Abstract
From an evolutionary point of view, it is likely that #epigeneticmarkers arose as a means of protecting genetic information [1]. The primary epigenetic marker is DNA methylation and DNA #methylation would furnish a way to distinguish between ‘self’ and ‘foreign’ #genetic material as, for example, for the selective action of the restriction #endonuclease system in bacteria [2]. Such an epigenetic marker might plausibly have become subsequently recruited to enable the stabilization of alternative #phenotypic states in differentiated tissues of multicellular organisms, as envisaged by Waddington [3,4]. For terminally differentiated #tissues in which no further cell division takes place, such as CNS neurons, there is no mechanistic difficulty in retaining the status quo, but in order to maintain the stable differentiated phenotype of cells with identical genomes undergoing replication it is necessary for the epigenetic information to be duplicated. The significance of DNA methylation in conferring phenotypic stability to differentiated proliferating cells was proposed by Holliday and Pugh [5] and Riggs [6].
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Epigenetic Error and Large-scale #Genomic Instability in Cancer by Patrick A Riley in BJSTR
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