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Research Article

Pyrimidine dimers block simian virus 40 replication forks.

C A Berger, H J Edenberg
C A Berger
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H J Edenberg
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DOI: 10.1128/MCB.6.10.3443
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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.

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Pyrimidine dimers block simian virus 40 replication forks.
C A Berger, H J Edenberg
Molecular and Cellular Biology Oct 1986, 6 (10) 3443-3450; DOI: 10.1128/MCB.6.10.3443

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Pyrimidine dimers block simian virus 40 replication forks.
C A Berger, H J Edenberg
Molecular and Cellular Biology Oct 1986, 6 (10) 3443-3450; DOI: 10.1128/MCB.6.10.3443
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