Functional organization of the simian virus 40 origin of DNA replication.

Li, J. J.; Peden, Keith; Dixon, Richard A. F.; Kelly, Thomas J.

doi:10.1128/mcb.6.4.1117

Cited by 180 publications

(186 citation statements)

References 74 publications

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“…1A). The ori core is the minimal SV40 sequence required for SV40 replication in vivo (12)(13)(14)(15)21) and in vitro (15,22) as well as ori-dependent DNA unwinding (22) and can be divided into three elements. These include a 15-bp imperfect inverted repeat (early palindrome), four contiguous GAGGC pentanucleotide sequences contained in a 27-bp perfect inverted repeat, and a 17-bp A/T-rich sequence.…”

Section: Resultsmentioning

confidence: 99%

“…DNase I protection studies ("footprinting") have shown that T antigen bound to site I protects sequences from approximately nucleotide 5175 to 5215, while site II is protected from nucleotide 5215 to 35 (10,11). T antigen site II is essential for SV40 replication, since mutations in this region can completely inhibit replication in vivo and in vitro, whereas site I can be removed with less severe effects (12)(13)(14)(15). However, many studies examining T antigen interactions with the SV40 ori in vitro were performed under conditions that do not support replicatione.g., incubations were at low temperatures (usually 00C) and lacked ATP.…”

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confidence: 99%

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ATP stimulates the binding of simian virus 40 (SV40) large tumor antigen to the SV40 origin of replication.

Borowiec¹,

Hurwitz²

1988

Proc. Natl. Acad. Sci. U.S.A.

128

110

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Simian virus 40 (SV40) large tumor antigen (T antigen) Past studies have indicated that there are two major binding sites for T antigen located in the ori region, designated binding sites I and II (9). T antigen has a 20-to 30-fold higher affinity for site I than site 11 (2). DNase I protection studies ("footprinting") have shown that T antigen bound to site I protects sequences from approximately nucleotide 5175 to 5215, while site II is protected from nucleotide 5215 to 35 (10, 11). T antigen site II is essential for SV40 replication, since mutations in this region can completely inhibit replication in vivo and in vitro, whereas site I can be removed with less severe effects (12-15). However, many studies examining T antigen interactions with the SV40 ori in vitro were performed under conditions that do not support replicatione.g., incubations were at low temperatures (usually 00C) and lacked ATP.The interactions between T antigen and ori have been examined recently under conditions that support SV40 DNA replication. The presence of ATP or dATP induced formation of a complex that was detected by electron microscopy and gel mobility-shift assays (16). In this paper, we have examined in greater detail the interaction of T antigen with ori in vitro, using DNase I footprinting and nitrocellulose filter binding. We have found that under conditions that support SV40 DNA replication, incubation at 37°C in the presence of ATP greatly stimulated the formation of a complex of T antigen with binding site II. We suggest that the ATPdependent formation of this complex is an essential prerequisite for the initiation of SV40 DNA replication. Similar results have also been obtained by Deb and Tegtmeyer (17). MATERIALS AND METHODSPreparation of T Antigen. T antigen was immunoaffinitypurified from COS-1 cells infected with SV40 cs1085 as described by Wobbe et al. (18).Preparation of End-Labeled SV40 ori Fragments. pSV01-AEP (18) plasmid ori DNA was used to prepare the ori wild-type (wt) fragment (Fig. 1B). The 5'-32P-labeled ori wt fragment was prepared by first cleaving pSV01AEP with EcoRI and, after dephosphorylation, labeling 5' ends with [y-32P]ATP and phage T4 polynucleotide kinase (Boehringer Mannheim). Fragments labeled uniquely on the top strand (the strand containing adenosine residues in positions 21 to 28) were produced by digestion with Sph I, whereas fragments specifically labeled on the bottom strand were prepared by cleavage with the restriction enzyme Hinf I. The digested DNA fragments were separated by electrophoresis on 8% polyacrylamide gels, and the desired fragment was localized by autoradiography and purified.pOR1 DNA (12) was used to prepare DNA fragments containing the SV40 "ori core" (defined in Results; Fig. 1A). ori core fragments, uniquely 5'-end-labeled on the top strand, were obtained by initial cleavage with restriction enzyme Nae I followed by end-labeling and Aha II digestion. The order of the two restriction digestions was reversed to prepare ori core DNA labeled on the bottom strand...

