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?
"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 points mutation to certain times and places. That is non-Darwinian, and is more inline with designed mechanisms than atelic processes.
"I noticed you also ignored the point that chromosome segregation is random. Convenient."
It's irrelevant.
"No, I'm saying that what we've observed is consistent with evolutionary theory."
It's more consistent with creationism. We keep on running into teleology in biochemistry.
"First of all, it's DNA Poly III, not IV or V, that performs large-scale replications in E.Coli."
That's precisely the point. Poly IV comes in when and (and possibly where) the organism needs modification. This is a purposeful, planned process.
"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."
Well-matched parts, multiple amino acid changes across multiple genes.
"How many base pairs are required to make an adapatation complex?"
If you are in the hundreds, I would count that as complex.
"Can a prokaryote even show a complex adapatation that would satisfy your criteria?"
There are many complex adaptations. The point is that none of them occur by Darwinian mechanisms. Take for instance Pseudomonas. It can adapt to new food sources within 9 days, by putting together pairs of entirely new genes. Now, if the mutational rate which produced the genes were present throughout the entire genome, error catastrophe would quickly occur. This indicates that the mutation was directed onto a single gene. In fact, the cell even knows to put the new gene on a plasmid to ship it to the rest of the colony that hasn't discovered it yet. I discuss it here:
http://crevo.blogspot.com/2005/06/evolution-chance-and-design-to-cb940.html
Likewise, Behe shows just how slow the Darwinian mechanism is in doing a change of only a few amino acids, if it is even possible at all:
http://www.proteinscience.org/cgi/content/abstract/ps.04802904v1
Our observations of beneficial change in organisms is almost entirely driven by mechanisms of purpose, not happenstance. The idea of Darwinism is almost completely foreign to everything that happens in biochemistry. Are there completely random mutations? Sure, they exist. But they aren't playing a major role in adaptation.