So, there is evidence that most biological mutations leading to variation are not external events but rather a consequence of different kinds of DNA replciation errors. Mutation probability is not equal across the genome in such cases and is in large part determined by how codons are encoded. The degenerate nature in which different BPs are combined to encode different codons which transcribe for the same amino acid allows for the same genotypic expression to have different mutation probabilities depending upon the encoding. This means that the mutation probability at particular loci is at least in part, susceptable to selection upon the different codon encoidings (and on other encoidng artifacts as well such as repeat sequences, etc) and there is recent research showing that it is selection upon mutation probability that has much to do with creating stable genome elements as well as areas which are more inclined to produce genotypic variation where such variation is advantageous. My term for this, which may actually mean something else in acedemic circles, is 'Genotypic Plasticity".
What this says to me is that an ALife system which provides only externally defined, fixed mutation probabilities and does not allow mutation probability to vary for different parts of the genome and be selected upon is incomplete. In fact, one could argue (I would) that the *primary* source of meaningful mutation and hence variation in nature is not being simulated and that the result is analogous to attempting to evolve in a highly radioactive environment. If the radiation is too high, all things complex wither. If too low, the pace of mutation is insufficient to achieve meaningful variation in finite time. Genotypic Plasticity allows for both I.e. high varation and fast paced mutation where such is advantageous, low mutation probability where such is not...
-E