I thought about including this in my previous thread, but it has grown so large that I suspect it would be lost in the abyss. If Skeptical Zone readers are interested I’ll write a series of these posts, in which I’ll develop a number of themes concerning why I abandoned evolutionary orthodoxy and became convinced that an inference to design is most reasonable.
As most of you know, I am a classical musician. All great musical compositions have a theme, and the theme of this site is “think it possible that you may be mistaken.” With that theme in mind, might I suggest some skepticism concerning probabilities?
One doesn’t need precise numbers to recognize when proposed probabilities are way of whack. When I was growing up and learning mathematics my dad (a professor of chemical physics) admonished me to always check my calculations to see if they made sense on the surface (in my engineering department we call this “using the beverage out the nose” test). If I punch 87 x 53 into my calculator and get 46,481 I immediately know something is wrong (in this case I hit the 7 key twice by accident) even if I don’t know exactly what is wrong, because the result should be somewhere in the hundreds, not thousands. I don’t need to know exactly what the problem is in order to recognize that the result makes no sense.
I apply this logic to probabilities concerning evolutionary theory. We have some good empirical evidence that it took about 10^20 reproductive events for malaria to evolve chloroquine resistance. It could be that Lucy turned into Lizzie in 3.2 million years by stochastic Darwinian mechanisms filtered by natural selection, but I apply the beverage-out-the-nose test concerning the probabilities. Even given the most generous assumptions (a few hundred thousand generations with a few million individuals in each generation) the probabilistic Lucy–to-Lizzie resources don’t pass the smell test, in my view.
So, I ask Skeptical Zone readers: Is my skepticism unwarranted, and if so, why?
Yes, indeed. Specifically genetic variations involved in brain development. There are some potentially interesting candidates.
Noam Ghish,
Once again, lets go back to the human specific TBC1D3 referenced in the paper you cited originally.
http://stke.sciencemag.org/cgi/content/full/sigtrans;2/89/pe59
TBC1D3 is a variant of the RabGTPase family TBC that appears to have evolved along the hominoid-lineage 35 million years ago by segmental duplication.
http://www.pnas.org/content/100/5/2507.short
Importantly, it’s human specific in that there has been a significant increase in *copy number*. Humans have 6 copies of the TBC1D3, chimps and orang-outangs have only two copies of this gene (go to PubMed protein, and do a BLAST search, then a similarity tree on BAK63846.1 TBC1 domain family member 3 [Pan troglodytes]).
Here’s the first 60 amino acids of the Human vs chimp TBC1D3
Query 1 MDVVEVAGSWWAQEREDIIMKYEKGHRAGLPEDKGPKPFGRYNNNVDHLGIVHETELPPL 60
MDVVEVAGSWWAQEREDIIMKYEKGHRAGLPEDKGPKPF YNNNVDHLGIVHETELPPL
Sbjct 1 MDVVEVAGSWWAQEREDIIMKYEKGHRAGLPEDKGPKPFRSYNNNVDHLGIVHETELPPL 60
Your “probability” calculations are completely meaningless, we know gene duplications occur, we know the rates they occur at. You are carrying around at least a couple of gene duplications your parents didn’t have. Mutations that expand the copy numbers of the CYP450 genes are well known in medicine because they have important impacts on drug metabolism.
Indeed if you look at the vast majority of “human specific” genes (and there was only 168 referenced in that paper), the story is the same one as for TBC1D3, where a human variant of an existing protein is expanded (in some cases not even expanded).
http://www.broadinstitute.org/mammals/alpheus/data/human_specific_genes.txt
Choosing a random gene from the above list, ENSG00000101446, this is the protein Kinase inhibitor SPINT3, a member of the KU superfamily. There are highly similar SPINT3 genes (better than 95% similarity) in chimps and orang-outangs, and very similar ones in other primates.
Same for ENSG00000204919 (a proline rich protein of as yet unassigned function), and so on.
There are three proteins that *are* unique to humans, which are frame shifts of genes that were present in the common ancestor of chimps and humans.
http://genome.cshlp.org/content/19/10/1752.full
Again, your “probability” calculations are irrelevant to the origin of these genes.
Since no new gene originates this way, why would you like to see this?
You conception of how new genes arise is a fantasy, which has no relationship to real biology.
I think there is a fundamental error at the base of much evolutionary thinking – a ‘confusion’ between what something is and what it does. Utility – that’s the point, not that something is sticky, but how the stickiness is ‘used’. Stickiness = lump, stickiness as part of a system could be endlessly useful.
damitall,
Damitall you’re way off the page. Binding proteins is exactly nothing, let alone an immune “system”. Enzymes are what they are, to have function they have to be used.
That also applies to your claimed attempts to correct the misunderstandings of others. I have little interest in discussion with one who cannot separate his philosophy from empirical study.