Is ID a scientific theory?

(1) The most often discussed ID prediction made in the 90s was related to so-called "junk dna" and how the majority of this information would not be junk at all. See junkdna.com for news related to that.

http://www.sciencedaily.com/releases/2008/01/080113161406.htm

"Estimates of the number of genes in the human genome have ranged wildly over the past two decades, from 20,000 all the way up to 150,000. By the time the working draft of the human genome was published in 2001, the best approximation stood at 35,000, yet even that number has fallen. A new analysis, one that harnesses the power of comparing genome sequences of various organisms, now reveals that the true number of human genes is about 20,500, thousands fewer than what is currently listed in human gene catalogs."

First this article demonstrates how little science really knows about the genome. If we can't even identify the number of words (genes) in a book (the Human Genome), how can we know what the book says?

But here is what is interesting. This article is rejecting words found in the book by others, not because we know they don't mean anything, but because they are not found in other books. Thus what looks like a word in the human genome, is now not a word because it is not found in the mouse genome. Hmm. What is the logic of that? Well, it's called Darwinian evolution. Because Darwinian evolution cannot be expected to produce 5000 words between the mouse and the human, we must conclude that the words are not words at all.

Really, the only way they can justify this seemingly arbitrary declaration is if they were to provide evidence that that this even-more-limited set of information was indeed capable of producing a human. As far as I'm aware they're quite clueless about what information marks the major differences and thus, like the junk dna concept which Darwinists promoted for years, if this idea becomes scientific consensus it might slow the progress of science for years.

Here is a very interesting opportunity for a very straight forward ID prediction: The Darwinist assumption is wrong and science will eventually discover that the apparent words are actual words.

Now, I can understand the reasoning behind this decision. Orphan genes in general pose a huge problem for Darwinism since if even half of the information is functional that means we have large islands of information that are specific to particular species and they are not modular. As an engineer having a combination of modular code combined with specific code makes sense to me. For example, in a project I'm working on I reuse a large chunk of modular code and modify specific portions to differentiate it from the other classes. Sometimes the resulting object appears completely different from all others from an external perspective (watching it in action) but I know that over half of the code is modular. And this is ignoring all the code reuse from libraries like .NET.

BTW, I'm not ignoring the fact of junk dna in general. Deleterious mutations do happen quite often. Some can be neutral, as in there is not any negative or positive selection pressure. So by any reasonable expectation there should be "some" amount of junk DNA.

(2) Heavy usage of modularity and common design.

(3) A fair-level of “front-loading” would be expected by some ID-compatible hypotheses. When they find genes for the expression of digits in sea anemones, this throws Darwinism for a loop, but is almost an expectation for ID.

(4) Again, because we’re dealing with “information systems”, one would expect high levels of redundancy built into the genome.This prediction was underscored when it was discovered that in some experiments the later generations would revert back to stored copies of the grandparents (!) in order to correct errors.

(5) Lots of environmental triggers: if you’re designing life that must deal with huge environmental changes, then there must be a way for the genome and the environment to interact. Although this particular prediction is primarily made by specific ID-compatible hypotheses and not core ID.

In the corner of OE you'll see a book called Design Of Life; here's a quote on page 296 from it:

"In fact, a strict Darwinian explanation for antibiotic resistance seems to be more the exception than the rule. In times of environmental stress, bacteria go into a programmed defense that constitutes a targeted search for gene combinations that will enable at least a few of the bacteria’s descendants to survive (the genetic changes here are therefore not random mutations as understood within neo-Darwinism)"

We can predict we’ll find a mechanism for these directed mutations triggered by an environmental cue.

(6) Now this is assuming Intelligent Evolution of some type, but gradualism would not be predicted by these classes of ID-compatible hypotheses.

(7) ID proponents in the 90s were predicting that we'd find ever increasing layers of encoded information. See the ENCODE project for how that prediction proved right.

