This is the authors' abstract. We don't add key points for this paper.
A model based on DNA methylation is proposed to explain the initiation and maintenance of mammalian X inactivation and certain aspects of other permanent events in eukaryotic cell differentiation. A key feature of the model is the proposal of sequence-specific DNA methylases that methylate unmethylated sites with great difficulty but easily methylate half-methylated sites. Although such enzymes have not yet been detected in eukaryotes, they are known in bacteria. An argument is presented, based on recent data on DNA-binding proteins, that DNA methylation should affect the binding of regulatory proteins. In support of the model, short reviews are included covering both mammalian X inactivation and bacterial restriction and modification enzymes.
Answers are grounded in this paper and cite their sources.
No takes yet. Share an insight, caveat, or question.
Arthur D. Riggs (1975) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: