Replication of Simian Virus 40 and Polyoma Virus Chromosomes

DePamphilis, Melvin L.

doi:10.1007/978-1-4613-2087-6_1

Cited by 17 publications

(8 citation statements)

References 157 publications

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“…The OBR resides in the IR at its junction with aux-l (38,39). Organization of Py on-core is strikingly similar to that of SV40 on-core (26,30,39) and presumably follows the same mechanism of action. transcription factors with a specific activation domain.…”

Section: Resultsmentioning

confidence: 82%

“…Nevertheless, despite the remarkable similarity between their on regions, they do not replicate in the same host cell, and their requirements for auxiliary components appear to differ significantly. SV40 and Py on-cores are strikingly similar in sequence composi-tion and organizational motifs (26,29). They contain all of the cis-acting genetic information necessary for initiating bidirectional DNA replication in the presence of its cognate T-ag and appropriate permissive cell factors (19,24,56,73).…”

mentioning

confidence: 99%

“…The only viral protein required for DNA replication is T-ag, which binds specifically to its cognate on-core and initiates DNA unwinding (8,83). Cellular proteins then initiate bidirectional DNA synthesis on the exposed DNA templates and assemble the newly replicated DNA into chromatin (13,26).…”

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confidence: 99%

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Specific transcription factors stimulate simian virus 40 and polyomavirus origins of DNA replication.

Guo¹,

DePamphilis²

1992

Mol. Cell. Biol.

102

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The origins of DNA replication (ori) in simian virus 40 (SV40) and polyomavirus (Py) contain an auxiliary component (aux-2) composed of multiple transcription factor binding sites. To determine whether this component stimulated replication by binding specific transcription factors, aux-2 was replaced by synthetic oligonucleotides that bound a single transcription factor. Spl and T-antigen (T-ag) sites, which exist in the natural SV40 aux-2 sequence, provided -75 and -20%, respectively, of aux-2 activity when transfected into monkey cells. In cell extracts, only T-ag sites were active. AP1 binding sites could replace completely either SV40 or Py aux-2. Mutations that eliminated API binding also eliminated AP1 stimulation of replication. Yeast GAL4 binding sites that strongly stimulated transcription in the presence of GAL4 proteins failed to stimulate SV40 DNA replication, although they did partially replace Py aux-2. Stimulation required the presence of proteins consisting of the GAL4 DNA binding domain fused to specific activation domains such as VP16 or c-Jun. These data demonstrate a clear role for transcription factors with specific activation domains in activating both SV40 and Py ori. However, no correlation was observed between the ability of specific proteins to stimulate promoter activity and their ability to stimulate origin activity. We propose that only transcription factors whose specific activation domains can interact with the T-ag initiation complex can stimulate SV40 and Py ori-core activity.Most, if not all, of the eukaryotic origins of DNA replication (on) characterized so far consist of two principal components: the core component that determines where replication begins in the chromosome and in which animal species replication occurs, and one or more auxiliary components that stimulate replication in certain cell types (28,30,96). on-core is the minimal cis-acting sequence required to initiate DNA replication under all conditions; it is analogous to a transcription promoter. on-auxiliary sequences generally consist of transcription factor binding sites that are dispensable under some conditions; they are analogous to transcription enhancers. The purpose of auxiliary components may be to regulate DNA replication by determining when initiation occurs. For example, the polyomavirus (Py) on functions only in those mouse cell types that can activate its enhancer (6,12,58,74). In mammalian chromosomes, active genes are replicated early during S phase while quiescent genes are replicated late (82), and initiation of replication may require specific transcription factors (76) that bind DNA sites where replication begins (11).To elucidate the function of on-auxiliary components in mammals, we turned our attention to the origins of DNA replication in simian virus 40 (SV40) and Py. These two closely related viral chromosomes replicate in the nuclei of mammalian cells and, with the exception of a single viral protein (large tumor antigen [T-ag]), rely entirely on the host to replicate their DNA (13,29)....

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Section: Resultsmentioning

confidence: 82%

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confidence: 99%

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Specific transcription factors stimulate simian virus 40 and polyomavirus origins of DNA replication.

Guo¹,

DePamphilis²

1992

Mol. Cell. Biol.

102

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“…The SV40 genome contains a single well-defined origin for DNA replication. In permissive host cells, the viral genome replicates bidirectionally and the newly replicated DNA complexes with histones, forming minichromosomes similar to cellular chromatin (9). Replication is dependent on cellular replication proteins with the exception of a single SV40-encoded protein, T antigen.…”

mentioning

confidence: 99%

Initiation of simian virus 40 DNA replication requires the interaction of a specific domain of human DNA polymerase alpha with large T antigen.

Dornreiter¹,

Copeland²,

Wang³

1993

Mol. Cell. Biol.

