I don’t see a way to approach design as a scientific explanation for amino acid sequences. It seems to me that design advocates like yourself propose that the mechanisms of evolution can produce small increments of sequence/information but not large. Further, the argument goes, since other kinds of design (e.g., engineering artifacts) are created by intelligent agency, intelligence is the only viable explanation for sequences/information unattainable by evolution.
However, I see no reason why an evolutionary mechanism that can produce 24 bits of information in 10 years (e.g, in bacteria) could not produce 2.4 kb in a thousand years and 2.4 gb in a billion years. Where does the uncrossable threshold come from? Truly I could not produce all heads in a single flip with 1024 coins even in a lifetime, but if I’m allowed to keep 10% of the heads from every flip I could do it in a couple of hours, tops. Since evolution has a mechanism (natural selection + inheritance) for conserving good flips, I don’t understand how design can be a scientific argument.
I do believe there is valid way to invoke Paley’s watchmaker argument. The watch is not the DNA sequences or the eukaryotic cell; the watch is evolution and its highly complex and interrelated mechanisms. This is a philosophical argument rather than a scientific one, but I find it compelling.
Provide some positive evidence and a way to test the hypothesis and science will consider it. Merely claiming a disembodied mind used magic to POOF! it into existence doesn’t qualify.
It amazes me that the immune system uses genetic variation and selection to produce the very things IDcreationists claim can’t be produced by evolution (specific binding and even enzymes) in a couple of weeks, then after they back themselves into an inescapable rhetorical corner, claim that God designed the system.
If God designed the immune system to use genetic variation and selection, why couldn’t he have designed life to do the same thing on a far grander scale?
It’s just another reason that IDcreationism is bad theology–it diminishes the very concept of God.
Recommended reading: The Perfect Predator: A Scientist’s Race to Save Her Husband from a Deadly Superbug by Steffanie A. Strathdee, for how this works in real life [and near death]. A war of genomes fought on the battlefield of a human life. Genetics as a thriller. The Perfect Predator
Hi Chris
The first problem with this claim is the statement I see no reason why. There are plenty of reasons why and a scientific explanation requires a tested model in order to be universally accepted. Until the eclipse experiment Einsteins theory of general relativity was not universally accepted.
This is the claim Behe argued against with irreducibly complexity. He shows that what we are observing are stepping stones larger than 1024 coins producing all heads.
Evolution as a complete explanation for Biology is an idea at this point. We see it working with simple adaptions. The grand claims have not been modeled or tested. The problem of functional information and irreducible complex structures is real and solved by a mind. This is the best explanation in my opinion as a mind along with other mechanisms has the power to account for what we are observing. This is the best we have at this point until someone identifies a deterministic mechanism in the cell that can account for all the diversity we are observing. This is what guys like James Shapiro are trying to do.
There you have it. Since Bill doesn’t understand how selection feedback works therefore selection doesn’t exist. Impeccable logic.
Actually Bill it’s arguably the most well supported scientific theory of all time. You really should read and learn about it some day. Especially the “natural selection” part.
Biologists have published many papers in recent years showing a series of neutral drift mutations being capped off by a final mutation that activates some new functionality. Behe’s assertion is that the set of mutations constitute an irreducibly complex mechanism; i.e., they all have to be present in order for the mechanism to work. Yet biologists keep finding this pattern and they keep publishing peer-reviewed papers about the finding.
This is perfectly normal, since gpuccio’s purpose with his wall example was not to mirror real biology. Not at all. Rather, it was intended to show that no TSS fallacy is committed by recognizing the function of protein post hoc. No more, no less.
That makes absolutely no logical sense. Nobody is claiming that the TSS fallacy is committed by recognizing the function of the protein. The TSS fallacy is committed by ignoring the missed shots. But Gpuccio is claiming there are no missed shots, hence his analogy is completely meaningless because it doesn’t show how he would infer design for the biologically real situation.
So Gpuccio, in an attempt to avoid the TSS fallacy, was forced to imagine a situation we are not actually in. Well then his analogy is of zero value or consequence as he has no reason to infer design for real biology.
