Abstract
Cytosine methylation in vertebrate genomes occurs predominantly at the dinucleotide CpG. This dinucleotide is deficient in vertebrate DNA, an observation which has hitherto been explained by passive deamination of S-methylcytosine to thymidine. Since the frequency and distribution of CpG may prove to be a useful indirect means to study the function of DNA methylation, it is of interest that the observed ‘CpG suppression’ is less apparent within and around coding sequences. A variety of different mechanisms now appear to be responsible for maintaining a relatively high CpG level in these regions despite the apparent attendant disadvantage of mutation.
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