-like antibiotics. Or how about restriction enzymes which enzymes that have evolved to cut the DNA of invading viruses?I maybe didn't use the best examples before, but they were just off the top of my head. Here, have some more.* The ability of a bacterium to digest nylon (Negoro et al. 1994; Thomas n.d.; Thwaites 1985)
* Adaptation in yeast to a low-phosphate environment (Francis and Hansche 1972; 1973; Hansche 1975);
* The ability of E. coli to hydrolyze galactosylarabinose (Hall 1981; Hall and Zuzel 1980);
* Evolution of multicellularity in a unicellular green alga (Boraas 1983; Boraas et al. 1998);
* modification of E. coli's fucose pathway to metabolize propanediol (Lin and Wu 1984);
* evolution in Klebsiella bacteria of a new metabolic pathway for metabolizing 5-carbon sugars (Hartley 1984)Even just one of these is sufficient to render yours statement "Evolution have never been known to produce new information" false.And stop saying evolution in this case. Mutations produce new information. Are you seriously trying to say that there is no such thing as a mutation that could produce a new protein with a new function?

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

I did, the nylon-eating bacterium the result of a frame-shift mutation that created a new enzyme which was not able to digest its previous food source, but only nylon.

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When the enzymes were first discovered about 1975 (Kinoshita, et al, 1981), it was at first thought the new enzymes arose through the modification of preexisting enzymes that had similar functions. To test this notion, the discoverers looked to see if the other enzymes in the same organism would react to antibodies made against the new enzymes. But by this criterion the new enzymes were unique. Antibodies against them found nothing similar with which to react among the array of other enzymes in the organism.

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Again it was reasoned that if the new enzymes were just old enzymes with minor changes to allow digestion of nylon byproducts, they should retain at least a slight amount of activity with their original substrates. But the new enzymes had no activity on biologically derived molecules having similar chemical structures. So, by this attribute as well, the new enzymes were seen to be unique.

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New Proteins Without God's Help | National Center for Science EducationHere's another example:Big-Benefit Mutations in a Bacteriophage Inhibited with Heat | Molecular Biology and Evolution | Oxford AcademicAdaptation of phage phiX174 to higher temperature results in 3 large-benefit mutations. The mutations occur in the structural proteins of the protein capsid which stabilize the the protein at the higher temperature, thus allowing them to function better at the higher temperature. There is no degradation of the proteins, there is no on-off switching. It's new proteins with a different amino acid sequence that optimizes the functioning of the phage a different temperature.Obviously, a mutation is not going to turn an enzyme into a carbohydrate, and a single mutation will not create an arm where there was none, but to say no mutation has ever produce any new information is patently false.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

Just because something happens predictably, doesn't mean it's not by chance. If I roll a 6 sided die, I will come up with a 2 at least once within an hour. EACH TIME! Holy moley! there must be something else besides chance happening here! Or, maybe it's that the probability of developing the mutation is such that within 9 days, and in the presence of nylon, the bacterium will develop the mutation that allows it to digest nylon. Yes, some bacteria have an adaptation that causes them to increase mutation rates when they are under stress. Sometimes they increase the overall mutation rate of the whole genome, sometimes they increase the mutation rate at a specific place. However, that does not mean that there is any particular mutation they are going for. Nylon is not a naturally occurring polymer. There's no possible way the bacterium could "know" what kind of mutation it could need. Instead, it increases it's mutation rate when under stress which gives it a better chance of creating a beneficial mutation. There is no predetermination. There is no guarantee that the right mutation will occur. But, lucky for the bacteria, there are billions upon billions of them, and even if the right mutation only has a 1 in 10000000000 chance of happening, chances are, in 9 days, through hundreds of generations, it will. It's still a novel mutation that confers a new function, not a physiological response

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

No kidding. But the same principle still applies. Just because it's by chance does not mean it's not predictable. There are a lot of things bacteria do only in the lab, and many things they do in predictable amounts of time. But it's always random mutation. No, they wouldn't have done it before, because nylon is not a naturally occurring polymer. You obviously did not understand what I said. Just because transposons start mutating a specific region, does not mean that they're specifically directing it to mutate to digest nylon. When stressed by a lack of their usual food source, the bacteria increase their mutation rate a specific site in the genome (one that has to do with digestive enzymes), just in case a beneficial mutation pops up. It just so happens, that a single frameshift mutation is all that is required for the bacteria to digest nylon. Another novel food source may require multiple mutations and may take longer to adapt to, if they can at all.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