Oh look, if we were in some imaginary situation completely unlike the real one, I could infer design without committing the TSS. But we are not in that situation, so… meh!
I have not seen any credible rebuttal. If you have one let me know. The flagellar motor is the most cited rebuttal but the rebuttals are speculative. This is a problem for universal common descent as the eukaryotic cells protein complexes are much more complex than the flagellar. Multicellular organisms have a series of leaps in functional information over the history of new animal forms.
To get an overarching theory a model is the minimum requirement to start to test a hypothesis. The design guys have a tested mechanism for generating a complex sequence. Their theory has other issues but it does meet the minimum requirement.
Bear in mind that I was not referring to a mechanical irreducible complexity (IC) but to a genetic IC that emerges from multiple correlated mutations in a gene. This conforms with the definition Behe offered in 2002:
“An irreducibly complex evolutionary pathway is one that contains one or more unselected steps (that is, one or more necessary-but-unselected mutations). The degree of irreducible complexity is the number of unselected steps in the pathway.”
I certainly wouldn’t expect you to just start reading biology literature without some guidance. I can think of a few articles that meet the criteria for genetic IC.
Hormones and their binding sites are IC, per Behe. However, the genetic origin of the pairing of aldosterone and its binding site was identified in 2006.
De novo genes would certainly qualify as IC. Ruiz-Orera, et al. were able to identify several that have functional signatures in this research. The paper is also interesting because it identifies some mechanisms that activate de novo genes.
Trotter, et al. actually laid the mathematical foundation for genetic IC in this 2014 paper.
Biologists - can you think of any other good papers for Bill to read on this topic?
I can’t say I agree with this.
The generation of functional information is the phenomenon that needs to be modeled. The putative identification of functional information from cross-species sequence conservation does not tell us anything about the origin of that sequence.
Dembski’s methodology is also unconvincing to me because he does not address the density of function in sequence space.
Axe’s research (and his famous 10-77 estimate) did not sample randomly from across functional space, therefore it cannot tell us anything about the density of function in the sequence space available to the biological domain. Moreover, samples from a different region of the space (beta-lactamases) have a density 69 orders of magnitude greater, per Art Hunt’s research.
If you read a little further he gives this example.
Let’s make our shooter a little less precise: let’s say that, out of 100 shots, only 50 hits are green bricks.
Now, the math becomes:
The probability of one succesful hit (where success means hitting a green brick) is still 0.01 (100/10000).
The probability of having 50 successes or more in 100 shots can be computed using the binomial distribution. It is:
6.165016e-72
Now, the system exhibits “only” 236 bits of functional information. Much less than in the previous example, but still more than enough, IMO, to infer aiming.
Consider that five sigma, which is ofetn used as a standard in physics to reject the nulll hypothesis , is just 3×10-7, less than 22 bits.
Now, DNA_Jock’s objection would be that our post-hoc specification is not valid because “we can make the probability arbitrarily small by making the specification arbitrarily precise”.
But is that true? Of course not.
Let’s say that, in this case, we try to “make the specification arbitrarily more precise”, defining the function of sharp aiming as “hitting only green bricks with all 100 shots”.
Analogies, even ones that make sense, are not examples.
What makes @gpuccio’s hypothesis so weak is the tiny number of cases (which I would not call examples because they are not representative) he used before claiming that he was right.
An archer is standing 100 yards from a heavily wooded area. He claims that he can hit a target the size of a dollar coin from 100 yards, on the first shot. Everyone scoffs and asks him to prove it. The archer draws back and fires an arrow. Predictably, the arrow hits one of the trees. The archer walks up and draws a target the size of a dollar coin around the arrow. The archer then proclaims that he had to be aiming at that spot because the probability of hitting that exact spot are just too improbable.
This is what @gpuccio has done. He starts with the arrow hit, the protein that has function. He then pretends that it is just too improbable that the sequence hit where it did, all the while ignoring all of the other sequences that also have function, places where the arrow could have hit.
To be fair to Axe, it was that 2004 paper that was so bad, not all of Axe’s research generally. It turns out that he did a far better sampling and published it in 1996:
