ArticleNucleic acids research2013
Early steps of active DNA demethylation initiated by ROS1 glycosylase require three putative helix-invading residues.
Article in Nucleic acids research, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Base Excision DNA Repair in Plants:International journal of molecular sciences · 2023Review
- Molecular basis of the plant ROS1-mediated active DNA demethylation.Nature plants · 2023Article
- Active DNA Demethylation in Plants.International journal of molecular sciences · 2019Review
- Peroxisomal β-oxidation regulates histone acetylation and DNA methylation inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Protecting DNA from errors and damage: an overview of DNA repair mechanisms in plants compared to mammals.Cellular and molecular life sciences : CMLS · 2017Review
- Measurement of Postreplicative DNA Metabolism and Damage in the Rodent Brain.Chemical research in toxicology · 2015Article
- The carboxy-terminal domain of ROS1 is essential for 5-methylcytosine DNA glycosylase activity.Journal of molecular biology · 2014Article
- 5-methylcytosine recognition by Arabidopsis thaliana DNA glycosylases DEMETER and DML3.Biochemistry · 2014Article
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4 authors.
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Abstract
Active DNA demethylation is crucial for epigenetic control, but the underlying enzymatic mechanisms are incompletely understood. REPRESSOR OF SILENCING 1 (ROS1) is a 5-methylcytosine (5-meC) DNA glycosylase/lyase that initiates DNA demethylation in plants through a base excision repair process. The enzyme binds DNA nonspecifically and slides along the substrate in search of 5-meC. In this work, we have used homology modelling and biochemical analysis to gain insight into the mechanism of target location and recognition by ROS1. We have found that three putative helix-intercalating residues (Q607, R903 and M905) are required for processing of 5-meC:G pairs, but dispensable for excision of mismatched 5-meC. Mutant proteins Q607A, R903A and M905G retain the capacity to process an abasic site opposite G, thus suggesting that all three residues play a critical role in early steps of the base extrusion process and likely contribute to destabilization of 5-meC:G pairs. While R903 and M905 are not essential for DNA binding, mutation of Q607 abrogates stable binding to both methylated and nonmethylated DNA. However, the mutant protein Q607A can form stable complexes with DNA substrates containing blocked ends, which suggests that Q607 intercalates into the helix and inhibits sliding. Altogether, our results suggest that ROS1 uses three predicted helix-invading residues to actively interrogate DNA in search for 5-meC.
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