Abstract:
:To further define the transcriptional regulation of the P38 promoter in the minute virus of mice (MVM) genome, we constructed a series of internal deletion and linker scanning mutations. The mutant P38 constructs were assayed for transcriptional activity in vitro by primer extension analysis with nuclear extracts from murine A92L fibroblasts. Mutations which disrupted the GC box and TATA box severely reduced transcription in vitro. DNase I footprinting analysis confirmed that the murine transcription factor Sp1 bound to the GC box; however, no factors were observed interacting with a putative transcriptional activation regulatory element, termed the TAR element. The linker scanning mutations were analyzed in vivo by using a chloramphenicol acetyltransferase expression assay system, in both the presence and absence of constructs expressing the viral nonstructural protein, NS1. The ability of NS1 to transactivate the P38 promoter (up to 1,000-fold) depended entirely on the presence of intact GC and TATA box sequences. Disruption of the TAR element by either linker insertion mutations or an internal deletion did not inhibit transactivation of the P38 promoter. These results suggest that NS1 transactivates the P38 promoter indirectly by interacting with one or more components of the P38 core-transcription complex.
journal_name
J Viroljournal_title
Journal of virologyauthors
Ahn JK,Pitluk ZW,Ward DCdoi
10.1128/JVI.66.6.3776-3783.1992subject
Has Abstractpub_date
1992-06-01 00:00:00pages
3776-83issue
6eissn
0022-538Xissn
1098-5514journal_volume
66pub_type
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journal_title:Journal of virology
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journal_title:Journal of virology
pub_type: 杂志文章
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pub_type: 杂志文章
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