Cloned mouse DNA fragments can replicate in a simian virus 40 T antigen-dependent system in vivo and in vitro.

Ariga, H; Tsuchihashi, Z; Naruto, M; Yamada, M

doi:10.1128/mcb.5.3.563

Cited by 12 publications

(6 citation statements)

References 30 publications

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“…Autonomous replication of isolated mammalian sequences has also been reported (1,31); however, autonomous replication of mammalian DNA shown to contain an OBR by biochemical methods (12,13,20,27) has not yet been observed. Our data strongly indicate that origins which initiate the replication of chromosomal sequences can also initiate the replication of extrachromosomal sequences.…”

Section: Discussionmentioning

confidence: 99%

Localization of a bidirectional DNA replication origin in the native locus and in episomally amplified murine adenosine deaminase loci.

et al. 1993

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Gene amplification is frequently mediated by the initial production of acentric, autonomously replicating extrachromosomal elements. The 4,000 extrachromosomal copies of the mouse adenosine deaminase (ADA) amplicon in B-1/50 cells initiate their replication remarkably synchronously in early S phase and at approximately the same time as the single-copy chromosomal locus from which they were derived. The abundance ofADA sequences and favorable replication timing characteristics in this system led us to determine whether DNA replication initiates in ADA episomes within a preferred region and whether this region is the same as that used at the corresponding chromosomal locus prior to amplification. This study reports the detection and localization of a discrete set of DNA fragments in the ADA amplicon which label soon after release of synchronized B-1/50 cells into S phase. A switch in template strand complementarity of Okazaki fragments, indicative of the initiation of bidirectional DNA replication, was found to lie within the same region. This putative replication origin is located approximately 28.5 kbp upstream of the 5' end of the ADA gene. The same region initiated DNA replication in the single-copy ADA locus of the parental cells. These analyses provide the first evidence that the replication of episomal intermediates involved in gene amplification initiates within a preferred region and that the same region is used to initiate DNA synthesis within the native locus.Amplification and consequent overexpression of oncogenes and growth factor receptor genes occurs in many human and rodent cancer cells in vivo. Amplification of a large number of target genes has also been shown to underlie the drug resistance of many mammalian cell lines propagated in vitro (see references 4, 5, 9, 43, and 44 for recent reviews). It is reasonable to infer that oncogene amplification contributes to tumor cell growth or survival since recent studies reveal that reducing the expression of oncogenes by antisense strategies (51) or by elimination of amplified oncogenes (49) reduces tumorigenicity.In many cases, the initial molecular intermediates of gene amplification are genetically unstable (see reference 26 for an early example and reference 50 for a review) and consist of chromosome fragments lacking centromeres (see reference 52 for a recent study and reference 53 for a review). These fragments often appear as heterogeneously sized, paired chromatin bodies called double minute chromosomes (DMs) (3,10,17,39). DMs can be formed by chromosome breakage (40, 52), resulting in the generation and subsequent oligomerization of submicroscopic circular precursors referred to as episomes or amplisomes (7,13,37,38,48,52), or by the generation of microscopically visible fragments in a single step (34,40,52 amplification suggests either that such structures are preferred intermediates or that they offer more substantial survival advantages than chromosomal amplicons in vivo (50).The common occurrence of DMs and their submicroscopic precursor...

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Section: Discussionmentioning

confidence: 99%

Localization of a bidirectional DNA replication origin in the native locus and in episomally amplified murine adenosine deaminase loci.

et al. 1993

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“…It is not yet clear whether SV40 T-antigen and the ori sequence are required for replication in embryos. Thus, SV40 replication may represent either a low level of T-antigen-dependent viral DNA replication that results from the large number of viral DNA molecules injected or it may be analogous to replication of a cellular o(i sequence similar to the one described by Ariga et al (3).…”

Section: -Cellmentioning

confidence: 99%

Sequence-dependent DNA replication in preimplantation mouse embryos.

Wirak¹,

Chalifour²,

Wassarman³

et al. 1985

Mol. Cell. Biol.

