Let’s recall that some of the most serious cases in triage get only palliative treatment; that’s the third category. Studies have shown that Bill isn’t helped by treatment.
2 Likes
Humans merit palliative care, but do arguments? I would have thought a prompt mercy killing would be kinder on all involved. Further evidence of the pitfalls of argument-by-analogy. 
1 Like
And then there is hospice care.
1 Like
William Dembski’s Hospice for Terminally Ill Arguments perhaps?
Unfortunately that site itself has joined the choir invisible. So where oh where can a poor, worn out, dying argument find solace in its last hours of existence?
1 Like
Right. So we have all of our homework still ahead of us, to show that random changes would break sequences down. Please, continue.
I don’t find that obvious at all. Please, cite a study documenting any such occurrence in nature. Otherwise, your argument that a sentence of some 39 characters is dysfunctional after ten (dubiously random) changes is a mere cartoon that illustrates nothing that could even hope to be applicable to biology, even if we were to pretend like character strings which only have meaning insofar as their users assign such, are in any way whatsoever comparable to DNA sequences, which have function inherently, in virtue of being chemical compounds that cannot help but interact with their environment through culturally independent electrostatic forces.
Why bother nobody takes him seriously.
This is the argument biologists have been hanging on to over the last 50 years since the Wistar conference where the idea of sequences breaking down when randomly changed was first introduced.
Since Francis Crick first discovered that genes code for proteins in the late 1950s it was known that DNA and proteins were sequence dependent. This meant they were under the same mathematical principles as a language where meaning is a tiny fraction of the possible arrangements. Richard Dawkins in the blind watchmaker tried to solve this problem with a target sequence essentially validating intelligent design. No one since has come close to showing how biology can generate new functional sequences through reproduction and associated variation. This is why God guided common descent is discussed.
The solution of gene duplication ignores genetic entropy after the duplication event. The entropy occurs when when function sequence space is smaller the total sequence space.
This is the bizarro alternative universe Bill inhabits. One in which the Wistar conference has any relevance whatsoever to the current practice of biology.
Please, cite a study documenting a parent-child pair in nature between whom over a quarter of coding DNA is mutated. I did not ask what one has to commit to for believing something, nor did I ask for a lesson on the field’s history. If biologists have been hanging on to this cartoon of an argument for half a century, I’m sure it should be trivial to produce more references than none at all to at least one of them at some point actually publishing anything even remotely like it. Let’s see it.
I already said I do not think a study like this exists.
Oh, my bad. It sounded like you were saying that it was obviously not true that between a parent and child having 25% dissimilarity was not likely possible. I guess you meant the opposite, that this was likely impossible. Very well.
In that case, it would seem that your illustration is grossly off-scale, such that despite sounding like a few, those ten changes you introduced into a 39 character long sequence are far more meaning-destructive than pretty much any naturally occurring single-generation mutation rate. In actuality, the effect of such mutations can as much alter function or produce new function, or fail to do anything, as it can damage function, and lineages that accumulate a detriment go extinct long before anything as cartoonish as ten destructive changes for every thirty-nine possible locations for change can accumulate. What was your mathematical challenge to any of this again?
1 Like
The problem with your argument is we see much more than 25% differences in proteins that the single origin theory asserts share a common ancestor like the WNT family. The differences occurred without extinction as they are separate designs.
We also know of single function killing mutations which is much more severe then a single letter change to a sentence.
I recently read Sanfords paper and it is worth reading as it summarizes the waiting time problem.
No math, no point. Show your math or go away.
1 Like
If those same differences arose thru unguided evolution, would extinction have occurred?
I fail to see why this is a problem. Perhaps a calculation may help.
Indeed. Do you reckon the unfortunate individual who dies from their lethal mutation gets to pass it on to many offspring of their own? If yes, how? If no, then why is this an interesting point to consider?
2 Likes
It directly contradicts your claim about a 25% change or difference in ancestral sequences not being real.
A lethal mutation to a gene/protein may or may not kill an individual species. It needs to be in the germline and needs to be mission critical to survival.
The problem is identifying the real cause of protein superfamilies like the WNT having vastly different sequences. This is very strong evidence for individual designs given random substitution of an amino acid has a 50% or greater chance of being deleterious.
I made no such claim and I would much appreciate it if in the future you could refrain from lying about what claims I made.
Is that so? Please, explain how a lethal mutation might kill an individual species. By what mechanism could an individual organism that undergoes it provide it to the rest of the current or some future population?
Please, show us a calculation that beginning with experimentally obtained data yields this estimate.
1 Like
Why are you comparing to a single generation mutation rate?
A single mutation to an APC gene can kill an organism by his mature cells going out of regulation. The death can happen in an individuals advanced adult years.
This estimate was made by @Rumraket as a counter to Behe’s 70%. Here is a quote from a paper that has been cited several times here.
An estimate of ρ can be inferred from studies of the tolerance of proteins to amino acid substitution. Although there is variation among different positions in a protein sequence, with surface residues in general being more tolerant of substitution than buried residues, it can be calculated that on average a given position will tolerate about six different amino acid residues and still maintain function (Reidhaar-Olson and Sauer 1988, 1990; Bowie and Sauer 1989; Lim and Sauer 1989; Bowie et al. 1990; Rennell et al. 1991; Axe et al. 1996; Huang et al. 1996; Sauer et al. 1996; Suckow et al. 1996). Conversely, mutations to an average of 14 residues per site will produce a null allele, that is, one coding for a nonfunctional protein
Because that’s how many generations of sentences there were in your analogy. You did not make but a few changes at a time, ensuring that the new sentence still had meaning before making the next change in it. Now maybe you meant to produce an inadequate analogy, understanding full well that this is not how genome changes propagate through a lineage. I chose to interpret you charitably instead, assuming that you did actually mean that this many coding DNA sequence changes could happen in a single generation, and were not intentionally mischaracterizing the process.
I see. So we just have different interpretations of the term “lethal”. I assumed you meant things that actually prevented the organism from being alive, rather than preventing it from growing particularly old. Evenso, do you reckon a gene that significantly shortens the carrier’s life span would find much success spreading through the population? Don’t you think that the shortened life span may impact the relative amount of offspring such a carrier can produce compared to his non-mutant competitors?