Methylation meets acetylation (original) (raw)

Gene silencing

Nature volume 393, pages 311–312 (1998)Cite this article

Promoters can sometimes be oblivious to transcription factors. For example, the ‘silent’ alleles of imprinted mammalian genes clearly have all the factors needed for their transcription, as shown by the active transcription of the other allele in the same nucleus. Such gene silencing depends on mitotic inheritance of transcriptionally repressed chromatin states. In vertebrates and flowering plants, repression is usually associated with methylation of the 5-position of cytosine residues in the underlying DNA.

Histone acetylation was first tied to transcriptional activation in the mid-1960s by Allfrey and colleagues3, and in 1977 Ingram et al. reported4 that n -butyrate can alter cellular differentiation by inhibiting histone deacetylation. The realization that many well-characterized transcriptional regulators exert histone deacetylase or acetyltransferase activity came much later (see ref. 5 for review). Some acetyltransferases are tightly associated with the RNA polymerase II holoenzyme, whereas other acetyltransferases and deacetylases act in concert with nuclear receptors. Moreover, the transcription of specific yeast and fruitfly promoters is abnormal in mutants that are deficient in histone acetylation or deacetylation. Although the effect on individual target genes has yet to be clarified, the different phenotypes indicate that there are many pathways of acetylation and deacetylation5.

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Figure 1: The effects of cytosine methylation and histone deacetylation on transcription.

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  1. the Department of Genetics and Development, College of Physicians and Surgeons of Columbia University, 701 West 168th Street, New York, 10032, New York, USA
    Timothy H. Bestor

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Bestor, T. Methylation meets acetylation.Nature 393, 311–312 (1998). https://doi.org/10.1038/30613

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