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PMID: 6321756 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't Research Support, U.S. Gov't, Non-P.H.S. Research Support, U.S. Gov't, P.H.S.

DNA methylation inhibits the transfecting activity of replicative- form phi X174 DNA.

Journal of virology ·Vol. 49 ·No. 3 ·1984-03-00 ·Pages 674-9

Wang RY, Shenoy S, Ehrlich M

Abstract

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.

MeSH Terms
5-Methylcytosine Bacteriophage phi X 174/genetics,pathogenicity Cytosine/analogs & derivatives,metabolism DNA (Cytosine-5-)-Methyltransferases/metabolism DNA Replication DNA Restriction Enzymes/metabolism DNA, Viral/biosynthesis Escherichia coli Methyltransferases/metabolism
Chemicals
DNA, Viral 5-Methylcytosine Cytosine Methyltransferases DNA (Cytosine-5-)-Methyltransferases DNA Restriction Enzymes
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Wang R Y
Shenoy S
Ehrlich M
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37 references, click to expand
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Article Info
Journal
Journal of virology
Abbr.
J Virol
ISSN
0022-538X
DOI
10.1128/JVI.49.3.674-679.1984
Published
1984-03-00
Pages
674-9
Language
English
Region
United States
NLM ID
0113724
PMCID
PMC255523
Subset
IM
Grants
NIGMS NIH HHS · GM26986 · United States
External Links
PubMed source DOI: 10.1128/JVI.49.3.674-679.1984 PMC Full Text View journal details
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