Abstract
Mutations in the Arabidopsis ROS1 locus cause transcriptional silencing of a transgene and a homologous endogenous gene. In the ros1 mutants, the promoter of the silenced loci is hypermethylated, which may be triggered by small RNAs produced from the transgene repeats. The transcriptional silencing in ros1 mutants can be released by the ddm1 mutation or the application of the DNA methylation inhibitor 5-aza-2'-deoxycytidine. ROS1 encodes an endonuclease III domain nuclear protein with bifunctional DNA glycosylase/lyase activity against methylated but not unmethylated DNA. The ros1 mutant shows enhanced sensitivity to genotoxic agents methyl methanesulfonate and hydrogen peroxide. We suggest that ROS1 is a DNA repair protein that represses homology-dependent transcriptional gene silencing by demethylating the target promoter DNA.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, Non-P.H.S.
MeSH terms
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Amino Acid Motifs
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Amino Acid Sequence
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Arabidopsis / genetics*
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Arabidopsis Proteins / genetics*
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Arabidopsis Proteins / physiology*
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Base Sequence
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Cloning, Molecular
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DNA Glycosylases
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DNA Methylation
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DNA Repair
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DNA, Complementary / metabolism
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Dose-Response Relationship, Drug
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Gene Silencing*
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Green Fluorescent Proteins
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Luminescent Proteins / metabolism
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Lyases / genetics*
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Molecular Sequence Data
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Mutation*
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N-Glycosyl Hydrolases / genetics*
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Nuclear Proteins / genetics*
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Nuclear Proteins / physiology*
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Promoter Regions, Genetic
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Protein Structure, Tertiary
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Recombinant Fusion Proteins / metabolism
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Sequence Homology, Amino Acid
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Transcription, Genetic*
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Transgenes
Substances
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Arabidopsis Proteins
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DNA, Complementary
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Luminescent Proteins
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Nuclear Proteins
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ROS1 protein, Arabidopsis
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Recombinant Fusion Proteins
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Green Fluorescent Proteins
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DNA Glycosylases
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N-Glycosyl Hydrolases
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Lyases