DNA methylation inhibits the transfecting activity of replicative- form phi X174 DNA.
Replacement of virtually all the cytosine residues with 5-methylcytosine residues in the complementary strand of the replicative form (RF) of phi X174 DNA caused a 300- to 500-fold loss in its transfecting activity. Similar results were obtained with analogously methylated M13 RF. Transfection experiments with phi X RF hemimethylated in only part of the molecule, as assessed by analysis with restriction endonucleases, indicated that gene A of phi X, which needs to be nicked at a specific site by the gene A protein for RF replication, was not the main target for this inhibition by DNA methylation. We propose that the loss of transfecting activity was due to hemimethylation of the phi X RF interfering with the processively catalyzed movement of the replication fork.
D044503:5-Methylcytosine; D010584:Bacteriophage phi X 174 / Q000235:genetics* / Q000472:pathogenicity; D003596:Cytosine / Q000031:analogs & derivatives / Q000378:metabolism; D004248:DNA (Cytosine-5-)-Methyltransferases / Q000378:metabolism*; D004261:DNA Replication; D004262:DNA Restriction Enzymes / Q000378:metabolism; D004279:DNA, Viral / Q000096:biosynthesis*; D004926:Escherichia coli; D008780:Methyltransferases / Q000378:metabolism*
D004279:DNA, Viral; D044503:5-Methylcytosine; D003596:Cytosine; D008780:Methyltransferases; D004248:DNA (Cytosine-5-)-Methyltransferases; D004262:DNA Restriction Enzymes