Abstract

The methylation of cytosine in mammalian DNA has proven to be an enigma to scientists since its discovery more than 30 years ago. There are several apparent roles for the methylation of DNA in eukaryotic cells, the exceptions being Drosophila yeast. The absence of DNA methylation in the latter two examples suggests that the fundamental mechanisms of DNA metabolism can exist without modification of cytosine. Probably the most common phenomenon ascribed in DNA methylation is the control of gene activity at the level of transcription (Bird, 1986; Lindsay and Bird, 1988). Methylation of key cytosine moieties is mediated by the mammalian DNA cytosine-5-methyltransferase (MeTase), and is specific for the dinucleotide sequence CpG (Bestor et al., 1988; Doerfler, 1983; Santi et al., 1983; Smith et al., 1991). The CpG sequences are often found localized in clusters and are referred to as “CpG islands” (Bird, 1986). Gene promoters which occupy such islands are susceptible to inactivation, but the process which determines what genes are to be selectively inactivated is currently unknown. A key feature of the regulation of gene activity by hypermethylation of CpG sequences is the epigenetic manner by which the cell strictly maintains DNA methylation patterns. The term “epigenetic” was introduced to permit the addition of another level of information, separate from alteration of the actual gene sequence, to allow the stable inheritance of, in this case, gene activity patterns (Holliday, 1990). The breakdown in the relaying of epigenetic information would result in the disarray of gene expression and ultimately cellular dysfunction.KeywordsHuman Immunodeficiency VirusHuman Immunodeficiency Virus TypeHuman Immune Deficiency VirusHuman Immunodeficiency Virus LatencyTranscriptional BlockThese keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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