What you need to show is a relevant example is for mutations to become fixed.
In the Lenski experiment a tiny fraction of total mutations became fixed and not lost to drift or other causes.
It is interesting that the delta variant held up and dominated the population for 4 months. Then omicron for 2 months. Do you know the sequence difference between these two variants.
The following link is an easy to use but very deep portal into global SARS-CoV-2 variant data. You can select hotspots on the phylogeny chart and click through view the sequence changes of individual samples.
The site has similar pages for influenza and monkeypox.
The hemagglutinin and neuraminidase of influenza display dizzying variation, constantly crossing over to different host species and avoiding antigenic detection, all the while maintaining critical ability to bind.
Just to be clear for Bill, all of these alleles have become fixed.
Bill, I would suggest that your understanding is hampered, in addition to your massive allergies to evidence and math, by thinking of variant alleles as mutations.
He did, Bill.
Not proteins in general - cell receptors in particular.
This paper has a table 1 with a selection of thirty or so receptors favored by respective viruses
Bill why does Behe say this in his paper?
Such numbers seem prohibitive. However, we must be cautious in interpreting the calculations. On the one hand, as discussed previously, these values can actually be considered underestimates because they neglect the time it would take a duplicated gene initially to spread in a population. On the other hand, because the simulation looks for the production of a particular MR feature in a particular gene, the values will be overestimates of the time necessary to produce some MR feature in some duplicated gene. In other words, the simulation takes a prospective stance, asking for a certain feature to be produced, but we look at modern proteins retrospectively. Although we see a particular disulfide bond or binding site in a particular protein, there may have been several sites in the protein that could have evolved into disulfide bonds or binding sites, or other proteins may have fulfilled the same role. For example, Matthews’ group engineered several nonnative disulfide bonds into lysozyme that permit function (Matsumura et al. 1989). We see the modern product but not the historical possibilities.
Why is that in the paper?
Because Behe knows his fans are incapable of actually understanding what it means and will simply believe Behe has owned the libtard atheists because he wrote some words. As @colewd is amply demonstrating.
ID QED.
Some things never change… That may be due to processes that interfere with migrating short term to long term memory.
When you think about it, it kind of blows the mind that we can reconstruct the genealogy of every living thing on earth just by looking at some chemicals in their cells. Creationists are missing out on so much.
You can understand the genealogy of every living thing on earth by understanding the process and limitations of reproduction.
Correct, so why do you refuse to do so?
Bill own-goals over on theskepticalzone yet again:
colewd : How do some deer have 70 chromosomes and others have 7 (…) There is no mechanism associated with reproduction that explains through any model these patterns yet it is an axiom of a current scientific theory with thousands of papers based on this axiom.
https://www.nature.com/articles/s41467-021-27091-0/
From the legend to Figure 1:
“a Maximum likelihood tree of muntjac and outgroup species with the respective sequencing technologies (red geometries), the divergence time (blue numbers) and number of chromosome fusion or fission events (red numbers) shown. Different combinations of black arrows represent different types of chromosome fusion and fission. The 31 fusion events leading to M. crinifrons are displayed in detail with the chromosome code (black numbers) of H. inermis , which are connected with the arrow mark on the phylogenic tree with dotted lines. Red hollow circles mark the nodes whose divergence times were used as calibration for estimating the divergence time among other species.”
Let me edit my prior assessment:
Bill, you would not be supported by any YEC organizations, as they do not acknowledge chromosome count as definitive of descent, and consider not just muntjac deer but many more to be all descended from one ark kind. Otherwise, the number of animals kinds would be too large to be accommodated on the ark. I do not know of any ID associates who would support you either.
So, the characteristics we see in deer around the world today were present in the genetic makeup of the deer kind aboard the Ark. Thinking about antlers as a trait, moose have palmate antlers, mule deer have tined antlers, and caribou have a mix of both. From this we can reason that the original deer kind had a mix of these features, and, over time, some species lost the genetic information to make the palmate antlers (elk and mule deer) and some species have become primarily palmate (moose). This is the kind of change that is consistent with what we find in Scripture and the kind of change I was referring to in the book.
Recent shifting of subfamilies based on new studies has caused the remaining subfamilies, Muntiacinae and Hydropotinae, to be placed in (or near) Cervinae and Odocoilinae (aka Capreolinae) respectively. This seems strong evidence that all members of this family are related.
Hi Ron
I realize this. Both evolutionists and YEC groups are tied to different Axioms. I am simply advocating to go where the evidence is leading and try to build models based on the evidence.
That is what the whole paper is about, top to bottom. The several lines of evidence all lead to chromosome fusion events.
Based on assuming they share ancestry. This use of common descent as an axiom is very problematic.
Based on population genetic models and other mammals chromosome variation why would we believe this?
Because the evidence is convincing, which is why pretty much everybody but you is convinced.
BTW, common descent is not an axiom. It is presumed because it is a well established hypothesis.
Hi Ron
It is a well established hypothesis based on older data. Why would you not put it to the test with the high frequency sequencing data we have now?
What if UCD turns out to be the wrong model? Isn’t it better to find out sooner than later?
This paper is very speculative but an interesting study because until I saw the chromosome differences I would have assumed that all deer share common ancestry.