114

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Initiation of cell-free simian virus 40 (SV40) DNA replication requires the interaction of DNA polymerase co/primase with a preinitiation complex containing the viral T antigen and cellular proteins, replication protein A, and topoisomerase I or IL To further understand the molecular mechanisms of the transition from preinitiation to initiation, the intermolecular interaction between human DNA polymerase a and T antigen was investigated. We have demonstrated that the human DNA polymerase a catalytic polypeptide is able to associate with SV40 large T antigen directly under physiological conditions. A physical association between these two proteins was detected by coimmunoprecipitation with monoclonal antibodies from insect cells coinfected with recombinant baculoviruses. A domain of human polymerase at physically interacting with T antigen was identified within the amino-terminal region from residues 195 to 313. This domain of human polymerase a was able to form a nonproductive complex with T antigen, causing inhibition of the SV40 DNA replication in vitro. Kinetics of the inhibition indicated that this polymerase domain can inhibit viral replication only during the preinitiation stage. Extra molecules of T antigen could partially overcome the inhibition only prior to initiation complex formation. The data support the conclusion that initiation of SV40 DNA replication requires the physical interaction of T antigen in the preinitiation complex with the amino-terminal domain of human polymerase a from amino acid residues 195 to 313.The papovavirus simian virus 40 (SV40) has been proven to be an exceptionally useful model with which to study the mechanisms of mammalian DNA replication (5, 23, 27, 34). The SV40 genome contains a single well-defined origin for DNA replication. In permissive host cells, the viral genome replicates bidirectionally and the newly replicated DNA complexes with histones, forming minichromosomes similar to cellular chromatin (9). Replication is dependent on cellular replication proteins with the exception of a single SV40-encoded protein, T antigen. The development of a cell-free SV40 DNA replication system has provided an effective functional approach to identifying and characterizing the cellular proteins required for the bidirectional replication of SV40 origin-containing duplex circular DNA (ori-DNA) (27).Several laboratories have identified and characterized seven cellular proteins which in combination with T antigen are sufficient to reconstitute SV40 replication in vitro (5,23,24,34). For initiation of SV40 replication, the first step is the recognition and binding of T antigen to the virus core origin. In the presence of ATP, T antigen forms a double-hexamer nucleoprotein complex and either concomitantly or subsequently induces structural changes in the origin region (2). Along with a multisubunit single-stranded DNA-binding cellular protein, replication protein A (RP-A), and topoisomerase I or II, T antigen further unwinds the origin in a bidirectional manner. This protein complex a...

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“…An alternative view is that viruses are appropriate models for how cells carry out various aspects of DNA replication, including the process of initiation of DNA replication. Studies of viral and mitochondrial genomes have led to the generally held view that DNA replication begins when specific trans-acting proteins (origin recognition proteins) bind to specific cis-acting DNA sequences that encompass from 50 to 1,000 bp of DNA and initiate DNA unwinding at or near the binding site followed rapidly by DNA synthesis on one or both strands (9, 11,13,22). The cis-acting sequence is genetically required for DNA replication and is referred to as an origin of replication (on).…”

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Papillomavirus contains cis-acting sequences that can suppress but not regulate origins of DNA replication

Nallaseth

DePamphilis

1994

J Virol

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Bovine papillomavirus (BPV) DNA has been reported to restrict its own replication and that of the lytic simian virus 40 (SV40) origin to one initiation event per molecule per S phase, which suggests BPV DNA replication as a model for cellular chromosome replication. Suppression of the SV40 origin required two cis-acting BPV sequences (NCOR-1 and-2) and one transacting BPV protein. The results presented in this paper confirm the presence of two NCOR sequences in the BPV genome that can suppress polyomavirus (PyV) as well as SV40 origin-dependent DNA replication as much as 40-fold. However, in contrast to results of previous studies on SV40, most of the suppression of the PyV origin was due to NCOR-1, a 512-bp sequence that functioned independently of distance or orientation with respect to the PyV origin and that was not required for BPV DNA replication. Moreover, NCOR-1 alone or together with NCOR-2 did not restrict the ability of the PyV ori to reinitiate replication within a single S phase and did not require any BPV protein to exert suppression. Furthermore, NCOR-1 did not suppress BPV origin-dependent DNA replication except in the presence of PyV large tumor antigen (T-ag). Since NCOR-1 suppression of PyV origin activity also varied with Tag concentration, suppression of origins by NCOR sequences appeared to require papovavirus Tag. Therefore, it is unlikely that NCOR sequences are involved in regulating BPV DNA replication. When these results are taken together with those from other laboratories, BPV appears to be a slowly replicating version of papovaviruses rather than a model for origins of DNA replication in eukaryotic cell chromosomes.

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Replication of Simian Virus 40 and Polyoma Virus Chromosomes

Cited by 17 publications

References 157 publications

Specific transcription factors stimulate simian virus 40 and polyomavirus origins of DNA replication.

Specific transcription factors stimulate simian virus 40 and polyomavirus origins of DNA replication.

Initiation of simian virus 40 DNA replication requires the interaction of a specific domain of human DNA polymerase alpha with large T antigen.

Papillomavirus contains cis-acting sequences that can suppress but not regulate origins of DNA replication

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