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Section: Resultsmentioning

confidence: 99%

mentioning

confidence: 99%

ATP stimulates the binding of simian virus 40 (SV40) large tumor antigen to the SV40 origin of replication.

Borowiec¹,

Hurwitz²

1988

Proc. Natl. Acad. Sci. U.S.A.

128

110

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“…The early domain is essential for both in vivo and in vitro replication. Its deletion reduces T-antigen-driven replication in COS-1 cell extracts 10-fold and SV40 replication in vivo 20-fold (24). Point mutants defective in replication also cannot bind the factor (41), suggesting a role for the early-domain-binding protein.…”

mentioning

confidence: 99%

“…Productive infection depends on prior synthesis of the viral T antigen (40). Replication starts at the viral origin (10,13,40), which spans a minimum of 64 base pairs (bp) (4,16,18,24,28,39) (Fig. 1).…”

mentioning

confidence: 99%

UV-induced early-domain binding factor as the limiting component of simian virus 40 DNA amplification in rodent cells.

Lücke‐Huhle¹,

Mai²,

Herrlich³

1989

Mol. Cell. Biol.

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“…Because of the uncertainty concerning what constitutes a cellular origin of replication, information has come mostly from viral systems where the origins are defined genetically (6,10,21). Among the papova-and adenoviruses, the involvement of transcription regulatory elements in replication control is very well documented (12,25,31). Conversely, template replication is typically required for late gene transcription (9,19).…”

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confidence: 99%

The replication activation potential of selected RNA polymerase II promoter elements at the simian virus 40 origin.

Hoang¹,

Wang²,

Gralla³

1992

Mol. Cell. Biol.

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Binding sites for cellular transcription factors were placed near the simian virus 40 origin of replication, and their effect on replication and TATA-dependent transcription was measured in COS cells. The hierarchy of transcriptional stimulation changed when the plasmids replicated. Only one of seven inserted sequences, a moderately weak transcription element, stimulated replication detectably. However, when two nonstimulatory sites were present in multiple copies they did activate replication. Multiple sites for the chimeric activator GAL4-VP16 did not stimulate replication even though transcription was stimulated strongly. The results indicate that the ability of a binding site to stimulate replication from the simian virus 40 ori is not based on its transcriptional activation potential but is instead related to a separate replication activation potential that can be increased by having multiple sites.The interrelationship between control of cellular replication and transcription has been the subject of extensive experimentation and discussion (10,11,19,38). Because of the uncertainty concerning what constitutes a cellular origin of replication, information has come mostly from viral systems where the origins are defined genetically (6,10,21). Among the papova-and adenoviruses, the involvement of transcription regulatory elements in replication control is very well documented (12,25,31). Conversely, template replication is typically required for late gene transcription (9,19). Thus, there is important communication between control of replication and transcription.The elements jointly controlling DNA and RNA synthesis are generally located near the replication origin in these viruses (5,12,22). These are binding sites for different factors in the different viruses, demonstrating that a variety of factors may play dual regulatory roles. These factors can be derived from the host or encoded by the virus. The host proteins are known to function as transcription factors for cellular genes and include, for example, NFI/CTF, used by BK virus and adenovirus, GC box binding factors such as Spl, used by simian virus 40 (SV40), and a variety of cellular proteins that bind viral enhancer regions (14,25,26,28). Some proteins that influence both processes appear to have separate domains for transcription and replication stimulation (18,32,33,37 to stimulate both replication and transcription was demonstrated. Stimulation of either process required the fused transcription activation domain. There was also a correlation between the strength of transcription activation and that of replication activation (2). This raised the possibility that nearly any transcription factor might have the capacity to stimulate replication when bound near an origin. A potential mechanism for this was that the factor activation domain might interact with a common mediating factor required for both transcription and replication.A different mechanism was suggested by experiments with the host NFI factor used in BK transcription (7). Those results sh...

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Functional organization of the simian virus 40 origin of DNA replication.

Cited by 180 publications

References 74 publications

ATP stimulates the binding of simian virus 40 (SV40) large tumor antigen to the SV40 origin of replication.

ATP stimulates the binding of simian virus 40 (SV40) large tumor antigen to the SV40 origin of replication.

UV-induced early-domain binding factor as the limiting component of simian virus 40 DNA amplification in rodent cells.

The replication activation potential of selected RNA polymerase II promoter elements at the simian virus 40 origin.

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