OK. This is obviously a really difficult concept for you. If you induce mutations, what that means is you increase the chance that a mistake is made in copying the code. However, the kind of mistake that is made is still random. The outcome of this mistake is random. This is still random mutation, there's just a higher probability that it will occur when it is induced. Inducing mutation is just like rolling multiple dice instead of just one (or rolling one die more often). It increases the chances of getting the desired roll, but it does not decrease the randomness of each individual roll. Just because there are mechanisms that allow for this increased mutation rate doesn't mean it's not random. Ah, they can't get resistance within the scope of the experiments, not no matter how long it takes. A key distinction. Yes, bacteria have ways of increasing the rate of mutation. But, you keep saying it's not random, and yet you also say it's not directed to a specific goal. So which is it? Be consistent. Either bacteria have the ability to direct their mutation to a specific goal, or they have the ability to increase the rate of random mutation at a specific site in order to take a chance that they will develop a beneficial mutation. I'll give you a hint, it's the latter.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

And yet we have observable, calculable mutation rates. Bacterial mutation rates are far higher than human mutation rates and your 99.99999999% correction rate is not based on any real information.

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The most common source of mutation is due to mistakes made during DNA replication when an incorrect nucleotide is incorporated into newly synthesized DNA. The mutation rate due to errors made by the DNA polymerase III replisome is one error for every one hundred million bases (nucleotides) that are incorporated into DNA. This is an error rate of 1/100,000,000, commonly written as 10^-8 in exponential notation. Technically, these aren't mutations; they count as DNA damage until the problem with mismatched bases in the double-stranded DNA has been resolved. The DNA repair mechanism fixes 99% of this damage but 1% escapes repair and becomes a mutation. The error rate of repair is 10^-2 so the overall error rate during DNA replication is 10^-10 nucleotides per replication (10^-8 10^-2) (Tago et al., 2005).

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Bacterial populations very often exceed 10^10, which means mutation solely due to replicaiton mistakes are pretty common. Well, the same thing any population does. A bacterium with a detrimental mutation will either a) die or b) not reproduce as fast as a wild type or beneficial mutant and that mutation "that it can't use" will disappear from the population. It's simply evolutionary theory. Read about it.Edited by Stagamancer, : clarification

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

By random I mean the frame shift/base pair change or whatever IS random. If I induce a die to roll is the outcome no longer random?!By saying random mutations have no cause I think you must be thinking of mutations that occur because of an error in replication. But UV light causes this error, are mutations that are caused by UV, or a chemical no longer random because they were "caused"? No, when a scientist says a random mutation they mean that the outcome (say getting a different, functional protein) is more or less random. Contradiction, anyone??? Yes, they wait for it to randomly occur! While mutating randomly (like a die rolling) there is a probability that a mutation will arise that gives the bacterium an advantage (like getting the desired number up on the die). Even if this increased mutation rate is induced, each time there is a mutation, it's a random mutation. Most of these mutation will be neutral or harmful, but with enough generations (rolls of the die) the right one will come up, and the bacteria that have that mutation will out-compete the others. It's really quite simple, and you seem to have a hard time grasping what random really means in this context. I've tried to explain it to you many times. This is my last. I'll respond to another argument that you have, but I'm done with this random mutation part. I don't see how it could be any clearer.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely

Well, that kind of thing can happen. It all depends on the situation. It is possible that a mutation could occur that in the current environment is neutral, but if the environment changes, it's effect on fitness could become either positive or negative. It's also possible that a neutral mutation could interact with a new mutation in such a way as to give a positive or negative fitness effect. Mutations are all about context. A set of strictly neutral mutations will not be adaptive, but if their put in an environment that causes them to have a fitness effect, they can start to have effects on adaptive evolution. One effect of genetic drift is the accumulation of neutral alleles (another is the fixation or loss of alleles regardless of their fitness advantage) Genetic drift, however has no adaptive power. This has been thoroughly tested, and no scientist claims that genetic drift causes adaptive evolution. However, it does cause evolution in the sense that it can cause a change in the frequency of alleles in a population simply due to sampling error of finite populations.

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We have many intuitions in our life and the point is that many of these intuitions are wrong. The question is, are we going to test those intuitions?
-Dan Ariely