(8) Using the analogy of a computer program, one would expect what I call “subroutines”, or, put another way, various parts of the genome that are used for a variety of purposes in an “on-demand” basis. These “subroutines” would be part of the “regulatory” system of the genome. Just as a computer must “compile” a program, there must be some kind of chromosomal system that associates the various “parts of the program” in a deterministic way. That is, the right parts have to be in the right place, and connected to one another in a ‘logical’ way.

(9) Due to the heavy usage of modularity with common design, the so-called "tree of life" would be a false picture. Instead ID would predict a bush-like pattern.

(10) Related to Behe's Edge of Evolution: "Bacteria/virus X will not evolve resistance to drug Y because it requires Z many mutations which is too many for Darwinian processes to account for.”

(11) The ID-compatible front-loaded genome hypothesis predicts that a mechanism exists for preserving unexpressed genomic information for geologic periods of time.

In a recent experiment 1.5 million base pairs of non-coding DNA containing over a thousand highly conserved sequences between mice and men were deleted from the mouse. There was no detectable difference between the GM mice and their unaltered parents. The experimenters were stunned. They expected to find all kinds of problems in the GM mice which they could then use to infer the function of the conserved sequences in humans and possibly get a handle on a large number of genetic defects in humans.

That result put a huge gaping rent in Darwinian theory. Natural selection can’t act on unexpressed genomic content. If natural selection didn’t conserve those sequences over 180 million years of divergent evolution between mice and men what the heck did preserve it? That question was shrugged off. The researchers were interested in ways to isolate and identify the function of DNA in humans and were not at all interested in DNA with no evident function. So instead of trying to figure out what worked to preserve that DNA they instead abandoned the mouse genome and started comparing sequences highly conserved between men and fish, men and reptiles, and men and amphibians. The Darwinian establishment at large seems to have little interest in testing their own hypothesis.

Of course, it's also possible this is due to lateral gene transfer.

(12) ID predicts that the majority of positively selected variation made by Darwinian processes will be destructive in nature (trench warfare). Very few will be constructive (arms race) and will also be limited in scope.

(13) DNA would be extremely optimized as a storage device.

http://www.sciencedaily.com/releases/2007/02/070220034152.htm

“Data encoded in an organism’s DNA, and inherited by each new generation, could be safely archived for hundreds of thousands of years, the researchers state.”

Hence the stasis noted for so many species.

(14) Some ID-compatible hypotheses predict Multiple OOL events. This would explain why scientists cannot derive a tree of life for lower lifeforms.

(15) If lateral gene transfer does in fact play a large role as a mechanism for evolution (micro or macro) then internal triggers and targeted information sectors will be involved and not simply chance events.

(16) Shared modular components where common descent is not expected. Like bacterial rhodopsin showing up in rice. That points to a network of shared modular genes...not Darwinian processes at work.

(17) Related to ID-compatible hypotheses that incorporate Genetic Entropy:

a. All genetic evidence points to accumulating degradation of the genome.
b. ID predicts that organisms comprise numerous complex functions with well tuned performance.
c. Mutations degrade or destroy biologic functions, causing disorder, disease and death.
d. Mutations with selection will progressively increase genetic mutational loads, increase the frequency of genetic diseases, reduce longevity, and eventually result in species death.
e. Accumulating genomic entropy, declining longevity, and genetic diseases point back to designed organisms with non-degraded function.

(18) Some have called Behe's new book a positive result for the major ID prediction that we would find evidence for limitations of Darwinian processes.

