Pyrimidine dimers block simian virus 40 replication forks.

C. A. Berger, H. J. Edenberg

Research output: Contribution to journalArticle

41 Scopus citations

Abstract

UV light produces lesions, predominantly pyrimidine dimers, which inhibit DNA replication in mammalian cells. The mechanism of inhibition is controversial: is synthesis of a daughter strand halted at a lesion while the replication fork moves on and reinitiates downstream, or is fork progression itself blocked for some time at the site of a lesion? We directly addressed this question by using electron microscopy to examine the distances of replication forks from the origin in unirradiated and UV-irradiated simian virus 40 chromosomes. If UV lesions block replication fork progression, the forks should be asymmetrically located in a large fraction of the irradiated molecules; if replication forks move rapidly past lesions, the forks should be symmetrically located. A large fraction of the simian virus 40 replication forks in irradiated molecules were asymmetrically located, demonstrating that UV lesions present at the frequency of pyrimidine dimers block replication forks. As a mechanism for this fork blockage, we propose that polymerization of the leading strand makes a significant contribution to the energetics of fork movement, so any lesion in the template for the leading strand which blocks polymerization should also block fork movement.

Original languageEnglish (US)
Pages (from-to)3443-3450
Number of pages8
JournalMolecular and cellular biology
Volume6
Issue number10
DOIs
StatePublished - Oct 1986
Externally publishedYes

ASJC Scopus subject areas

  • Molecular Biology
  • Cell Biology

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