Journal
CURRENT BIOLOGY
Volume 12, Issue 16, Pages 1360-1367Publisher
CELL PRESS
DOI: 10.1016/S0960-9822(02)00976-4
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- NIGMS NIH HHS [GM60398] Funding Source: Medline
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Background: The heterochromatin of many eukaryotes is marked by both DNA methylation and histone H3 lysine 9 (H3-K9) methylation, though the exact relationship between these epigenetic modifications is unknown. In Neurospora, H3-K9 methylation is required for the maintenance of all known DNA methylation. In Arabidopsis, H3-K9 methylation directs some of the CpNpG and asymmetric methylation. However, it is not known in any organism whether DNA methylation may also direct histone H3 methylation. Results: Using chromatin immunoprecipitation (ChIP) assays, we show that Arabidopsis heterochromatin is associated with H3-K9 methylation. This histone methylation is dependent on the KRYPTONITE and DDM1 genes (SU[VAR]3-9 and SWI2/SNF2 homologs, respectively). We also find that a decrease in DNA methylation does not directly cause a loss of H3-K9 methylation. Instead, a decrease in H3-K9 methylation is only seen at loci where transcription is derepressed. Conclusions: We conclude that DNA methylation does not control the methylation of histone H3-K9. We propose that loss of H3-K9 methylation is due to transcriptional reactivation, coupled with deposition of unmethylated nucleosomes. These findings are consistent with recent observations of DNA replication-independent deposition of histone H3.3 in Drosophila. Our results also suggest that, in Arabidopsis, DNA methylation is sufficient for gene silencing, but H3-K9 methylation is not.
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