I'll deal with the easier answer first, if you don't mind:
As to the stopping evolution, I was under the impression that mutation -and- selection were required. Thus it would take more than change in the way mitosis and meiosis occur.
Yes. It takes both. But mutation is primary. If there is no mechanism of variation, we just have static alleles. So yes, one phenotype would still be selected for, but you would have a finite number of phenotypes because of a finite number of genotypes.
This is primary to mitosis and meiosis. We mutate because A) nucleic acid chains have only so much stability, which is how we get 'induced' mutations; B) the processes of replication and transcription have a certain basal inaccuracy (~10^-6 to 10^-9 depending on the type of creature and which polymerases are used) which gives us 'spontaneous' mutations. Further variation is induced through recombination, also dependent on the biochemical properties of DNA. Some organisms are also lucky enough to be able to use plasmids, conjugation, transformation, and transduction, not us though (although we are working towards transduction with viral gene therapy).
Once this variation occurs two things happen 1) certain changes are selected against (if for no other reason than that any
mutation tends to lower survivability regardless of its benefit); 2) certain changes are selected for (and if this selection overcomes their cost, then they stick around). Now, not all selection is natural selection. In fact, the first chapter of the Origin of Species
is about artificial selection (the mechanism by which we converted wolves to dogs and a undifferentiated cabbage-like ancestor to like 7 different types of edible plant). There is also sexual selection, where one sex determines a sexually desirable feature regardless of its survival benefit (e.g. if overnight all men started only wanting redheads).
So in essence, mutation (and recombination, etc) provides the mechanism, selection (regardless of type) provides the direction.
I have no doubt that there are small scale local adaptions to various environmental conditions - sickle cell, ApoE mutation, and so on. I was thinking more of the large scale macro-level changes that might lead to speciation. The kind of thing that would be to us as we are to various proto-humans.
Am I conceptualising this incorrectly?
A little. Macro-level changes do not occur in leaps (with incredibly
rare exception). This is for several reasons: 1) Genes aren't all they are cracked up to be. This is why I often talk of the "failed promise of genomics". There isn't an X gene (damn you Marvel comics!!!). No one gene works completely alone and the vast majority work in headache inducingly complex networks, one of the features of which is redundancy (this is why we can generally only say you have a pre-disposition to cancer, because it generally takes 3 specific separate gene mutations to get a single benign tumor and 5 for malignancy); 2) Unlike bacteria, we have large non-coding regions and mutations that fall there tend to be silent; 3) only genes in our gametogenic (is that a word ?_?) cells pass on. This is why gene therapies aren't hereditary. So of all the cells in your body, only certain baseline stuff tends to matter for your offspring. Again, this is why if one of your parents was pre-disposed to cancer and indeed contracted cancer, you would still be only pre-disposed and have a chance not to contract cancer.
All of these mechanisms work to ensure that grandiose changes don't happen. And for a very good reason, this is what makes macroscopic life possible. We don't have the luxury of being able to have half of our body die off to select for the resistant bits and let them regenerate into a whole (like say a bacteria colony would). No one gene can make or break us, not even those which we generally think of as causing single gene disorders (like sickle cell, active HbF provides a suppressor mutation). I posted about this a while back when I made reference to the wonderful paper: "Human disease classification in the postgenomic era: A complex systems approach to human pathobiology." Loscalzo, et al. 2007.
The end result is that mutation at the animal level is much less dynamic than under the microscope; and this goes double when you are dealing with humans who are one of the most extreme K-selectors.
I tend to dislike Dawkins (more for his attitude than his actual views), but he does have something relevant to say here:
"Take a rabbit, any female rabbit (arbitrarily stick to females for convenience: it makes no difference to the argument). Place her mother next to her. Now place the grandmother next to the mother and so on back in time, back, back, back through the megayears, a seemingly endless line of female rabbits, each one sandwiched between her daughter and her mother. We walk along the line of rabbits, backwards in time, examining them carefully like an inspecting general. As we pace the line, we'll eventually notice that the ancient rabbits we are passing are just a little different from the modern rabbits we are used to. But the rate of change will be so slow that we shan't notice the trend from generation to generation, just as we can't see the motion of the hour hand on our watches - and just as we can't see a child growing, we can only see later that she has become a teenager, and later still an adult. An additional reason why we don't notice the change in rabbits from one generation to another is that, in any one century, the variation within the current population will normally be greater than the variation between mothers and daughters. So if we try to discern the movement of the 'hour hand' by comparing mothers with daughters, or indeed grandmothers with granddaughters, such slight differences as we may see will be swamped by the differences among the rabbits' friends and relations gamboling in the meadows round about."
-The Greatest Show on Earth Dawkins, 2009