For years evolutionists have been making hay over the claim that Chimps and Humans are genetically similar to about 99%.  Well it seems that much of that was hype.  The similarities are less than thought and now it appears they are converging on a figure near 94%.  Well below the similarity for mice at nearly 98%.  This is significant because at the same time we have learned how evolution has not been able to produce even one new protein interaction in the billions and billions and billions of lab organisms observed and yet these genetic differences between humans and chimps include thousands of them. 

How can it be?  Evolutionists estimate that the population pool involved in the presumed evolution of humans from ancestral apes is less than 20 billion and in that pool thousands of significant protein structure differences must have occurred if evolution is correct.  Well if so, this completely contradicts experimental biology and molecular biology studies which show that known evolutionary processes don't generate these kinds of changes given the low population density and probability analysis provides the theoretical basis to demonstrate why this is the case.  In order to generate these changes given observed processes, the population pool must be increased billions and billions and billions and billions of time over.

The conclusion should be obvious.  Some process other than random mutation, and the other evolutionary processes along with natural selection had to be involved.

The article below describes how genetics researchers are backing away from the 1% difference claim but it does not discuss the implications directly.  I have added that here for additional possible discussion.

Truth be Told about Human Chimp DNA

Similarities are interesting but they only tell part of the story.  It is the differences that reveal inherent weaknesses in the  evolutionary narrative.  How do you address them?

Well first off it isn't "The Truth Is Now Told About Chimp DNA"; this implies there was a lie, and there wasnt. They were simply incorrect, off by a bit. Could be they're still wrong. Could be we find out in 10 years it's 99% like ours, or more alike with 'more important' dna. This happens when you're actually looking for an answer rather than simply sitting back re-assured in any answer you come up with and prove with mere faith is the right one.


I don't see why that conclusion is obvious in the least. In fact I don't even see what it has to do with it. There is only one thing to conclude when faced with an unknown: that it is unknown. Blackness. A big question mark. Nothing 'obvious' about it. It's not a cue to insert any answer.



Ahk

Thomas Hunt Morgan (Nobel prize in 1933). Almost all known mutant fruit flies with drastic phenotype changes (result of changed protein-protein interaction) were produced in the lab.

It is interesting that RF is ignoring COS, who has responded with scientific, not scientistic, answers. Its a shame that Creationists simply refuse to see real science and focus on propaganda.

Morgan was working (among other things) on how fast do mutations develop, what are the consequences of mutations, where on the chromosome is the cause of mutation. The DNA and protein level of his experiments was explained later.

A typical gene regulatory protein has 2 domains. A DNA binding domain and kinase domain (that interact with protein). A gene is switched on/off either by mutation in DNA binding domain (won't go into details as you are interested in protein:protein) or by mutation in kinase domain. Now mutation in this region does not necessarily cause on/off. It can also result in changed affinity with binding protein (resulting in over expression or lower expression of gene regulated by this protein), or that it binds with a different protein altogether. So yes, there is a changed/new protein:protein interaction.

An even better example is sickle cell anemia in human medicine (but I left this one out, because the initial mutation was not observed in the laboratory, for obvious reasons). One single nucleotide mutation in one of the globin genes changes amino acid sequence in the protein, causing to fold differently, causing to interact with other protein components of hemoglobin in a different way, causing multiple haemoglobin to bind into a cristal structure, interacting with components in the cytoskeleton and on the cell surface to misshape the cell. A whole bunch of new protein:protein interaction from one single nucleotide change.


In know people are often frustrated why fundamental genetics is done on flies, E.coli and mice. There is a very good reason... ethics.


RF is not ignoring me, we have discussed this issues several times before. From my perspective, it is difficult to find simple examples to explain them to forum members. For RF, he tried to explained me in details about ID, but we ended that debate on weather a cloud in the shape of Austria is complex enough or not. It's the criteria of what is complex enough and what not that I don't accept from ID.

About real science vs propaganda vs religion, I am sick of that subject.

I second this COS, I am fascinated by your explanations.

Again I would ask you to recheck your information.  Can you provide a specific example of a new binding site or are you only speaking of changes to existing binding sites resulting in changed binding affinities as you indicated?  Evolution has demonstrated that it can change and in the process break existing function including over and under expression of regulated genes and the out of order expressions I described earlier.  I have asked specifically about new binding sites and new interactions.


Actually this is another example of a change but not in a binding site but rather in a folded area that normally prevents the heme portion of the mutiprotein hemoglobin to contact other areas of the structure that have modest affinity to it and also to other heme structures that are otherwise also protected but only when the heme is not bound to Oxygen.  The result of the change is that existing (unitended)  binding sites are exposed, but these are not new binding sites.  More importantly is the impact of this change.  This change causes the hemoglobin to form up into a gelatinous mess and alters the entire shape of the blood cell causing it to clump in capillaries when the heme is not bound to oxygen and more importantly the spleen recognizes that these cells are deformed and destroys them leading of course to anemia.

The primary point is that this change in the fold only exposed otherwise protedted heme causing a major misfuntion.  These areas that are now exposed existed already.  They are not new.

So do those of you who see the kinds of examples offered as valid indicators of ability to generate the actual observed differences?  Do you believe these examples are "close enough"?

I ask this because if these examples did represent the mechanisms the generated new protein protein interactions and since these single step mutations are relatively frequent (1 per 100,000 base pairs) why is it that the examples are so sparce and why is it that we can't identify even one example of a mutation that exposes a previously concealed potential binding site that builds useful new function?  In other words, why does the narrative not match observation?  


Did you misunderstand? The bizzare effects demonstrated with mutations to regulatory control genes in fruit flies are not in the same category of differences as those between apes and humans and therefore do not offer a solution to the issue I have raised.  They represent changes in control function that dramatically messes up normal developmental function.  They are not new proteins, new protein binding sites and new protein function that make up the differences in expressed genes that this article and this discussion focuses.


Actually I agreed that a cloud shape is absolutely complex enough.  My point was that the shape could not be specified inependently from the event prior to the actual stipulated occurance.  It was not detatchable in that we cannot say that we regularly observe clouds in the shape of countries. The marker for design requires complexity and specification but the cloud represents only complexity.