cis-acting sequences that control the level of viral DNA synthesis in the polyomavirus late region

Melucci-Vigo, Gianna; Ciotta, Carmela; Risuleo, Gianfranco

doi:10.1128/jvi.63.11.4979-4981.1989

Cited by 7 publications

(2 citation statements)

References 17 publications

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“…These mutated Py-RR determine by themselves the ability of the virus to replicate in the nonpermissive cells, except for the mutant carrying the shortest duplication (30 base pairs). This mutant displays a second mutation in the region defined by Melucci-Vigo et al (20), which causes the virus to lose its ability to replicate in myoblasts, when separated from the duplicated regulatory region by in vitro recombination.…”

Section: Resultsmentioning

confidence: 99%

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Maione

Felsani

Pozzi

et al. 1989

J Virol

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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...

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Section: Resultsmentioning

confidence: 99%

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Maione

Felsani

Pozzi

et al. 1989

J Virol

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“…Despite this result, however, we cannot rule out the possibility that the 6-bp deletion may alter a viral regulatory region. In this context, Melucci-Vigo et al (22) have shown that consistent alterations (deletion or substitutions) of a large fragment (1,165 bp) of the late coding region inhibit Py DNA replication in a cis-dominant manner. We show here that a similar deletion (spanning nt 3627 to 3632) occurs in the VP1 coding region of the PyMB27 mutant, which displays a wt RR.…”

Section: Discussionmentioning

confidence: 99%

Mutations in the VP1 coding region of polyomavirus determine differentiating stage specificity

Ricci

Maione

Passananti

et al. 1992

J Virol

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Polyomavirus mutants capable of replicating in undifferentiated murine C2 myoblasts were selected and characterized. These mutants grow normally in 3T6 mouse fibroblast cells, and they do not complement the wild-type virus in coinfection experiments of C2 myoblasts. Of 12 isolates, 10 possess duplications of the regulatory region including the enhancer A domain. On the bases of the regulatory region structure and the presence and length of the enhancer duplication, the mutant viruses could be grouped into three classes. One mutant class (e.g., PyMB3) possesses an enhancer duplication of 91 bp identical to that of a previously characterized polyomavirus mutant, PyNB11/1. We have demonstrated that this enhancer duplication gives rise at its junction to a novel recognition motif for the transcriptional factor NF-1 (M. Caruso, C. Iacobini, C.

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Mouse polyomavirus late region mutants expressing a defective VP2 capsid protein exhibit an enhanced viral DNA replication

1994

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We have constructed mouse polyomavirus mutants with deletions or insertions in the late region. These viral constructs exhibit two different phenotypes, characterized by a differential replication ability. The first type shows a twofold higher level of DNA synthesis with respect to wild type, while mutants of the second type are virtually unable to replicate. In this paper we investigate the replicative behavior of the first class of mutants, which expresses defective viral coat proteins. Our data raise the possibility that, of the three late gene viral products, VP2 is involved in the formation of an encapsidation intermediate that, in an indirect fashion, affects the rate of viral DNA synthesis.

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cis-acting sequences that control the level of viral DNA synthesis in the polyomavirus late region

Abstract: A deletion in the polyomavirus late region results in a drastic reduction of viral replication, as shown after transfection of viral DNA into 3T6 cells. This mutation is cis acting, since cotransfection with wild-type DNA

Cited by 7 publications

References 17 publications

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Polyomavirus genome and polyomavirus enhancer-driven gene expression during myogenesis

Mutations in the VP1 coding region of polyomavirus determine differentiating stage specificity

Mouse polyomavirus late region mutants expressing a defective VP2 capsid protein exhibit an enhanced viral DNA replication

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