No kidding. I recall from a botany course a species that was almost identical to another except that one had 14 chromosomes while the other had 18. Two of the additional chromosomes were clearly just duplicates of two of the 14; the exciting thing about the other two is that they were very good matches to two chromosomes from another plant that was found in the same ecosystem – apparently somehow two chromosomes from a plant of one species got into a seed of another species and the mess worked!
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Cant resist . . . .
Where do the ferrets fit into this? 
Thinking of psychosocial effects, I’ve observed that chest hair also has some – I recently even encountered some twenty-something guys who shaved their chests allegedly because they could get more gals!
If my understanding is correct, hotspots experience higher mutation rates than other regions of the genome. It’s not so much of an allowance, but a higher rate due to the specific features of that region of the genome.
Yes and no. By “allowed” certainly no conscious involvement is meant to be implied. There is only that a number of mechanisms make some regions of the genome more susceptible to variation than others. Any so called “intent” is in hindsight of selected advantage.
Hotspots have a variety of causes, including the inhibition of repair mechanisms and the weakness of the bonds in the AT sequence. But in this case we are talking about “recombination hotspots” where the mechanics of the recombination process are the cause.
In my mind, it is like saying more rain is allowed to fall in the tropics. In the end, perhaps it’s just semantics.
The hotspots are contrasted with “highly conserved regions,” which show that some parts of the genome are more protected from variation. This is expected because natural selection would favor protection of portions of the genome which are more crucial to survival. Since there is obviously no such selection process in weather formation, your analogy is a poor one.
Certainly semantics is involved. But it is more a matter of finding (or inventing) the right terminology to describe what is happening with the greatest accuracy.
What we are trying to decipher is the background mutation rate separate from the effects of selection. In the case of mutational hotspots it is suggesting that the background mutation rate is higher in this region compared to the majority of the genome.
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But our DNA also repairs copy errors as well as more extensive damage, so this goes both ways, not just more mutation in some regions than some “background” mutation rate but also less mutation in conserved regions.
Now this doesn’t happen in viruses. They have mutation right on the edge of population lethality. But that doesn’t work for more complex organisms.
It could be that DNA repair is not consistent across the genome which could contribute to the uneven distribution of inherited mutations. Either way, the result is the same: some regions of the genome tend to have more mutations than others.
From my understanding, RNA viruses mutate at a higher rate because there are no RNA repair mechanisms to fix mutations.
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RNA viruses have a high mutation rate but even they seem to have evolved mechanisms that affect the rate of mutation. Some may be internal as large genomes have a lower mutation rate than small ones, some seem to depend on the host-virus interaction, like varying depending on the host type or lysis time:
Combe & Sanjuan. 2014. Variability in the mutation rates of RNA viruses. Future Virology 9:605-615. DOI:10.2217/fvl.14.41
It would make sense that there are mechanisms in addition to lack of proofreading in viral RNA polymerases.
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