trans-Activation of parvovirus P38 promoter by the 76K noncapsid protein

Rhode, Solon L.

doi:10.1128/jvi.55.3.886-889.1985

Cited by 126 publications

(101 citation statements)

References 33 publications

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“…The most striking observation from the in vivo experiments was that deletion of a 46-bp fragment (-167 to -121, nt 1838 to 1884) containing the 30-bp TAR motif resulted in a threeto eightfold increase in transcription over the wild-type promoter. Given the reports on trans activation of P38 by the viral NS proteins in both H-1 virus (21,24) and MVM(i) (10), these data suggested that trans activation might be due to the relief of repression rather than to positive regulation. Furthermore, the proximity of the TAR element to the CCAAT box and the demonstrated functionality of the CCAAT motif in the fully active (derepressed) promoter in vivo, suggest that repression at P38 may be mediated through this sequence.…”

Section: Discussionmentioning

confidence: 72%

“…Although the majority of the viral message (65 to 70%) in a productive infection is transcribed from the P38 promoter, the cloned P38 promoter has proven to be relatively weak both in vivo and in vitro, while the cloned P4 promoter is quite strong (1). This apparent paradox has been resolved by recent findings which demonstrate that the NS proteins of the autonomous parvoviruses activate the P38 promoter in trans, apparently by increasing the rate of transcription (10,21,24). This type of genomic organization suggested a classic early-to-late switch in viral gene expression; however, evidence that the appearance of viral mRNA coding for the NS proteins precedes viral capsid mRNAs has only recently been presented (8).…”

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confidence: 99%

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Positive and negative regulation of the minute virus of mice P38 promoter

Gavin

Ward

1990

J Virol

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mutants of the minute virus of mice P38 promoter were constructed and analyzed for transcriptional activity in vitro and in vivo. In uninfected mouse A9 cell extracts, 107 base pairs upstream of the RNA start sites are required for optimal activity. Within this region, the only readily recognizable cis-acting control elements are a GC box and a TATA box. However, in infected cell extracts, deletion of a sequence between -167 and -121, which shares homology with the 30-base-pair trans-activation region (TAR) of H-1 virus (S. L. Rhode and S. M. Richard, J. Virol. 61:2807-2815, 1987, results in a threeto fourfold decrease in transcriptional activity. Interestingly, in vivo transfection experiments demonstrate a threeto eightfold increase in transcription relative to the wild-type promoter when the TAR element homology region is deleted and reveal a functional role for a CCAAT motif which lies immediately downstream of the TAR element. These results indicate both positive and negative regulation of the P_u promoter.

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Section: Discussionmentioning

confidence: 72%

mentioning

confidence: 99%

Positive and negative regulation of the minute virus of mice P38 promoter

Gavin

Ward

1990

J Virol

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“…The growth medium was replaced with MEM containing 10% dialyzed serum 12 h before the addition of 20 ,uCi of [35S]methionine (1,000 Ci/mmol; New England Nuclear Corp., Boston, Mass.) per ml, and lysates were prepared 24 h after the addition of the isotope. The serum used as the first antibody was anticapsid antibody (rabbit 0118) or serum from a calf experimentally infected and immunized with BPV (calf 86).…”

Section: Methodsmentioning

confidence: 99%

Genomic clones of bovine parvovirus: construction and effect of deletions and terminal sequence inversions on infectivity

Shull

Chen

Lederman

et al. 1988

J Virol

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Genomic clones of the autonomous parvovirus bovine parvovirus (BPV) were constructed by blunt-end ligation of reannealed virion plus and minus DNA strands into the plasmid pUC8. These clones were stable during propagation in Escherichia coli JM107. All clones tested were found to be infectious by the criteria of plaque titer and progressive cytopathic effect after transfection into bovine fetal lung cells. Sequencing of the recombinant plasmids demonstrated that all of the BPV inserts had left-end (3')-terminal deletions of up to 34 bases. DNA isolated from progeny virions arising from transfected infectious clones was found to be indistinguishable from wild-type DNA by restriction enzyme analysis. Defective genomes could also be detected in the progeny DNA even though the infection was initiated with homogenous, cloned DNA. Full-length genomic clones with 3' flip and 3' flop conformations were constructed and were found to have equal infectivity. Analysis of low-molecular-weight DNA isolated from lysates of cells transfected with these clones demonstrated that rescue and replication of BPV DNA could be detected 3 to 8 days after transfection. Expression of capsid proteins from transfected genomes was demonstrated by hemagglutination, indirect immunofluorescence, and immunoprecipitation of [35S]methionine-labeled cell lysates. Use of appropriate antiserum for immunoprecipitation showed the synthesis of BPV capsid and noncapsid proteins after transfection. Independently, a series of genomic clones with increasingly larger 3'-terminal deletions was prepared from separately subcloned 3'-terminal fragments. Transfection of these clones into bovine fetal lung cells revealed that deletions of up to 34 bases at the 3' end lowered but did not abolish infectivity, while deletions of greater than 52 bases were lethal. End-label analysis showed that the 34-base deletion was repaired to wild-type length in the progeny virus.

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“…According to recent studies one or more of the nonstructural proteins of AAV are involved in trans-regulation of AAV gene expression [24,25]. Finally, Rhode [26] has shown that the P38 promoter of the parvovirus H-1 is transactivated by the NS-1 protein.…”

Section: Structure and Organization Of The Genomementioning

confidence: 99%

Parvoviruses: agents of distinct pathogenic and molecular potential

Siegl

Tratschin

1987

FEMS Microbiology Letters

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Parvoviruses are small, spherical and extremely stable particles with a genome of linear single‐stranded DNA. They are widespread in nature and thus have been in virtually every animal species and in man. Many parvoviruses were initially isolated by chance and could not be associated with clinical disease. Today, however, a considerable number of these agents are known to cause a broad spectrum of syndromes including fetal death, malformations, dwarfism, cerebellar hypolasia and ataxia, enteritis, panleukopenia, aplastic anemia, and immunologic disorders. Biological, pathological, and molecular studies revealed that all these syndromes are explainable on the basis of two predominant requirements for productive cytolytic parvovirus replication: the availability of cellular helper function(s) provided exclusively by mitotically active cells in the phase of cellular DNA replication, and by apparently specific, yet so far undefined cellular functions

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trans-Activation of parvovirus P38 promoter by the 76K noncapsid protein

Cited by 126 publications

References 33 publications

Positive and negative regulation of the minute virus of mice P38 promoter

Positive and negative regulation of the minute virus of mice P38 promoter

Genomic clones of bovine parvovirus: construction and effect of deletions and terminal sequence inversions on infectivity

Parvoviruses: agents of distinct pathogenic and molecular potential

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