Polyomavirus origin for DNA replication comprises multiple genetic elements

Muller, William J.; Mueller, C.W.; Mes, A.; Hassell, John A.

doi:10.1128/jvi.47.3.586-599.1983

Cited by 124 publications

(109 citation statements)

References 45 publications

Supporting

Mentioning

105

Contrasting

Order By: Relevance

“…The suggestion that other Py genomic regions play an essential role in determining the expression of viral function, is in agreement with recent results (20) segment in the late Py region as necessary for DNA replication in cis, even though in plasmids the enhancer, the ORI regions, and the large T gene present in trans are by themselves sufficient to ensure DNA replication (7,23,28). This suggestion is further supported by the results obtained (manuscript in preparation) with Py mutants capable of growth in both myoblasts and PR8 cells.…”

Section: Resultssupporting

confidence: 91%

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Maione

Felsani

Pozzi

et al. 1989

J Virol

View full text Add to dashboard Cite

The mRNAs for myogenic functions are coordinately transcribed with polyomavirus (Py) early mRNA during in vitro differentiation of mouse C2 myoblast cells. Sequence analysis shows that the A domain of the Py enhancer includes an ElA-like consensus sequence that is also found in the 5' upstream region of two genes expressed during myoblast differentiation: a-actin and myosin light chain. Therefore, the coordinate expression of such genes with Py early mRNA may be activated by a common cellular regulatory factor. In the present work, we report that C2 cells surviving Py infection are unable to differentiate and do not express a-actin and myosin light-chain mRNAs. Hybrids between such Py-resistant myoblast cells and the parental cells exhibited dominance of the permissibility to Py growth and of the expression of myogenic mRNAs. In C2 cells transiently transfected with a chimeric plasmid (pSVPy12CAT) harboring the bacterial chloramphenicol acetyltransferase (CAT) gene driven by the Py enhancer-promoter region, the CAT gene was expressed irrespective of their stage of differentiation. Moreover, undifferentiated stably transfected cells expressing the CAT gene restricted viral growth. Py-resistant C2 myoblasts transiently transfected with pSVPyl2CAT also expressed the CAT gene driven by the Py enhancer. This contradictory finding is similar to results previously obtained by other investigators with cloned genes specific for myogenic functions, and it may be explained by a structural difference between the pSVPy12CAT and the Py genomic organizations in which the viral enhancer operates.The interaction of oncogenic viruses with differentiating cells has been investigated in different tissue culture systems. The replication of polyomavirus (Py) in murine cells provides valuable insights into gene regulation during the differentiation process, because the expression of viral functions is related to changes in the Py regulatory region (Py-RR) (for a recent review, see reference 1; M.-H. Kryszke and M. Yaniv, Crit. Rev. Biochem., in press). One of the most interesting systems is that of Py expression during differentiation of muscle cells. Fogel and Defendi (11) first reported that explanted myoblasts are susceptible to Py infection. Recently, by using established cell lines, our knowledge of the myogenic process has greatly developed (2,24,26,33). The regulation of myogenic functions occurs at many different stages and levels from transcription to posttranslational control (9). We have previously shown (10) that infecting or transfected Py genomes are unable to express their early functions and replicate in undifferentiated C2 myoblasts, whereas they replicate during myogenesis. Preliminary experiments indicated that early Py mRNA is transcribed in differentiating myoblasts concomitantly with the expression of typical myogenic functions, such as transcription of ox-actin and myosin light-chain (MLC1) mRNA. Sequence analysis of the 5' regulatory regions of several genes coding for myogenic functions (5) reveals the presence...

show abstract

Section: Resultssupporting

confidence: 91%

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Maione

Felsani

Pozzi

et al. 1989

J Virol

View full text Add to dashboard Cite

show abstract

“…The transcription enhancer located on the late side of the ori core was shown to stimulate Py DNA replication by -200to 1000fold (de Villiers et al, 1984). The enhancer contains two cores, designated A and B or a and , (Muller et al, 1983;Veldman et al, 1985). Within the A core there exist binding sequences for the transcription factors AP1/PEAl (Piette and Yaniv, 1987), PEA3 (an Ets family factor; Martin et al, 1988;Wasylyk et al, 1990a;Martin et al, 1992;Xin et al, 1992) /PEBP5 and PEA2 (Piette and Yaniv, 1987) /PEBP2 (Satake et al, 1988;Yamaguchi et al, 1989;Ogawa et al, 1993), each of which contributes to both the stimulation of Py DNA replication and transcription (Muller et al, 1988;Asano et al, 1990;Murakami et al, 1990;Wasylyk et al, 1990b;Guo and DePamphilis, 1992).…”

