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Interference with protein binding at AP2 sites by sequence‐specific methylation in the late E2A promoter of adenovirus type 2 DNA
Author(s) -
Hermann Ralf,
Doerfler Walter
Publication year - 1991
Publication title -
febs letters
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.593
H-Index - 257
eISSN - 1873-3468
pISSN - 0014-5793
DOI - 10.1016/0014-5793(91)80391-f
Subject(s) - biology , ap 1 transcription factor , microbiology and biotechnology , dna , promoter , methylation , dna methylation , epigenetics of physical exercise , transcription (linguistics) , consensus sequence , transcription factor , creb , nucleic acid sequence , binding site , dna binding site , genetics , gene , gene expression , linguistics , philosophy , base sequence
The in vitro methylation of the +6, +24, and −215 located 5′‐CCGG‐3′ sequences in the late E2A promoter of adenovirus type 2 (Ad2) DNA abrogates promoter function. 3‐Methyldeoxycytidine (5‐mC) at positions +6 and +24 in both or either of the two DNA complements in the late E2A promoter abolishes the formation of high‐molecular‐mass DNA‐protein complex that is essential for promoter function. The formation of this complex can be competed for by an oligodeoxyribonucleotide with a consensus AP2 sequence, but not by AP1, AP3, and CREB sequences, The AP2 sites comprise the +6 and +24 located 5′‐CCGG‐3′ sequences in the late E2A promoter; the AP1, AP3, and CREB sequences are in their immediate vicinity, Methylation of either the +6 or the +24 5′‐CCGG‐3′ sequence also compromises formation of the DNA‐protein complex. A 40 nucleotide pair oligodeoxyribonucleotide encompassing the −215 5′‐CCGG‐3′ site in the late E2A promoter can also form DNA‐protein complexes which is not affected by the introduction of a 5‐mC residue in the −215 position. The data suggest that the AP2 protein together with other proteins is involved in the generation of a transcription‐activating complex with the late E2A promoter of Ad2 DNA, and the formation of this complex is completely abolished when both the +6 and +24 5′‐CCGG‐3′ sequences are methylated.