A region of the polyoma virus genome between the replication origin and late protein coding sequences is required in cis for both early gene expression and viral DNA replication

Tyndall, Chiara; Mantia, Girolama La; Thacker, Colin; Favaloro, Jenny M.; Kamen, Robert

doi:10.1093/nar/9.23.6231

Cited by 302 publications

(221 citation statements)

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“…Viral enhancers were originally identified in SV40 and polyoma virus as "far-upstream" promoter elements required for efficient early transcription (Benoist and Chambon, 1981;Gruss et al, 1981;Fromm and Berg, 1982;Tyndall et al, 1981). More recently, enhancer elements have been found in a variety of other viruses (reviewed in Gluzman and Shenk, 1983;Gruss, 1984;Picard, 1985).…”

Section: Introductionmentioning

confidence: 99%

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Boshart

Weber

Jahn

et al. 1985

Cell

1,091

648

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SummaryA strong transcription enhancer was identified in the genomic DNA (235 kb) of human cytomegalovirus (HCMV), a ubiquitous and severe pathogen of the herpesvirus group. Cotransfection of enhancerless SV40 DNA with randomly fragmented HCMV DNA yielded two SV40-HCMV recombinant viruses that had incorporated overlapping segments of HCMV DNA to substitute for the missing SV40 enhancer. Within HCMV, these enhancer sequences are located upstream of the transcription initiation site of the major immediate-early gene, between nucleotides -118 and -524. Deletion studies with the HCMV enhancer, which harbors a variety of repeated sequence motifs, show that different subsets of this enhancer can substitute for the SV40 enhancer. The HCMV enhancer, which seems to have little cell type or species preference, is severalfold more active than the SV40 enhancer. It is the strongest enhancer we have analyzed so far, a property that makes it a useful component of eukaryotic expression vectors.

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Section: Introductionmentioning

confidence: 99%

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Boshart

Weber

Jahn

et al. 1985

Cell

1,091

648

View full text Add to dashboard Cite

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“…Several reports about proteins interacting with enhancer sequences have been published recently (16,17,18,19,20,21). The enhancer of polyoma virus that is studied here is necessary both for transcription from the early promoter and for the replication of viral DNA (22,23,24). It could be subdivided into two fragments conserving partial activity: the PvuII-BclI fragment or A enhancer and the PvuII-4 fragment or B enhancer (25).…”

Section: Intkroduionmentioning

confidence: 99%

Molecular analysis of the interaction between an enhancer binding factor and its DNA target

Piette

Yaniv

1986

Nucl Acids Res

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ABSTRATTIei fine contacts of a mouse nuclear factor, called PEB1, with the B enhancer of polyoma virus were analyzed. It protects against DNaseI attack a region of about 50 base pairs that can be divided in two domains. The first contains a GC-rich palindrome and the homology to the SV40 enhancer. The second is homologous to a sequence in the immunoglobulin (Ig) heavy chain gene enhancer. Methylation interference and protection experiments reveal strong specific contacts only with a purine rich track on the late coding strand of the early proximal part of the palindrome. Deletion analysis show that the minimal sequences necessary for binding include only the first domain. The Ig homology contributes only weakly to the binding. The minimal core is similar to the core of the B enhancer defined in vivo. The interactions we observe here are reminiscent of those of TFIIIA positive transcription factor and the 5SRNA gene of Xenopus. INTKRODUIONDNA-protein interactions play an essential role in the regulation of gene expression and DNA replication. Characterization of these interactions can help unravel the mechanisms involved in these processes. Repressor-operator interactions in prokaryotes were the first to be analyzed in great detail: in essence, a repressor dimer interacts with both parts of a palindromic sequence in a symmetric way; a conserved c-helix-turn-a-helix motif fits into the large groove of right-handed B-DNA (1). This model was found to be applicable to activator proteins like the CAP protein (2) or even yeast proteins involved in mating type control (3).In higher eukaryotes only a few cases of specific DNA-protein interactions have been studied in detail so far. The positive transcription factor TF III A of Xenopus laevis contacts the DNA mainly along the non coding strand (4) and the helical configuration of the DNA may be altered by this binding (5). Knowledge of the primary structure of the protein has led to a model in which small Zn++ binding, fingerlike domains interact with the DNA in a way quite different from bacterial repressors or activators (6). Another

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“…Recombinants carrying polyoma virus DNA produced slightly higher numbers of colonies compared to vector DNA alone. This is most probably due to the effect of polyoma virus enhancer elements (De Villiers & Schaffner, 1981 ;Tyndall et al, 1981 ;Herbomel et al, 1984) present in these constructs which function only weakly in the Chinese hamster cells. Since transformation frequencies correlate with enhancer activity in so many systems (Spandidos & Wilkie, 1983, 1984b and references therein), we take this to be a measure of enhancer function.…”

Section: (Accepted 23 January 1986)mentioning

confidence: 99%

Polyoma Virus Middle T Gene Can Trigger Malignant Transformation of Early Passage Rodent Cells

Spandidos

Riggio

1986

Journal of General Virology

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A region of the polyoma virus genome between the replication origin and late protein coding sequences is required in cis for both early gene expression and viral DNA replication

Cited by 302 publications

References 51 publications

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

A very strong enhancer is located upstream of an immediate early gene of human cytomegalovirus

Molecular analysis of the interaction between an enhancer binding factor and its DNA target

Polyoma Virus Middle T Gene Can Trigger Malignant Transformation of Early Passage Rodent Cells

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