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Cytosine methylation and the ecology of intragenomic parasites

Yoder, Jeffrey A., Walsh, Colum P., Bestor, Timothy H.·1997·Trends in Genetics
DOI 10.1016/s0168-9525(97)01181-5
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Abstract

Most of the 5-methylcytosine in mammalian DNA resides in transposons, which are specialized intragenomic parasites that represent at least 35% of the genome. Transposon promoters are inactive when methylated and, over time, C-->T transition mutations at methylated sites destroy many transposons. Apart from that subset of genes subject to X inactivation and genomic imprinting, no cellular gene in a non-expressing tissue has been proven to be methylated in a pattern that prevents transcription. It has become increasingly difficult to hold that reversible promoter methylation is commonly involved in developmental gene control; instead, suppression of parasitic sequence elements appears to be the primary function of cytosine methylation, with crucial secondary roles in allele-specific gene expression as seen in X inactivation and genomic imprinting.

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  • A number of epigenetic gene silencing mechanisms, such as cytosine methylation, genomic imprinting and heterochromatin, are thought to have evolved as defense mechanisms against transposition.

    “A number of epigenetic gene silencing mechanisms, such as cytosine methylation [52], genomic imprinting [53] and heterochromatin [54] are thought to have evolved as defense mechanisms against transposition.”

    From A Family of Human MicroRNA Genes from Miniature Inverted-Repeat Transposable Elements (2007) · cites this paper as [52]

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Metadata

Authors
Yoder, J. A., Walsh, C. P., & Bestor, T. H.
Venue
Trends in Genetics
Publisher
Elsevier BV
Published
1997-08
Volume
13
Issue
8
Pages
335-340
ISSN
0168-9525
DOI
10.1016/s0168-9525(97)01181-5
Cited by
1,562
References
0
Language
en
Licence

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