"Even genes on the same chromosome are randomly recombined due to crossing over."
But the points at which the recombination take place are not.
"On top of that, if you're going to define a complex mutation by the number of base pairs involved (since you effectively disregard recombination as nonrandom) and you want to see this scale of viable mutation in the last hundred years in order to demonstrate evolution in action - then you're actually asking for evidence against evolutionary theory, which indicates that random mutation causes large changes over millions of years, not hundreds."
What you seem to be saying here is that neo-Darwinism is untestable. However, there are ways to speed up frequency of mutations in the lab, without affecting their distribution.
"No. Errors in replication are a fundamental part of the chemistry involved in DNA polymerase activity. We understand it very well."
We understand _some_ of it very well. But, for instance, it seems that E. Coli can actually regulate how well DNA polymerase operates, based on stress conditions:
http://www.pubmedcentral.gov/articlerender.fcgi?tool=pubmed&pubmedid=14617178
So, the regulation of the error-production/correction mechanism is controlled by the cell itself. It appears that if it senses that it needs adaptation, it will employ more error-prone methods of gene duplication.
I don't doubt that in the future, it will also be determined that _which_ genes are the subject of mutagenesis will be shown to be influenced by the cellular control system. Perhaps it already has, and I am just not yet aware of the article.
Sure they are. Recombination varies linearly with distance. The further apart two genes are, the more likely a recombination will occur between them, because crossing over is random.
I noticed you also ignored the point that chromosome segregation is random. Convenient.
What you seem to be saying here is that neo-Darwinism is untestable. However, there are ways to speed up frequency of mutations in the lab, without affecting their distribution.
No, I'm saying that what we've observed is consistent with evolutionary theory.
We understand _some_ of it very well. But, for instance, it seems that E. Coli can actually regulate how well DNA polymerase operates, based on stress conditions:
First of all, it's DNA Poly III, not IV or V, that performs large-scale replications in E.Coli.
Second of all, this doesn't change the fact that random errors are introduced by all polymerases; regulating the activity of an error-prone polymerase does not change the random nature of the mutagenesis. It's just another way that prokaryotes can encourage diversity, which is necessary for survival by natural selection - which is consistent with evolutionary theory.
Finally, I notice you didn't answer my question about complexity, which is at the heart of the issue here. You want to see a complex adaptation, but you refuse to precisely define it.
How many base pairs are required to make an adapatation complex?
Can a prokaryote even show a complex adapatation that would satisfy your criteria?