Requirement of CHROMOMETHYLASE3 for Maintenance of CpXpG Methylation

American Association for the Advancement of Science (AAAS) - Tập 292 Số 5524 - Trang 2077-2080 - 2001
Anders M. Lindroth1, Xiaofeng Cao1, James P. Jackson1, Daniel Zilberman1, Claire M. McCallum2, Steven Henikoff2,3, Steven E. Jacobsen1
1Department of Molecular, Cell, and Developmental Biology, University of California, Los Angeles, CA 90095, USA
2Fred Hutchinson Cancer Research Center, Seattle, WA 98109, USA
3Howard Hughes Medical Institute

Tóm tắt

Epigenetic silenced alleles of the Arabidopsis SUPERMAN locus (the clark kent alleles) are associated with dense hypermethylation at noncanonical cytosines (CpXpG and asymmetric sites, where X = A, T, C, or G). A genetic screen for suppressors of a hypermethylated clark kent mutant identified nine loss-of-function alleles of CHROMOMETHYLASE3 ( CMT3 ), a novel cytosine methyltransferase homolog. These cmt3 mutants display a wild-type morphology but exhibit decreased CpXpG methylation of the SUP gene and of other sequences throughout the genome. They also show reactivated expression of endogenous retrotransposon sequences. These results show that a non-CpG DNA methyltransferase is responsible for maintaining epigenetic gene silencing.

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Supported by NIH grant GM60398 a Beckman Young Investigator grant a Searle Scholar award (S.E.J.) NIH training grants GM07104 (J.P.J.) and GM07185 (D.Z.) and NIH grant GM29009 (S.H.). We thank C. Hyun M. Huang L. Cahoon and H. Le for technical assistance; S. Kaeppler and N. Springer for helpful discussions; and E. Richards for the met1 mutant.