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Circular, double-stranded DNA molecules were injected into nuclei of mouse oocytes and one-or two-cell embryos to determine whether specific sequences were required to replicate DNA during mouse development.Although all of the injected DNAs were stable, replication of plasmid pML-l DNA was not detected unless it contained either polyomavirus (PyV) or simian virus 40 (SV40) DNA sequences. Replication occurred in embryos, but not in oocytes. PyV DNA, either alone or recombined with pML-l, underwent multiple rounds of replication to produce superhelical and relaxed circular monomers after injection into one-or two-cell embryos. SV40 DNA also replicated, but only 3% as well as PyV DNA. Coinjection of PyV DNA with either pML-1 or SV40 had no effect on the replicating properties of the three DNAs. These results are consistent with a requirement for specific cis-acting sequences to replicate DNA in mammalian embryos, in contrast to sequence-independent replication of DNA injected into Xenopus eggs. Furthermore, PyV DNA replication in mouse embryos required PyV large T-antigen and either the a-,8-core or ,-core configuration of the PyV origin of replication. Although the a-core configuration replicated in differentiated mouse cells, it failed to replicate in mouse embryos, demonstrating cell-specific activation of an origin of replication. Replication or expression of PyV DNA interfered with normal embryonic development. These results reveal that mouse embryos are permissive for PyV DNA replication, in contrast to the absence of PyV DNA replication and gene expression in mouse embryonal carcinoma cells.Although ori sequences have not yet been demonstrated as functional elements of eucaryotic chromosomes, they are implicated strongly by the temporal order of gene replication (11, 36); the selective amplification of specific genes (53,65,74); the existence of autonomously replicating sequences (26,76); and the fact that all bacterial, viral, plasmid, and organelle genomes require one or more unique cis-acting sequences that act as origins of replication (ori) and interact with specific gene products. However, some observations suggest that DNA replication during the early stages of embryonic development may not require sequence-specific origins of replication to carry out DNA replication.Analysis of DNA replication in Drosophila melanogaster (6,56,85) has revealed that the average distance between chromosome replication bubbles in preblastomere embryos is at least five times smaller than that in differentiated cells, suggesting that embryos initiate replication at many more sequences than do differentiated cells of the same species. Furthermore, injection of DNA into Xenopus eggs revealed that semiconservative DNA replication can occur under the apparent control of the cell division cycle but with no apparent requirement for specific DNA sequences (34,57,58). All of the DNA molecules examined, including simian virus 40 (SV40) and polyomavirus (PyV) DNA which normally replicate only in differentiated cells of a specific m...

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“…With the advent of soluble systems capable of initiating SV40 DNA replication in vitro (21)(22)(23)(24), it was possible to determine which DNA sequence exhibited the strongest affinity for replication initiation factors by its ability to inhibit replication of a second plasmid containing the SV40 oriregion. Surprisingly, the DNA binding site for a limiting factor(s) required to initiate SV40 DNA replication did not coincide with ori-core and did not include the strongest T-Ag binding sequences, although it was specific for SV40.…”

mentioning

confidence: 99%

DNA binding site for a factor(s) required to initiate simian virus 40 DNA replication.

Yamaguchi¹,

DePamphilis²

1986

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

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Efficient initiation of DNA replication in the absence of nonspecific DNA repair synthesis was obtained by using a modification of the system developed by J. J. Li and T. J. Kelly [(1984) Proc. Natl. Acad. Sci. USA 81, [6973][6974][6975][6976][6977].Circular double-stranded DNA plasmids replicated in extracts of CV-1 cells only when the plasmids contained the cis-acting origin sequence for simian virus 40 DNA replication (on) and the extract contained simian virus 40 large tumor antigen. Competition between plasmids containing on and plasmids carrying deletions in and about on served to identify a sequence that binds the rate-limiting factor(s) required to initiate DNA replication. The minimum binding site (nucleotides 72-5243) encompassed one-half of the simian virus 40 on sequence that is required for initiation of replication (oni-core) plus the contiguous sequence on the late gene side of on-core containing G+C-rich repeats that facilitates initiation (oni-auxiliary). This initiation factor binding site was specific for the simian virus 40 on region, even though it excluded the high-affmlity large tumor antigen DNA binding sites.With the exception of initiation of DNA replication, all subsequent steps in the replication and assembly of simian virus 40 (SV40) chromosomes utilize host-cell components exclusively (1, 2). Initiation ofviral DNA replication requires the cis-acting 63-base-pair (bp) ori-core sequence, SV40 large tumor antigen (T-Ag), and permissive cell factors from monkey or human cells. Bidirectional replication then originates at the junction between the strongest DNA binding site for T-Ag and ori-core (Fig. 1). The 40-45 bp flanking either side of ori-core (ori-auxiliary; Fig. 1) are not required for replication, although they do stimulate replication 3-to 5-fold.Purified SV40 T-Ag binds most strongly to the early gene-side auxiliary sequence (site I), less strongly to the ori-core sequence (site II), and marginally to the late geneside auxiliary sequence and beyond (site III; Fig. 1). Mutations within sites I and II alter the affinity of T-Ag for DNA (6)(7)(8)19). These sites are biologically significant because mutations within ori that reduce or prevent replication can be suppressed by mutations in T-Ag (20), and mutations within site I that reduce the ability of T-Ag to regulate its own synthesis are overcome by mutations in T-Ag (7). Since most of binding sites I and III can be deleted with only a marginal effect on replication, initiation of DNA replication must involve binding of T-Ag to site II (ori-core), perhaps aided by the strong affinity of T-Ag to site I. Thus, one might expect ori-core and perhaps T-Ag binding site I to be the primary binding site for the protein complex responsible for initiating SV40 DNA replication.With the advent of soluble systems capable of initiating SV40 DNA replication in vitro (21-24), it was possible to determine which DNA sequence exhibited the strongest affinity for replication initiation factors by its ability to inhibit replication of a s...

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Cloned mouse DNA fragments can replicate in a simian virus 40 T antigen-dependent system in vivo and in vitro.

Cited by 12 publications

References 30 publications

Localization of a bidirectional DNA replication origin in the native locus and in episomally amplified murine adenosine deaminase loci.

Localization of a bidirectional DNA replication origin in the native locus and in episomally amplified murine adenosine deaminase loci.

Sequence-dependent DNA replication in preimplantation mouse embryos.

DNA binding site for a factor(s) required to initiate simian virus 40 DNA replication.

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