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DNA demethylation by the base‐excision DNA repair pathway in Arabidopsis
Author(s) -
Fischer Robert,
Huh JinHoe,
Penterman Jon,
Gehring Mary,
Zilberman Daniel,
Ballinger Tracy,
Henikoff Steve
Publication year - 2007
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.21.5.a206
Subject(s) - dna glycosylase , dna demethylation , ap site , base excision repair , dna repair , biology , microbiology and biotechnology , dna , nucleotide excision repair , ap endonuclease , methyltransferase , dna methylation , genetics , chemistry , gene , methylation , gene expression
DNA glycosylases repair DNA by excising modified, damaged, or mispaired bases, creating an abasic site. AP endonuclease and DNA polymerase complete the repair process by incorporating a new base at the abasic site. In Arabidopsis, the DEMETER (DME) DNA glycosylase excises 5‐methylcytosine. Abasic sites opposite 5‐methylcytosine inhibit DME activity and might prevent DME from generating double‐stranded DNA breaks. DME DNA glycosylase functions in vivo to demethylate and activate maternal allele transcription of imprinted genes. In flowering plants, the egg and the adjacent central cell are both fertilized to generate the embryo and endosperm, which is a placenta‐like tissue that supports embryo growth. DME is transcribed in the central cell where it demethylates and activates maternal allele expression of imprinted genes. Mutations that suppress dme mutant phenotypes reside in the MET1 DNA methyltransferase gene, which maintains cytosine methylation and is related to the Dnmt1 DNA methyltransferase in mammals. Thus, imprinting is established by DNA demethylation mediated by the DME DNA glycosylase. The role of DNA demethylation in Arabidopsis will be discussed.