Thursday, January 05, 2006
Ideas for Creationist Research in the Secular World
Anyway, if you are in the biological sciences, or are thinking about getting into the biological sciences, but don't know what to research on, this post is for you. Of course, you, actually being in the biological sciences, probably know more about this than I do. But hopefully as an outsider I can provide a fresh perspective on the situation. This should be both (a) interesting to a creationist, and (b) able to get secular support for such research.
Look for more examples of the directed adaptation of an organism through mobile elements
There is already at least one example of an insertion sequence as an activator of cryptic genes
Some suggested studies for this area might include:
- A study of C3, C4, and C3/C4 photosynthesis, and try to induce a change from one to the other. Todd Wood has hypothesized that this could be because of inactivated genes. If you could simulate sufficient environmental conditions to do the switch, that would be fabulous.
- A study of symbiotic mechanisms. I personally have a gut feeling that symbionts are an adaptive process, and that organisms detect what other organisms are in the area, and can, most likely using transposons, develop appropriate symbiotic behavior with those creatures. A good study specimen might be orchids, which seem to produce symbiotic behavior quite easily. Showing that animals have pre-coded adaptations to certain types of organisms indicates that these adaptations do not arise a piece at a time, and are a part of a plan, not happenstance.
Generation of de novo genes
Studying the nylon bug could prove interesting. It has applications to all sorts of areas of creationary theory. For example, the generated gene occurs in both flavobacterium and pseudomonas with a high homology between the two genes. What does it say when generated genes have a high homology? What does that do to arguments from homology? In addition, it appears that this gene is actually pre-prepped for change, with a lack of stop codons in the antisense strand [the abstract says "the presence of such rare NSFs on all three antisense strands of the nylB gene family suggests that there is some special mechanism for protecting these NSFs from mutations that generate the stop codons. Such a mechanism may enable NSFs to evolve into new functional genes and hence seems to be a basic mechanism for the birth of new enzymes."]. In addition, there were many point mutations and transposon activity in the birth of the new gene. So, by what process did this new gene arise? Note that this also has a lot of impact into the environment, so that we can know if we can mutate bacteria to eat some of our trash.
What does having a gene that is open to mutation say? For one thing, it says (a) it is really rare that a gene is open to so much mutation. It also says (b) that such mutations require specified mechanisms to occur -- the evidence doesn't indicate happenstance. Finally it says (c) the mutations were directed at this particular gene (imagine what kind of error catastrophe would occur if this kind of mutation happened genome-wide).
A good research topic would be adaptive mutagenesis. Some ideas along this line would be:
- What are the actions of the different DNA polymerases, and why do cells use one over the other
- What kind of specificity occurs during adaptive mutagenesis. It is widely claimed by this experiment that adaptive mutagenesis is just a lot of random mutation + natural selection. However, I still don't see the mutation process as being random, for several reasons.
- While the environmental stress affected more than just the Lac- genes, it did not affect all genes, which is evidenced in their paper with the follow quote: "Thus many, but apparently not all, chromosomal loci hypermutate in association with Lac+ adaptive reversion." (there were no Fruc- mutants in the revertant colonies). This indicates that there may be some mechanism that the cell uses to figure out what to mutate. Even if it is just selected amplification with a mutagenic DNA Polymerase, how is the gene to amplify (and thus mutate) get selected?
- What are the specific mechanisms of the DNA Polymerases? I'm sure this is already covered in the literature, but a more relevant question is "which DNA Polymerase activity promotes adaptive mutagenesis of which genes, and how does the cell know which one to use?"
- If there was a spout of hyper-random-mutation, such that in nearly every case there was adaptability, it seems like this would have to be large-scale genome bombardment, such that would lead to error catastrophe. The fact that it does not indicates that there is a mechanism which either partially specifies the mutation or prevents error catastrophe in critical components.
- Above, we discussed a certain gene which is activated by an insertion sequence. What causes an insertion sequence to be activated in one stress condition, while adaptive mutagenesis is activated in another one?
- What types of genes can undergo adaptive mutagenesis, and which ones cannot?
The Function of Alternative Splicing
Alternative splicing will change the way we view DNA. What we need to know is (a) how does the cell know when to change the splicing, and (b) is there a way to detect within the DNA where splicing can occur. I'll present some good papers on alternative splicing (hopefully) shortly.
The Semantics of the Genome
Semantics is probably the greatest evidence of intentionality in a coded system. Semantics are the constraints under which change operates. In general, when coding a computer program, each design purpose (apobetic information) gets coded as at least one semantic constraint. While there are some apobetics which do not reflect this, the existance of semantics in the genome imply an apobetic origin. Quantifying the genome semantics using something akin to Type Theory in computer science would go a long way to showing design.
I'll probably add to this list as the week goes on. Note that almost always the "random mutation" is the presupposition, which is easily refuted by examination. The Darwinist idea is that life is contingent, but contingent on happenstance. All that needs to happen is when a secular biologist gives up and says "it was random", you go in and say "no, here's how the design works".
If you have any ideas for research projects, please post them in the comments!