The initiation of SV40 DNA synthesis is not unique to the replication origin

Martin, Robert G.; Setlow, Valerie Petit

doi:10.1016/0092-8674(80)90624-8

Cited by 56 publications

(24 citation statements)

References 18 publications

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“…This is as expected, since there is no fixed termination site in SV40 (15) 6,1986 A. 100 present to such a large extent (1/3 to 1/2 of the potential RIs) in both control and irradiated populations that this explanation is unlikely; rolling circles generally represent fewer than 2% of the RIs (17). These Y-shaped molecules are most z readily explained as a consequence of breakage at the short regions of single-stranded DNA located at the replication fork (Fig.…”

Section: Methodsmentioning

confidence: 62%

“…In unirradiated SV40, replication forks are symmetrically distributed around the origin of replication ( Fig. 5-7; Tables 1 and 2), showing that the two forks move at approximately equal rates (17,27). UV dramatically changes that situation: a very large proportion of the replicating molecules are asymmetrical ( Fig.…”

Section: Discussionmentioning

confidence: 99%

“…During normal SV40 replication, the two replication forks diverge from a fixed origin (about 30 bp from the BglI site) at approximately equal rates (14,17,27). Thus, the replication forks in a single molecule will usually be at equal distances from the origin (17, 27; see Fig.…”

Section: Methodsmentioning

confidence: 99%

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Pyrimidine dimers block simian virus 40 replication forks.

Berger¹,

Edenberg²

1986

Mol. Cell. Biol.

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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.A variety of chemical and physical agents damage DNA within cells, causing inhibition of DNA replication and transcription, alteration of gene expression, mutagenesis, carcinogenesis, or cell death. Inhibition of DNA replication, when it occurs, is crucial to the fate of the cell: although cells may tolerate some mutations, they must replicate their full complement of DNA before dividing. The structures that result from attempting to replicate a damaged DNA template are the substrates for subsequent repair and recovery processes. Understanding the initial interaction between lesions and the replication fork will therefore provide insight into the mechanisms of recovery.UV light is one of the best-studied of DNA-damaging agents. The primary lesion produced by UV irradiation is the cis-syn cyclobutane pyrimidine dimer (31). The mechanism by which UV inhibits eucaryotic DNA replication remains controversial, especially the question of whether dimers inhibit all, most, or no replication forks. The earliest model (16) proposed that a pyrimidine dimer in the template blocked elongation of a daughter strand without affecting the progression (unwinding and movement) of the replication fork, which reinitiated synthesis about 1,000 nucleotides downstream, leaving a long single-stranded gap that could later be filled de novo (Fig. 1B). This resembles a situation in Escherichia coli, except that in E. coli the gaps are filled by recombination (23,24). An alternative hypothesis (7) is that lesions block the movement of the replication fork itself, as in Fig. 1C. With increasing awareness of the semidiscontinuous nature of DNA replication in mammalian cells (Fig. 1A), the latter model was modified to suggest that lesions in the template for the continuously synthesized (leading) strand block...

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Section: Methodsmentioning

confidence: 62%

Section: Discussionmentioning

confidence: 99%

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Pyrimidine dimers block simian virus 40 replication forks.

Berger¹,

Edenberg²

1986

Mol. Cell. Biol.

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“…Plasmids containing ARS elements, isolated from the Xenopus genome by ARS function in S. cerevisiae, also replicated equally as well as plasmids without the ARS in this system (35). In addition, a simian virus 40 mutant defective in T antigen continued replication at a much lower rate but from many initiation sites (30), suggesting that T antigen might confer specificity but that other replication sites may be utilized without the T antigen.…”

mentioning

confidence: 82%

“…Having documented where replicons typically open in a particular region of the rDNA repeat, it was of interest to learn something about the temporal pattern of replication through' out the S period of the cell cycle. cdc7-1 cells were assayed for bubbles at 10,20,30,40, and 60 min after the release of the block for replication. If cdc7-1 cells have an S period similar to that of cdc74 cells, then their S period is between 40 (38) and 75 (6) min.…”

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confidence: 99%

Electron microscopic study of Saccharomyces cerevisiae rDNA chromatin replication.

Saffer¹,

Miller²

1986

Mol. Cell. Biol.

113

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An electron microscopic study was made of the replication of rDNA chromatin of Saccharomyces cerevisiae. Two different methods were used to synchronize cells. cdc7-1 cells were raised to a restrictive temperature, whereas A364a cells were blocked with mating factor. Replication bubbles typically opened in the nontranscribed spacers of rDNA repeats in both cell types. The mean position of the center of these bubbles corresponds closely to a position where an autonomously replicating sequence previously has been mapped in an rDNA repeat. Clusters of replication bubbles containing up to four bubbles spaced one to three genes apart were seen opening in early S phase.

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Replication of Simian Virus 40 and Polyoma Virus Chromosomes

DePamphilis¹

1987

Molecular Aspects of Papovaviruses

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The initiation of SV40 DNA synthesis is not unique to the replication origin

Cited by 56 publications

References 18 publications

Pyrimidine dimers block simian virus 40 replication forks.

Pyrimidine dimers block simian virus 40 replication forks.

Electron microscopic study of Saccharomyces cerevisiae rDNA chromatin replication.

Replication of Simian Virus 40 and Polyoma Virus Chromosomes

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