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cis-acting sequences in the Aleutian mink disease parvovirus late promoter important for transcription: comparison to the canine parvovirus and minute virus of mice
journal contribution
posted on 1993-04-01, 00:00 authored by T Storgaard, J Christensen, B Aasted, Soren AlexandersenSoren AlexandersenWe are currently investigating the regulation of transcription of the Aleutian mink disease parvovirus (ADV). ADV causes a chronic immune complex-mediated condition known as classical Aleutian disease, characterized by slow viral replication. This slow replication is an intrinsic property of ADV and distinguishes it from the more prototypic parvoviruses such as minute virus of mice (MVM) and canine parvovirus (CPV). We have previously suggested a role for the weak ADV promoters in the slow replication and thereby the absence of acute cytopathology and instead establishment of persistent ADV infection with progressive immune complex-mediated chronic lesions. In this study, we have mapped the cis-acting sequences around the ADV P36 promoter responsible for both constitutive transcription and transactivation mediated by the nonstructural protein 1. The mapping was performed by using endpoint deletions of the ADV P36 promoter and by making chimeras between the ADV P36 and MVM P38 promoters. We found the weak constitutive activity of the ADV P36 promoter to be caused by suboptimal promoter proximal sequences, while the low level of transactivation was caused mainly by an upstream region including sequences with homology to the transactivation responsive element (tar) of the H-1 parvovirus (M.-L. Gu, F.-X. Chen, and S. L. Rhode, Virology 187:10-17, 1992). We also found the corresponding regions in the MVM and CPV P38 promoters to be important for transactivation of these promoters by making 5' deletions of the promoter region. In addition, it was found that MVM tar-like and upstream sequences could transfer high nonstructural protein 1 responsiveness to the ADV promoter even though the distance between the tar-like element and the TATA box was significantly changed. On the basis of comparative data for ADV, MVM, CPV, and H-1, a new clustered motif (TTGGTT) is proposed to be the responsive cis-acting element for transactivation. Homology comparison of the specific transcriptional elements of the ADV P36, MVM P38, and CPV P38 promoters suggests that few, but crucial, changes in the ADV P36 promoter and upstream region are responsible for the weak constitutive activity and low level of transactivation of the ADV P36 promoter.
History
Journal
Journal of virologyVolume
67Issue
4Pagination
1887 - 1895Publisher
American Society for MicrobiologyLocation
Washington D.C.ISSN
0022-538XLanguage
engPublication classification
C1.1 Refereed article in a scholarly journalCopyright notice
1993, American Society for MicrobiologyUsage metrics
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No categories selectedKeywords
Aleutian Mink DiseaseAleutian Mink Disease VirusAnimalsBase SequenceCatsCells, CulturedDogsGene Expression Regulation, ViralIn Vitro TechniquesMinute Virus of MiceMolecular Sequence DataParvoviridaePromoter Regions, GeneticRNA, MessengerRNA, ViralRegulatory Sequences, Nucleic AcidSequence AlignmentSequence DeletionStructure-Activity RelationshipTranscription, GeneticTranscriptional ActivationScience & TechnologyLife Sciences & BiomedicineVirologyTRANS-ACTIVATIONNUCLEOTIDE-SEQUENCEP38 PROMOTERINTERSTITIAL PNEUMONIAAUTONOMOUS PARVOVIRUSVIRAL REPLICATIONENTERITIS VIRUSINFECTIONPROTEINKITS
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