Cooper, David Neil ![]() |
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.
Item Type: | Article |
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Date Type: | Publication |
Status: | Published |
Schools: | Medicine |
Subjects: | R Medicine > R Medicine (General) |
ISSN: | 0045-6039 |
Last Modified: | 27 Oct 2022 08:22 |
URI: | https://orca.cardiff.ac.uk/id/eprint/62082 |
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