1- Code for an amino acid
2- Code for the angle/orientation of the amino acid.

The second point would explain why two identical amino acids coded for by two ‘supposedly’ functionally identical codon triplets could result in a different folding pattern in the protein.

So in short, when the TRNA goes into the ribosome, the codon sequence it has can actually rotate the amino acid it codes for as well as bind to the its relevant amino acid.

Whether this will happen for all codon – amino acid pairs… dunno.

For example, in the last paragraph the author states, “One interesting observation is that the sequence divergence between chimp and human is quite large, in excess of 20% for a few regions… These observations suggest that complex processes, presumably involving repeated sequences and possible conversion events, may occur that will require detailed study to understand. The uncertainty in the estimate of 3.4% indels on Table 1 cannot be directly evaluated. In the first place, the sample of 779 kb is small, and the variation between the different BACs is large. Further, there may be large gaps that were missed as part of chimpanzee BAC sequences that could not be aligned with the human genome.” Based on this, one could predict that the genomic difference between human and chimp will continue to increase in line with continued study.

And I loved the closing statement of the article: “Nevertheless, the conclusion is clear that comparison of the DNA sequences of closely related species reflects many events of insertion and deletion. It is the result of a major evolutionary process.” (I suspect the author meant “Darwinian evolutionary process” as opposed to anything remotely teleological.)

Thanks for all your help!

Eric

P.S. I still would like to see any reference that can show definitively whether, for purposes of determining similarity of nucleotide sequences, it is assumed that synonymous codons are considered “identical,” thus showing closer similarity between the genomes being compared. I assume the current paradigm would prefer a smaller difference rather than larger, thus a tendency to ignore SNPs since with our past understanding we “know” that synonymous codons make “absolutely no difference at all” (a real science stopper here!). Thankfully, however, the engineering instincts of many scientists motivate them to still figure out those things that Darwinian theories don’t care to explore.

As I’ve been following this thread, I couldn’t help but wonder: when computing the reported DNA difference between humans and chimps (somewhere between 1% and 4%), how are SNPs handled in the counting — are they ignored, and the codons considered identical? I suspect this is one area that will be impacted by this new understanding of the “silent” mutations.

The SNPs account for the 1.5% difference. When indels are added the number goest to 5%. Just a rote comparison of base-pair numbers

Man 3.4 giga base pairs
Chimp 3.57 giga base pairs indicate a 6% difference.

See:
Genbank

The difference between pan an homo is about 180,000,000 just based on base pair count, and that’s about 6%. This indicates comparisons of nucleotides that are non-coding. I argue the non-coding 6% need to be accounted for.

Also, see this article from PNAS:

Divergence between samples of chimpanze and human DNA is 5% counting indels

Five chimpanzee bacterial artificial chromosome (BAC) sequences
(described in GenBank) have been compared with the best matching
regions of the human genome sequence to assay the amount
and kind of DNA divergence. The conclusion is the old saw that we
share 98.5% of our DNA sequence with chimpanzee is probably in
error. For this sample, a better estimate would be that 95% of the
base pairs are exactly shared between chimpanzee and human
DNA. In this sample of 779 kb, the divergence due to base
substitution is 1.4%, and there is an additional 3.4% difference due
to the presence of indels. The gaps in alignment are present
in about equal amounts in the chimp and human sequences.
They occur equally in repeated and nonrepeated sequences, as
detected by REPEATMASKER (http:

ftp.genome.washington.edu
RM

RepeatMasker.html).

I had some thoughts trickling thru my mind the other night about pain thresholds related Biblically to Eve. It is a weird thought for most I’m sure.

But it popped into my mind and this article prompted the thought again. What if birthing pain was genetically related? I realize this is a stretch, no pun intended.

Embedded in this article posted by Dr. Dembski is this little jewel,

The gene Diatchenko’s team studied encodes a neurotransmitter-degrading enzyme called human catechol-O-methyltransferase, or COMT. This enzyme is central to the regulation of pain perception. The COMT gene exists in three common variants, each one consisting of both silent and nonsilent codon changes.

Depending on which variant a person has, he or she is likely to have low, average, or high pain sensitivity. The researchers found that differences in COMT production derive far more from differences in synonymous codons in the COMT gene than in nonsynonymous ones that lead to amino acid changes.

Put this together with other recent research(Wnt signals – limb regeneration), the “zipcode” pattern of body placement for cell location, body repair, blood clotting and healing proceses.

Could there be more series of switches, folds, body mapping that can be manipulated to shut off pain in different regions?

I know this is way out there – speculative. But this new fidning of pain threshold differences in such unexecpted areas should alert us to the fact that it can be controlled subtly instead of direct medical feeds like local or general anesthesia. And if controllable, then shut off completely in specific regions by a “zipcode” process, or blanket altogether.

What about a switch or synonomous areas that turn pain off for good or minimize the pain? That is three billion happy people. This eliminates mass doses of pain medication for childbirth sometimes which may possibly harm a child.

If one exerts a “literal” interpretation on Genesis, pain was not intended for childbirth in the beginning, but after sin. Realize this brings all sorts of arguments to the table. I’m not trying to make any, just asking questions that think on these issues. Like if pain associated with childbirth were a single point mutation or larger? In this case, it appears larger areas of concern. And does that point to design that can be tweaked backwards toward a more “original” design?

Finally, pain is beneficial. But the find in the article made me think a bit on my original thought of what may be “designed pain”.

Are you silly IDers doubting the all-purpose resourcefullness of natural selection? Linguist, poet, creator, engineer, innovator. My goodness, the phrase does just about anything you want it to.

I’m glad you brought up viral insertions of beneficial genes. In another thread we were making things up to solve Haldane’s Dilemma. Someone divided natural selection into two parts (hard and soft) and said Haldane uses only hard selection while soft selection has no cost and happens an unknown amount of the time.

Soft selection was rather a brilliant invention. It works like this – if a creature is missing a beneficial mutation and dies before reproducing, well maybe he was going to die anyway whether or not he had the mutation so even though he is helping to fix the mutation there’s no substitution cost because he would’ve died anyhow. Absolutely brilliant. All one has to do is ignore the fact that creatures WITH the mutation also die because of other factors so it doesn’t become obvious that it’s a self-nullifying mechanism.

At any rate, I thought I’d solve Haldane’s Dilemma too so I proposed that beneficial genes are spread through a population by kissing. I didn’t yet outline how it works by kissing (I was saving that for my forthcoming book “How I Solved Haldane’s Dilemma”) but since you mentioned the mechanism I might as well ‘fess up. A virus that implants the beneficial gene is passed during the kiss.