Despite being generally under-represented in the genome, CpG sequences represent 
a disproportionately high fraction of sites involved in mutational events 
leading to human genetic disease. Cytosine within CpG dinucleotides is often 
modified to 5-methylcytosine. Deamination of 5-methylcytosine in situ yields a 
thymine, which being mispaired with guanine, is potentially mutagenic. Previous 
reports have indicated that most mutations recovered at these sites appear to 
originate on the non-transcribed strand as C-->T transitions. This trend may 
however, reflect the lack of detectable mutant phenotypes resulting from this 
transition at the complementary positions on the transcribed strand. To date, 
there has not been a good model system in which mutations can be recovered on 
both strands at the same CpG site. The human hprt gene has MeCpG sites contained 
within arginine codons for which mutations have been recovered on both strands. 
From an analysis of a database of hprt mutations, a statistically significant 
strand bias is observed in mutations recovered at CpG sites. We describe some 
models for the bias of mutation distribution observed at MeCpG sites in light of 
this and previous work are described.