Induction and maintenance of nonsymmetrical DNA methylation in Neurospora.

Abstract:

:One can imagine a variety of mechanisms that should result in self-perpetuating biological states. It is generally assumed that cytosine methylation is propagated in eukaryotes by enzymes that specifically methylate hemimethylated symmetrical sites (e.g., (5')CpGGpC(5') or (5')CpNpGGpNpC(5')). Although there is wide support for this model, we and others have found examples of methylation that must be propagated by a different mechanism. Most methylated regions of the Neurospora genome that have been examined are products of repeat-induced point mutation, a premeiotic genome defense system that litters duplicated sequences with C.G to T.A mutations and typically leaves them methylated at remaining cytosines. In general, such relics of repeat-induced point mutation are capable of triggering methylation de novo. Nevertheless, some reflect a mechanism that can propagate heterogeneous methylation at nonsymmetrical sites. We propose that de novo and maintenance methylation are manifestations of a single mechanism in Neurospora, catalyzed by the DIM-2 DNA methyltransferase. The action of DIM-2 is controlled by the DIM-5 histone H3 Lys-9 methyltransferase, which in turn is influenced by other modifications of histone H3. DNA methylation indirectly recruits histone deacetylases, providing the framework of a self-reinforcing system that could result in propagation of DNA methylation and the associated silenced chromatin state.

authors

Selker EU,Freitag M,Kothe GO,Margolin BS,Rountree MR,Allis CD,Tamaru H

doi

10.1073/pnas.182427299

keywords:

subject

Has Abstract

pub_date

2002-12-10 00:00:00

pages

16485-90

eissn

0027-8424

issn

1091-6490

pii

182427299

journal_volume

99 Suppl 4

pub_type

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