Did you know that not all genes have the same mutation rates?
As a matter of fact I did:
"Rates and patterns of molecular evolution:
We observed a total of 199 differences between the human and chimpanzee sequences: 131 transitions (66%), 52 transversions (26%), and 16 insertion-deletion variants (8%). Insertion-deletion variants were less than one-tenth as common as nucleotide substitutions and consisted of changes of 1 bp (8 mutations), 2 bp (5 mutations), 3 bp (1 mutation), and 4 bp (2 mutations). Thus, 15/16 of these insertion-deletion variants would have resulted in frameshift mutations in coding regions. Approximately one-fifth of all single nucleotide mutations were transitions at CpG dinucleotides...
Table 3. Estimates of mutation rate assuming different divergence times and different ancestral population sizes
4.5 mya, pop.= 10,000 mutation rate is 2.7 x 10^-8
4.5 mya, pop.= 100,000 mutation rate is 1.6 x 10^-8
5.0 mya, pop.= 10,000 mutation rate is 2.5 x 10^-8
5.0 mya, pop.= 10,0000 mutation rate is 1.5 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 2.3 x 10^-8
5.5 mya, pop.= 10,000 mutation rate is 1.4 x 10^-8
6.0 mya, pop.= 10,000 mutation rate is 2.1 x 10^-8
6.0 mya, pop.= 100,000 mutation rate is 1.3 x 10^-8
Table 4. Estimates of mutation rate for different sites and different classes of mutation
Transition at CpG mutation rate 1.6 x 10^-7
Transversion at CpG mutation rate 4.4 x 10^-8
Transition at non-CpG mutation rate 4.4 x 10^-8
Transversion at non-CpG mutation rate 5.5 x 10^-9
All nucleotide subs mutation rate 2.3 x 10^-8
Length mutations mutation rate 2.3 x 10^-9
All mutations mutation rate 2.5 x 10^-8
Rates calculated on the basis of a divergence time of 5 mya, ancestral population size of 10,000, generation length of 20 yr, and rates of molecular evolution given in Table 1.
Calculations are based on a generation length of 20 years and average autosomal sequence divergence of 1.33%
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Estimate of the Mutation Rate per Nucleotide in Humans (Michael W. Nachmana and Susan L. Crowella
Genetics, 297-304, September 2000) "
Since this was published the known divergence has grown by 5X:
"Gene families are groups of homologous genes that are likely to have highly similar functions. Differences in family size due to lineage-specific gene duplication and gene loss may provide clues to the evolutionary forces that have shaped mammalian genomes. Here we analyze the gene families contained within the whole genomes of human, chimpanzee, mouse, rat, and dog. In total we find that more than half of the 9,990 families present in the mammalian common ancestor have either expanded or contracted along at least one lineage. Additionally, we find that a large number of families are completely lost from one or more mammalian genomes, and a similar number of gene families have arisen subsequent to the mammalian common ancestor. Along the lineage leading to modern humans we infer the gain of 689 genes and the loss of 86 genes since the split from chimpanzees, including changes likely driven by adaptive natural selection. Our results imply that humans and chimpanzees differ by at least 6% (1,418 of 22,000 genes) in their complement of genes, which stands in stark contrast to the oft-cited 1.5% difference between orthologous nucleotide sequences. This genomic “revolving door” of gene gain and loss represents a large number of genetic differences separating humans from our closest relatives."(The Evolution of Mammalian Gene Families, PLoS ONE. December 20, 2006
And that there are different types of selective pressure that can have a different effect on the rate at which mutations are fixed? (I don't think selection affects the rate of the appearance of mutations, though - it's only that sometimes more, sometimes less of them are weeded out before they can spread)
Considering that the vast majority of mutations are selectively neutral with the bulk of the rest being deleterious I'd say your point is moot.
If selective pressures are stabilising - i.e. deviation from the current sequence in any way would decrease the organism's fitness - then mutations (more precisely, nonsynonymous mutations, those that actually change the gene product) are going to be fixed at a very slow rate. However, directional selection (i.e when deviation in a certain way is advantageous) can accelerate the process immensely.
If and only if a mutation with a beneficial effect happens in the first place.