Abstract
DNA methylation has been implicated in a wide range of biological processes including gene regulation (Razin and Cedar 1991; Finnegan et al. 1993), determination of chromatin structure (Lewis and Bird 1991), timing of DNA replication (Lewis and Bird 1991), genomic imprinting (Sasaki et al. 1993), increasing the spontaneous mutation rate (Coulondre et al. 1978; Duncan and Miller 1980), as the basis for epigenetic phenomena (Holliday 1993), and as a defense mechanism to protect against foreign or invading DNA (Bird 1986; Bestor 1990; Doerfler 1991). Despite this, the existence of organisms such as yeast and Drosophila that lack DNA methylation has led to debate about the role of DNA methylation. There can be no doubt that DNA methylation plays a fundamental role in mouse development following the establishment of a targeted mutation of the DNA methyltransferase gene in the germ line of transgenic mice. Embryos that were homozygous for the mutation had methylation levels reduced to about 30% of wild-type levels. These embryos were stunted and delayed in development compared to their normal siblings and spontaneously aborted in mid-gestation. Although the underlying cause for the embryo-lethal phenotype has not been determined, it has been proposed that inappropriate gene expression resulting from the reduced level of DNA methylation is involved (Li et al. 1992). In contrast, mutants of Neurospora crassa that abolish all detectable methylation showed only minor changes in vigor and growth morphology, suggesting that DNA methylation is not absolutely essential for development of this organism (Foss et al. 1993). This...
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