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Discussion
Acknowledgements
This work was supported by National Basic Research Program of China (Grant No. 2006CB100106), National Natural Science Foundation of China (NSFC 30571196, 0933ZF11C1, and 0933Z411C1), The Ministry of Science and Technology of China (Grant No. 2007AA10Z187).
Keywords
CpG island; CpG cluster; CG clusters; Methylation; Epigenetics; Promoter; Prediction algorithm
CpG dinucleotides have been commonly observed to be only ～20 to 25% as what expected in most sequenced mammalian genomes [1] and [2]. Such a great deficit PluriSIn 1 attributed to the hypermutability of methylated CpGs to TpGs/CpAs [3]. It has been estimated ～80% of CpGs are methylated in mammalian genomes [4]. In contrast, CpGs in GC-rich regions such as CpG clusters and CGIs are usually unmethylated, which is an important feature in the promoter regions of genes and for the regulation of gene expression [4]. For example, hypermethylation of promoter-associated CGIs in tumor suppressor genes were found to cause carcinogenesis [5]. Although most promoter-associated CGIs remain unmethylated [6], recent studies revealed a sizable fraction of CGIs might be fully methylated in normal cells [6], [7], [8] and [9].