Section: Introductionmentioning

confidence: 99%

c-Jun stimulates origin-dependent DNA unwinding by polyomavirus large Tantigen.

et al. 1996

View full text Add to dashboard Cite

The AP1 protein c‐Jun has previously been shown to stimulate polyomavirus (Py) DNA replication in vivo. In order to define the mechanism, we added purified c‐Jun protein to the origin‐dependent and large T antigen (LT)‐dependent in vitro DNA unwinding assay. c‐Jun protein was found to stimulate by approximately 5‐fold the unwinding of a 290 bp linear DNA fragment containing both the Py origin and the AP1 recognition sequence to which c‐Jun binds. Efficient levels of stimulation were specifically observed at limiting concentrations of LT for unwinding. Under similar conditions, Py DNA replication was stimulated to a comparable extent by AP1 in a purified in vitro replication assay. Mobility shift and DNase I footprinting assays showed that c‐Jun stimulates the ATP‐dependent binding of LT to the origin core by approximately 7‐fold. Furthermore, c‐Jun was found to interact directly with LT, but not with replication protein A. The activities of c‐Jun to stimulate unwinding and origin binding of LT were found to be harbored within the N‐terminal region of c‐Jun, which is distinct from the DNA binding domain. We speculate that certain transcription factors may possess specific DNA replication domains that function to stimulate the loading of replication factors at the origin during the initiation of DNA synthesis.

show abstract

“…Murine polyomavirus (Py) has been used as a model system to study the genetic requirements of regulatory DNA (enhancers) for cell-specific transcription and DNA replication. Py has two enhancers, A and B, found on the late side of the origin of replication (7,15,27). Numerous consensus sequences and binding sites for cellular trans-acting nuclear factors have been identified within the Py enhancer (for a review, see reference 10).…”

mentioning

confidence: 99%

Polyomavirus DNA replication in the pancreas and in a transformed pancreas cell line has distinct enhancer requirements

Rochford

Villarreal

1991

J Virol

View full text Add to dashboard Cite

The regulatory DNA (enhancer) of polyomavirus (Py) is a major determinant of tissue-specific DNA replication during acute infection of newborn mice. Previously, we reported that the combination of one of the two Py enhancers (A enhancer) and the repeated Moloney murine leukemia virus (Mo-MuLV) enhancer gave a chimeric Py genome (Py-MuLV) that replicates predominantly in the acinar cells of the pancreas, a tissue not permissive for wild-type PyA2 replication (R. Rochford, B. A. Campbell, and L. P. Villareal, Proc. Nat. Acad. Sci. USA 84: [449][450][451][452][453] 1987). In this report, we further examine the combined enhancer requirements for acinar cell-specific Py replication. We also compare enhancer requirements for Py replication in the acinar cells of the pancreas with those of a transformed acinar cell line (266-6 cells). The deletion of sequences within the A enhancer of Py-MuLV (nucleotides 5098 to 5132) results in a virus with 10-fold-reduced levels of pancreasspecific replication. The deletion, however, of one of the 72-bp repeated Mo-MuLV enhancer sequences from Py-MuLV results in a complete loss of pancreas-specific DNA replication. Thus, the Py A enhancer is required for efficient replication of Py in the pancreas without otherwise altering organ specificity, but both of the repeated copies of the Mo-MuLV enhancer are essential for pancreas-specific Py replication. In contrast to the enhancer requirements for in vivo pancreas replication, in transformed acinar cells (266-6), PyA2 wild-type replicated efficiently and the Py-MuLV recombinant replicated inefficiently. These data suggest that the cellspecific control of DNA replication is different between normal pancreas cells and their transformed cell line counterparts and that this difference is apparent in the enhancer requirement of cell-specific Py DNA replication.

show abstract

Polyomavirus origin for DNA replication comprises multiple genetic elements

Cited by 124 publications

References 45 publications

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

c-Jun stimulates origin-dependent DNA unwinding by polyomavirus large Tantigen.

Polyomavirus DNA replication in the pancreas and in a transformed pancreas cell line has distinct enhancer requirements

Contact Info

Product

Resources

About