On page 138 of Dr. Behe’s Edge of evolution:

As one study put it “Each and Every possible single-point mutation occurs between 10^4 and 10^5 times per day in an HIV-infected individual.” (HIV population dynamics in vivo Collin J.M., 1995). Every double point mutation, where two amino acids are changed simultaneously, in each person once a day. (This means a chloroquine-type resistance mutation-where two particular amino acids had to appear before there was a net beneficial effect-would occur in each aids patient every day. Not that’s mutational firepower!) In fact, just about every possible combination of up to six point mutations would be expected to have occurred in an HIV particle somewhere in the world in the past several decades-double the number that could occur in the slower mutating P. falciparum. In addition to all those point mutations, enormous numbers of insertions, deletions, duplications and other sorts of mutations would occur as well.
An exactly what has all that evolution of HIV wrought? Very little. Athough news stories rightly emphsize the ability of HIV to quickly develop resistance, and although massive publicity makes HIV seem to the public to be an evolutionary powerhouse, on a functional biochemical level the virus has been a complete stick_in_the_mud. Over the years its DNA sequence has certainly changed. HIV has killed millions of people, fended off the human immune system, and become resistant to whatever humanity could throw at it. Yet through all that, there have been no significant basic biochemical changes in the virus at all…

(19) So you want other applications that would require acceptance of ID? How about designer drugs that take into account the limitations of Darwinian mechanisms predicted by ID?

What one needs to know to do that:

a) A drug and how the drug breaks the bacteria or virus
b) All possible stepwise evolutionary pathways for developing resistance to that drug (potentially the most difficult aspect)
c) How fast on average the drug kills the virus or bacteria
d) Rate of replication/estimated limits of Darwinian mechanisms

http://www.sciencemag.org/cgi/content/abstract/1152725

Short version is that they’ve identified the host proteins required by HIV. Perhaps Behe’s work could be applied to this line of research. How?

Several hundred of these genes might make good drug targets, since they can reduce HIV infection without killing the host cell. Blocking 28 of these genes could even prevent the formation of functional viruses (obviously the preferred scenario). HIV is dependent on its host for the functionality of parts of the nuclear pore, RNA transcription machinery, Golgi complex, and controls for proteins on the cell surface.

Now first note my previous comment where I quote Behe’s discussion of HIV. As parts of the host genome, these genes do not possess the replication rates nor the selective pressures that allow HIV to rapidly evolve around therapies. The virus could still evolve to be less dependent on these specific genes but, given the fundamental nature of the host proteins required to sustain life, this seems fairly unlikely. In fact, if there is a particular host gene that plays a critical function for HIV I say researchers should examine it to see what sort of modifications would be required for HIV to work around it. If they are beyond Behe’s edge then that should be the primary target for designer drugs.

Still…as Behe pointed out in his book (in regards to malaria) this seems to be an indirect way to attacking the problem. Perhaps there is a way to modify the host’s immune system or something else. Using the trench warfare analogy, why not build a defensive fortified wall instead of blowing up a bridge?

(20) Jonathan Wells. In a 2005 paper (”Do centrioles generate a polar ejection force?” Rivista di Biologia 98(1), 2005: 71-95), he makes the ID-based inference that centrioles are microscopic turbines:

Centrioles consist of nine microtubule triplets arranged like the blades of a tiny turbine. Instead of viewing centrioles through the spectacles of molecular reductionism and neo-Darwinism, this hypothesis assumes that they are holistically designed to be turbines. Orthogonally oriented centriolar turbines could generate oscillations in spindle microtubules that resemble the motion produced by a laboratory vortexer. The result would be a microtubule-mediated ejection force tending to move chromosomes away from the spindle axis and the poles.

From this ID hypothesis, several solid, testable predictions follow:

A. It predicts that spindle microtubules in animal cells begin to oscillate at the beginning of prometaphase, and that those oscillations rapidly accelerate until metaphase.

B. It predicts that the centriole contains a helical pump powered by dynein molecules located in the inner wall of its lumen.

C. It predicts that the polar ejection force is regulated, at least in part, by intracellular calcium concentration.

(21) Other links

http://www.researchintelligentdesign.org/wiki/Predictions_of_intelligent_design

http://www.evolutionnews.org/2006/01/intelligent_design_is_empirica.html

http://www.researchintelligentdesign.org/wiki/Empirical_ID_research#Gonzalez.E2.80.99s_lunar_research_proposals

http://www.discovery.org/scripts/viewDB/index.php?command=view&id=4072